Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide

D. H. Sigmon, Ivan Florentino, R. A. Van Dyke, W. H. Beierwaltes

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Background: The endogenous vasodilator endothelium-de-rived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods: Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by N(W)- nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results: N(W)-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 ± 2 (P < 0.001) and 20 ± 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 ± 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). N(W)- nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions: Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

Original languageEnglish (US)
Pages (from-to)135-143
Number of pages9
JournalAnesthesiology
Volume82
Issue number1
DOIs
StatePublished - Feb 3 1995
Externally publishedYes

Fingerprint

Halothane
Nitric Oxide
NG-Nitroarginine Methyl Ester
Hemodynamics
Endothelium
Anesthesia
Cardiac Output
Heart Rate
Vascular Resistance
Anesthetics
Kidney
Renal Circulation
Regional Blood Flow
Vasodilator Agents
Microspheres
Blood Vessels
Perfusion
barbituric acid
Blood Pressure

Keywords

  • Anesthetics, volatile: barbiturate; halothane
  • Endothelium: endothelium- derived nitric oxide
  • Hemodynamics: blood flow; vascular resistance

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide. / Sigmon, D. H.; Florentino, Ivan; Van Dyke, R. A.; Beierwaltes, W. H.

In: Anesthesiology, Vol. 82, No. 1, 03.02.1995, p. 135-143.

Research output: Contribution to journalArticle

Sigmon, D. H. ; Florentino, Ivan ; Van Dyke, R. A. ; Beierwaltes, W. H. / Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide. In: Anesthesiology. 1995 ; Vol. 82, No. 1. pp. 135-143.
@article{3d157bcc504646b8a076e99869a4fc41,
title = "Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide",
abstract = "Background: The endogenous vasodilator endothelium-de-rived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods: Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by N(W)- nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results: N(W)-nitro-L-arginine methyl ester decreased blood flow to the brain by 23{\%} (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 ± 2 (P < 0.001) and 20 ± 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132{\%} (P < 0.001) and 105{\%} (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 ± 1 mmHg) and the increase in TPR (only 22{\%}) were greatly diminished (P < 0.001). N(W)- nitro-L-arginine methyl ester decreased cardiac output (CO) by 47{\%} (P < 0.001) and heart rate (HR) by 28{\%} (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38{\%} (P < 0.005) and HR by 13{\%} (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30{\%}) and kidneys (47{\%}). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35{\%} (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions: Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.",
keywords = "Anesthetics, volatile: barbiturate; halothane, Endothelium: endothelium- derived nitric oxide, Hemodynamics: blood flow; vascular resistance",
author = "Sigmon, {D. H.} and Ivan Florentino and {Van Dyke}, {R. A.} and Beierwaltes, {W. H.}",
year = "1995",
month = "2",
day = "3",
doi = "10.1097/00000542-199501000-00018",
language = "English (US)",
volume = "82",
pages = "135--143",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide

AU - Sigmon, D. H.

AU - Florentino, Ivan

AU - Van Dyke, R. A.

AU - Beierwaltes, W. H.

PY - 1995/2/3

Y1 - 1995/2/3

N2 - Background: The endogenous vasodilator endothelium-de-rived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods: Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by N(W)- nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results: N(W)-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 ± 2 (P < 0.001) and 20 ± 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 ± 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). N(W)- nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions: Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

AB - Background: The endogenous vasodilator endothelium-de-rived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods: Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by N(W)- nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results: N(W)-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 ± 2 (P < 0.001) and 20 ± 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 ± 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). N(W)- nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions: Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

KW - Anesthetics, volatile: barbiturate; halothane

KW - Endothelium: endothelium- derived nitric oxide

KW - Hemodynamics: blood flow; vascular resistance

UR - http://www.scopus.com/inward/record.url?scp=0028877735&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028877735&partnerID=8YFLogxK

U2 - 10.1097/00000542-199501000-00018

DO - 10.1097/00000542-199501000-00018

M3 - Article

C2 - 7832295

AN - SCOPUS:0028877735

VL - 82

SP - 135

EP - 143

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 1

ER -