Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis

Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the ear...
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Autor*in:	Miura, Arisa [verfasserIn] Hino, Hirofumi [verfasserIn] Uchida, Kazuhide [verfasserIn] Inoue, Soichiro [verfasserIn] Tateda, Takeshi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Sepsis Critical illness polyneuropathy Nerve conduction study Threshold

Übergeordnetes Werk:	Enthalten in: Journal of anesthesia - Tokyo, 1987, 30(2016), 6 vom: 09. Sept., Seite 961-969
Übergeordnetes Werk:	volume:30 ; year:2016 ; number:6 ; day:09 ; month:09 ; pages:961-969

Links:	Volltext

DOI / URN:	10.1007/s00540-016-2247-5

Katalog-ID:	SPR006800440

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245	1	0	\|a Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
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520			\|a Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment.
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700	1		\|a Uchida, Kazuhide \|e verfasserin \|4 aut
700	1		\|a Inoue, Soichiro \|e verfasserin \|4 aut
700	1		\|a Tateda, Takeshi \|e verfasserin \|4 aut
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author_variant	a m am h h hh k u ku s i si t t tt
matchkey_str	article:14388359:2016----::eihrlevcnutoanraiisrcdmrhlgclleainiae
hierarchy_sort_str	2016
bklnumber	44.66
publishDate	2016
allfields	10.1007/s00540-016-2247-5 doi (DE-627)SPR006800440 (SPR)s00540-016-2247-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.66 bkl Miura, Arisa verfasserin aut Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment. Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213 Hino, Hirofumi verfasserin aut Uchida, Kazuhide verfasserin aut Inoue, Soichiro verfasserin aut Tateda, Takeshi verfasserin aut Enthalten in Journal of anesthesia Tokyo, 1987 30(2016), 6 vom: 09. Sept., Seite 961-969 (DE-627)300185065 (DE-600)1481564-3 1438-8359 nnns volume:30 year:2016 number:6 day:09 month:09 pages:961-969 https://dx.doi.org/10.1007/s00540-016-2247-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.66 ASE AR 30 2016 6 09 09 961-969
spelling	10.1007/s00540-016-2247-5 doi (DE-627)SPR006800440 (SPR)s00540-016-2247-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.66 bkl Miura, Arisa verfasserin aut Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment. Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213 Hino, Hirofumi verfasserin aut Uchida, Kazuhide verfasserin aut Inoue, Soichiro verfasserin aut Tateda, Takeshi verfasserin aut Enthalten in Journal of anesthesia Tokyo, 1987 30(2016), 6 vom: 09. Sept., Seite 961-969 (DE-627)300185065 (DE-600)1481564-3 1438-8359 nnns volume:30 year:2016 number:6 day:09 month:09 pages:961-969 https://dx.doi.org/10.1007/s00540-016-2247-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.66 ASE AR 30 2016 6 09 09 961-969
allfields_unstemmed	10.1007/s00540-016-2247-5 doi (DE-627)SPR006800440 (SPR)s00540-016-2247-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.66 bkl Miura, Arisa verfasserin aut Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment. Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213 Hino, Hirofumi verfasserin aut Uchida, Kazuhide verfasserin aut Inoue, Soichiro verfasserin aut Tateda, Takeshi verfasserin aut Enthalten in Journal of anesthesia Tokyo, 1987 30(2016), 6 vom: 09. Sept., Seite 961-969 (DE-627)300185065 (DE-600)1481564-3 1438-8359 nnns volume:30 year:2016 number:6 day:09 month:09 pages:961-969 https://dx.doi.org/10.1007/s00540-016-2247-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.66 ASE AR 30 2016 6 09 09 961-969
allfieldsGer	10.1007/s00540-016-2247-5 doi (DE-627)SPR006800440 (SPR)s00540-016-2247-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.66 bkl Miura, Arisa verfasserin aut Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment. Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213 Hino, Hirofumi verfasserin aut Uchida, Kazuhide verfasserin aut Inoue, Soichiro verfasserin aut Tateda, Takeshi verfasserin aut Enthalten in Journal of anesthesia Tokyo, 1987 30(2016), 6 vom: 09. Sept., Seite 961-969 (DE-627)300185065 (DE-600)1481564-3 1438-8359 nnns volume:30 year:2016 number:6 day:09 month:09 pages:961-969 https://dx.doi.org/10.1007/s00540-016-2247-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.66 ASE AR 30 2016 6 09 09 961-969
allfieldsSound	10.1007/s00540-016-2247-5 doi (DE-627)SPR006800440 (SPR)s00540-016-2247-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.66 bkl Miura, Arisa verfasserin aut Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment. Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213 Hino, Hirofumi verfasserin aut Uchida, Kazuhide verfasserin aut Inoue, Soichiro verfasserin aut Tateda, Takeshi verfasserin aut Enthalten in Journal of anesthesia Tokyo, 1987 30(2016), 6 vom: 09. Sept., Seite 961-969 (DE-627)300185065 (DE-600)1481564-3 1438-8359 nnns volume:30 year:2016 number:6 day:09 month:09 pages:961-969 https://dx.doi.org/10.1007/s00540-016-2247-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.66 ASE AR 30 2016 6 09 09 961-969
language	English
source	Enthalten in Journal of anesthesia 30(2016), 6 vom: 09. Sept., Seite 961-969 volume:30 year:2016 number:6 day:09 month:09 pages:961-969
