Mechanisms of collateral development and hemodynamics of gradual coronary occlusion

Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Scheel, K. W. [verfasserIn] Granger, H. J. [verfasserIn] Brody, D. A. [verfasserIn] Keller, F. W. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	1974

Schlagwörter:	Coronary Flow Coronary Reserve Flow Peripheral Vasculature Coronary Reserve Collateral Growth

Übergeordnetes Werk:	Enthalten in: Basic research in cardiology - [Darmstadt u.a.] : Steinkopff, 1937, 69(1974), 4 vom: 01. Juli, Seite 338-360
Übergeordnetes Werk:	volume:69 ; year:1974 ; number:4 ; day:01 ; month:07 ; pages:338-360

Links:	Volltext

DOI / URN:	10.1007/BF01905940

Katalog-ID:	SPR004883993

Internformat


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245	1	0	\|a Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
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520			\|a Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired.
650		4	\|a Coronary Flow \|7 (dpeaa)DE-He213
650		4	\|a Coronary Reserve Flow \|7 (dpeaa)DE-He213
650		4	\|a Peripheral Vasculature \|7 (dpeaa)DE-He213
650		4	\|a Coronary Reserve \|7 (dpeaa)DE-He213
650		4	\|a Collateral Growth \|7 (dpeaa)DE-He213
700	1		\|a Granger, H. J. \|e verfasserin \|4 aut
700	1		\|a Brody, D. A. \|e verfasserin \|4 aut
700	1		\|a Keller, F. W. \|e verfasserin \|4 aut
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912			\|a GBV_ILN_2093
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2107
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952			\|d 69 \|j 1974 \|e 4 \|b 01 \|c 07 \|h 338-360

