Clinical review: Vasopressin and terlipressin in septic shock patients

Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopr...
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Autor*in:	Delmas, Anne [verfasserIn] Leone, Marc Rousseau, Sébastien Albanèse, Jacques Martin, Claude

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2004

Schlagwörter:	catecholamines diuresis mesenteric circulation noradrenaline (norepinephrine) renal function septic shock shock vasopressin

Anmerkung:	© BioMed Central Ltd 2004

Übergeordnetes Werk:	Enthalten in: Critical care - London : BioMed Central, 1997, 9(2004), 2 vom: 09. Sept.
Übergeordnetes Werk:	volume:9 ; year:2004 ; number:2 ; day:09 ; month:09

Links:	Volltext

DOI / URN:	10.1186/cc2945

Katalog-ID:	SPR029762618

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520			\|a Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock.
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allfields	10.1186/cc2945 doi (DE-627)SPR029762618 (SPR)cc2945-e DE-627 ger DE-627 rakwb eng Delmas, Anne verfasserin aut Clinical review: Vasopressin and terlipressin in septic shock patients 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2004 Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213 Leone, Marc aut Rousseau, Sébastien aut Albanèse, Jacques aut Martin, Claude aut Enthalten in Critical care London : BioMed Central, 1997 9(2004), 2 vom: 09. Sept. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:9 year:2004 number:2 day:09 month:09 https://dx.doi.org/10.1186/cc2945 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2004 2 09 09
spelling	10.1186/cc2945 doi (DE-627)SPR029762618 (SPR)cc2945-e DE-627 ger DE-627 rakwb eng Delmas, Anne verfasserin aut Clinical review: Vasopressin and terlipressin in septic shock patients 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2004 Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213 Leone, Marc aut Rousseau, Sébastien aut Albanèse, Jacques aut Martin, Claude aut Enthalten in Critical care London : BioMed Central, 1997 9(2004), 2 vom: 09. Sept. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:9 year:2004 number:2 day:09 month:09 https://dx.doi.org/10.1186/cc2945 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2004 2 09 09
allfields_unstemmed	10.1186/cc2945 doi (DE-627)SPR029762618 (SPR)cc2945-e DE-627 ger DE-627 rakwb eng Delmas, Anne verfasserin aut Clinical review: Vasopressin and terlipressin in septic shock patients 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2004 Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213 Leone, Marc aut Rousseau, Sébastien aut Albanèse, Jacques aut Martin, Claude aut Enthalten in Critical care London : BioMed Central, 1997 9(2004), 2 vom: 09. Sept. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:9 year:2004 number:2 day:09 month:09 https://dx.doi.org/10.1186/cc2945 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2004 2 09 09
allfieldsGer	10.1186/cc2945 doi (DE-627)SPR029762618 (SPR)cc2945-e DE-627 ger DE-627 rakwb eng Delmas, Anne verfasserin aut Clinical review: Vasopressin and terlipressin in septic shock patients 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2004 Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213 Leone, Marc aut Rousseau, Sébastien aut Albanèse, Jacques aut Martin, Claude aut Enthalten in Critical care London : BioMed Central, 1997 9(2004), 2 vom: 09. Sept. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:9 year:2004 number:2 day:09 month:09 https://dx.doi.org/10.1186/cc2945 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2004 2 09 09
allfieldsSound	10.1186/cc2945 doi (DE-627)SPR029762618 (SPR)cc2945-e DE-627 ger DE-627 rakwb eng Delmas, Anne verfasserin aut Clinical review: Vasopressin and terlipressin in septic shock patients 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2004 Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213 Leone, Marc aut Rousseau, Sébastien aut Albanèse, Jacques aut Martin, Claude aut Enthalten in Critical care London : BioMed Central, 1997 9(2004), 2 vom: 09. Sept. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:9 year:2004 number:2 day:09 month:09 https://dx.doi.org/10.1186/cc2945 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2004 2 09 09
language	English
source	Enthalten in Critical care 9(2004), 2 vom: 09. Sept. volume:9 year:2004 number:2 day:09 month:09
sourceStr	Enthalten in Critical care 9(2004), 2 vom: 09. Sept. volume:9 year:2004 number:2 day:09 month:09
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institution	findex.gbv.de
topic_facet	catecholamines diuresis mesenteric circulation noradrenaline (norepinephrine) renal function septic shock shock vasopressin
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container_title	Critical care
authorswithroles_txt_mv	Delmas, Anne @@aut@@ Leone, Marc @@aut@@ Rousseau, Sébastien @@aut@@ Albanèse, Jacques @@aut@@ Martin, Claude @@aut@@
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fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR029762618</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519070050.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2004 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/cc2945</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR029762618</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)cc2945-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Delmas, Anne</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Clinical review: Vasopressin and terlipressin in septic shock patients</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2004</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="500" ind1=" " ind2=" "><subfield code="a">© BioMed Central Ltd 2004</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. 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author	Delmas, Anne
spellingShingle	Delmas, Anne misc catecholamines misc diuresis misc mesenteric circulation misc noradrenaline (norepinephrine) misc renal function misc septic shock misc shock misc vasopressin Clinical review: Vasopressin and terlipressin in septic shock patients
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topic_title	Clinical review: Vasopressin and terlipressin in septic shock patients catecholamines (dpeaa)DE-He213 diuresis (dpeaa)DE-He213 mesenteric circulation (dpeaa)DE-He213 noradrenaline (norepinephrine) (dpeaa)DE-He213 renal function (dpeaa)DE-He213 septic shock (dpeaa)DE-He213 shock (dpeaa)DE-He213 vasopressin (dpeaa)DE-He213
topic	misc catecholamines misc diuresis misc mesenteric circulation misc noradrenaline (norepinephrine) misc renal function misc septic shock misc shock misc vasopressin
topic_unstemmed	misc catecholamines misc diuresis misc mesenteric circulation misc noradrenaline (norepinephrine) misc renal function misc septic shock misc shock misc vasopressin
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title	Clinical review: Vasopressin and terlipressin in septic shock patients
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title_full	Clinical review: Vasopressin and terlipressin in septic shock patients
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title_sort	clinical review: vasopressin and terlipressin in septic shock patients
title_auth	Clinical review: Vasopressin and terlipressin in septic shock patients
abstract	Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. © BioMed Central Ltd 2004
abstractGer	Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. © BioMed Central Ltd 2004
abstract_unstemmed	Abstract Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via $ V_{1} $ receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01–0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. © BioMed Central Ltd 2004
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title_short	Clinical review: Vasopressin and terlipressin in septic shock patients
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