sourceStr	Enthalten in Journal of anesthesia 30(2016), 6 vom: 09. Sept., Seite 961-969 volume:30 year:2016 number:6 day:09 month:09 pages:961-969
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Sepsis Critical illness polyneuropathy Nerve conduction study Threshold
dewey-raw	610
isfreeaccess_bool	false
container_title	Journal of anesthesia
authorswithroles_txt_mv	Miura, Arisa @@aut@@ Hino, Hirofumi @@aut@@ Uchida, Kazuhide @@aut@@ Inoue, Soichiro @@aut@@ Tateda, Takeshi @@aut@@
publishDateDaySort_date	2016-09-09T00:00:00Z
hierarchy_top_id	300185065
dewey-sort	3610
id	SPR006800440
language_de	englisch
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In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. 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author	Miura, Arisa
spellingShingle	Miura, Arisa ddc 610 bkl 44.66 misc Sepsis misc Critical illness polyneuropathy misc Nerve conduction study misc Threshold Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
authorStr	Miura, Arisa
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topic_title	610 ASE 44.66 bkl Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis Sepsis (dpeaa)DE-He213 Critical illness polyneuropathy (dpeaa)DE-He213 Nerve conduction study (dpeaa)DE-He213 Threshold (dpeaa)DE-He213
topic	ddc 610 bkl 44.66 misc Sepsis misc Critical illness polyneuropathy misc Nerve conduction study misc Threshold
topic_unstemmed	ddc 610 bkl 44.66 misc Sepsis misc Critical illness polyneuropathy misc Nerve conduction study misc Threshold
topic_browse	ddc 610 bkl 44.66 misc Sepsis misc Critical illness polyneuropathy misc Nerve conduction study misc Threshold
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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title	Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
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title_full	Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
author_sort	Miura, Arisa
journal	Journal of anesthesia
journalStr	Journal of anesthesia
lang_code	eng
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author_browse	Miura, Arisa Hino, Hirofumi Uchida, Kazuhide Inoue, Soichiro Tateda, Takeshi
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author-letter	Miura, Arisa
doi_str_mv	10.1007/s00540-016-2247-5
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author2-role	verfasserin
title_sort	peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
title_auth	Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
abstract	Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment.
abstractGer	Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment.
abstract_unstemmed	Purpose The pathological mechanisms of critical illness polyneuropathy (CIP), an acute neuromuscular disorder, remain unknown. In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. Conclusions Our findings suggest that primary electrophysiological deterioration is due to threshold alterations rather than morphological alterations after 48 h of LPS treatment.
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container_issue	6
title_short	Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis
url	https://dx.doi.org/10.1007/s00540-016-2247-5
remote_bool	true
author2	Hino, Hirofumi Uchida, Kazuhide Inoue, Soichiro Tateda, Takeshi
author2Str	Hino, Hirofumi Uchida, Kazuhide Inoue, Soichiro Tateda, Takeshi
ppnlink	300185065
mediatype_str_mv	c
isOA_txt	false
hochschulschrift_bool	false
doi_str	10.1007/s00540-016-2247-5
up_date	2024-07-04T00:44:02.437Z
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In this study, we evaluated nerve and vascular properties that might account for electrophysiological abnormalities, including reduced nerve conduction amplitude, in the early phase of CIP. Methods Rats were administered intravenous saline (C-group; n = 31) or lipopolysaccharide (3 mg/kg/day; L-group; n = 30) for 48 h. Subsequently, tracheotomy was performed and sciatic nerves exposed bilaterally. A catheter was inserted into the left internal carotid artery to measure the mean arterial pressure (MAP). Nerve conduction velocity (NCV), nerve blood flow (NBF), evoked amplitudes, chronaxie, rheobase, and the absolute refractory period (ARP) were measured from the sciatic nerves. Degeneration, myelination, and neutrophil infiltration were examined in the sciatic nerves using histology and electron microscopy. Results The NBF (C-group 25 ± 3 ml/100 g/min, L-group 13 ± 3 ml/100 g/min, p < 0.001) was lower in the L-group, but the MAP was similar between groups (C-group 119 ± 17 mmHg, L-group 115 ± 18 mmHg, p = 0.773). LPS also caused a severe reduction in amplitude (C-group 0.9 ± 0.2 mV, L-group 0.2 ± 0.1 mV, p < 0.001), while latency and NCV were not affected. Of note, response amplitudes partially recovered with an increase in stimulus intensity. LPS treatment increased the rheobase and decreased the chronaxie (rheobase: C vs L-group; 0.35 ± 0.07 vs 1.29 ± 0.66 mA, p < 0.001; chronaxie 171 ± 24 vs 42 ± 20 µs, p < 0.001), while ARP was unchanged. No primary axonal degeneration or inflammatory infiltration was observed. 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Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis

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