Indexfelder

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matchkey_str	article:14351803:1974----::ehnssfoltrleeomnadeoyaisfrd
hierarchy_sort_str	1974
bklnumber	44.85
publishDate	1974
allfields	10.1007/BF01905940 doi (DE-627)SPR004883993 (SPR)BF01905940-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Scheel, K. W. verfasserin aut Mechanisms of collateral development and hemodynamics of gradual coronary occlusion 1974 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired. Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213 Granger, H. J. verfasserin aut Brody, D. A. verfasserin aut Keller, F. W. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 69(1974), 4 vom: 01. Juli, Seite 338-360 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:69 year:1974 number:4 day:01 month:07 pages:338-360 https://dx.doi.org/10.1007/BF01905940 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_224 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 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_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_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 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_2808 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 44.85 ASE AR 69 1974 4 01 07 338-360
spelling	10.1007/BF01905940 doi (DE-627)SPR004883993 (SPR)BF01905940-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Scheel, K. W. verfasserin aut Mechanisms of collateral development and hemodynamics of gradual coronary occlusion 1974 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired. Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213 Granger, H. J. verfasserin aut Brody, D. A. verfasserin aut Keller, F. W. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 69(1974), 4 vom: 01. Juli, Seite 338-360 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:69 year:1974 number:4 day:01 month:07 pages:338-360 https://dx.doi.org/10.1007/BF01905940 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_224 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 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_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_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 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_2808 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 44.85 ASE AR 69 1974 4 01 07 338-360
allfields_unstemmed	10.1007/BF01905940 doi (DE-627)SPR004883993 (SPR)BF01905940-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Scheel, K. W. verfasserin aut Mechanisms of collateral development and hemodynamics of gradual coronary occlusion 1974 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired. Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213 Granger, H. J. verfasserin aut Brody, D. A. verfasserin aut Keller, F. W. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 69(1974), 4 vom: 01. Juli, Seite 338-360 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:69 year:1974 number:4 day:01 month:07 pages:338-360 https://dx.doi.org/10.1007/BF01905940 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_224 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 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_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_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 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_2808 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 44.85 ASE AR 69 1974 4 01 07 338-360
allfieldsGer	10.1007/BF01905940 doi (DE-627)SPR004883993 (SPR)BF01905940-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Scheel, K. W. verfasserin aut Mechanisms of collateral development and hemodynamics of gradual coronary occlusion 1974 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired. Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213 Granger, H. J. verfasserin aut Brody, D. A. verfasserin aut Keller, F. W. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 69(1974), 4 vom: 01. Juli, Seite 338-360 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:69 year:1974 number:4 day:01 month:07 pages:338-360 https://dx.doi.org/10.1007/BF01905940 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_224 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 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_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_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 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_2808 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 44.85 ASE AR 69 1974 4 01 07 338-360
allfieldsSound	10.1007/BF01905940 doi (DE-627)SPR004883993 (SPR)BF01905940-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Scheel, K. W. verfasserin aut Mechanisms of collateral development and hemodynamics of gradual coronary occlusion 1974 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired. Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213 Granger, H. J. verfasserin aut Brody, D. A. verfasserin aut Keller, F. W. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 69(1974), 4 vom: 01. Juli, Seite 338-360 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:69 year:1974 number:4 day:01 month:07 pages:338-360 https://dx.doi.org/10.1007/BF01905940 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_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_224 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 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_2018 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_2043 GBV_ILN_2044 GBV_ILN_2048 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_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_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 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_2808 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 44.85 ASE AR 69 1974 4 01 07 338-360
language	English
source	Enthalten in Basic research in cardiology 69(1974), 4 vom: 01. Juli, Seite 338-360 volume:69 year:1974 number:4 day:01 month:07 pages:338-360
sourceStr	Enthalten in Basic research in cardiology 69(1974), 4 vom: 01. Juli, Seite 338-360 volume:69 year:1974 number:4 day:01 month:07 pages:338-360
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Coronary Flow Coronary Reserve Flow Peripheral Vasculature Coronary Reserve Collateral Growth
dewey-raw	610
isfreeaccess_bool	false
container_title	Basic research in cardiology
authorswithroles_txt_mv	Scheel, K. W. @@aut@@ Granger, H. J. @@aut@@ Brody, D. A. @@aut@@ Keller, F. W. @@aut@@
publishDateDaySort_date	1974-07-01T00:00:00Z
hierarchy_top_id	253390265
dewey-sort	3610
id	SPR004883993
language_de	englisch
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W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Mechanisms of collateral development and hemodynamics of gradual coronary occlusion</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1974</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. 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author	Scheel, K. W.
spellingShingle	Scheel, K. W. ddc 610 bkl 44.85 misc Coronary Flow misc Coronary Reserve Flow misc Peripheral Vasculature misc Coronary Reserve misc Collateral Growth Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
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topic_title	610 ASE 44.85 bkl Mechanisms of collateral development and hemodynamics of gradual coronary occlusion Coronary Flow (dpeaa)DE-He213 Coronary Reserve Flow (dpeaa)DE-He213 Peripheral Vasculature (dpeaa)DE-He213 Coronary Reserve (dpeaa)DE-He213 Collateral Growth (dpeaa)DE-He213
topic	ddc 610 bkl 44.85 misc Coronary Flow misc Coronary Reserve Flow misc Peripheral Vasculature misc Coronary Reserve misc Collateral Growth
topic_unstemmed	ddc 610 bkl 44.85 misc Coronary Flow misc Coronary Reserve Flow misc Peripheral Vasculature misc Coronary Reserve misc Collateral Growth
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title	Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
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title_full	Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
author_sort	Scheel, K. W.
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author_browse	Scheel, K. W. Granger, H. J. Brody, D. A. Keller, F. W.
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title_sort	mechanisms of collateral development and hemodynamics of gradual coronary occlusion
title_auth	Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
abstract	Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired.
abstractGer	Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired.
abstract_unstemmed	Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. It was concluded that neither ischemia nor a pressure differential can solely account for collateral development It is believed that ischemia begins the collateral growth process and it is sustained by the pressure differential (or some manifestation thereof) during the post-ischemic phase. Assumption 2 is most consistent with both physiological and clinical data. The autoregulatory capacity of the peripheral coronary bed allows a constriction of 76% before the resting coronary flow is impaired.
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title_short	Mechanisms of collateral development and hemodynamics of gradual coronary occlusion
url	https://dx.doi.org/10.1007/BF01905940
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W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Mechanisms of collateral development and hemodynamics of gradual coronary occlusion</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1974</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The mechanisms for development of collaterals following a gradual occlusion (Ameroid technique) of one the coronary arteries in the dog were investigated. A control systems approach, based on quantitative experimental data, was utilized. The peripheral coronary pressure, peripheral coronary flow, coronary reserve flow, collateral resistance, peripheral coronary resistance, oxygen availability and demand were among the parameters studied. These variables were followed through the preocclusion phase, occlusion phase, ischemic phase, and post-ischemic phase of a gradual coronary constriction. The simulation studies were examined for the following basic assumptions: 1) ischemia is the sole stimulus for collateral development, 2) the peripheral coronary vasculature exhibits autoregulation and the peripheral coronary resistance increases during ischemia, 3) autoregulation occurs but during ischemia the peripheral vasculature remains maximally dilated without increase in resistance, and 4) the peripheral coronary vasculature is non-autoregulatory. 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Mechanisms of collateral development and hemodynamics of gradual coronary occlusion

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