Pulmonary vasoregulation by cyclooxygenase metabolites and angiotensin II after hypoperfusion in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs

David Fehr, D. P. Nyhan, B. B. Chen, P. A. Murray

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The authors investigated the extent to which endogenously produced metabolites of the cyclooxygenase pathway and angiotensin II modulate the pulmonary vascular response to increasing pulmonary blood flow after a period of systemic and pulmonary hypotension and hypoperfusion (defined as posthypoperfusion) in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs. The authors tested the hypothesis that vasodilator metabolites of the cyclooxygenase pathway offset the vasoconstrictor influence of angiotensin II to prevent pulmonary vasconstriction posthypoperfusion. Baseline and posthypoperfusion pulmonary vascular pressure-cardiac index (P/Q̇) plots were constructed by stepwise inflation and deflation, respectively, of a hydraulic occluder implanted around the inferior vena cava to vary Q̇. In intact (no drug), conscious dogs, the pulmonary vascular P/Q̇ relationship posthypoperfusion was not altered significantly compared with baseline. In contrast, after cyclooxygenase inhibition, active flow-independent pulmonary vasoconstriction (12-17%; P < 0.01) was observed posthypoperfusion, and this response was abolished entirely by angiotensin converting-enzyme inhibition. During pentobarbital anesthesia, significant pulmonary vasoconstriction (27%; P < 0.01) occurred posthypoperfusion in the no-drug condition. However, the magnitude of the posthypoperfusion vasoconstriction was not increased by cyclooxygenase inhibition, nor was it reduced by converting-enzyme inhibition. During halothane anesthesia, pulmonary vasoconstriction was not observed posthypoperfusion in the no-drug condition, but it was unmasked (8-13%; P < 0.05) by cyclooxygenase inhibition and attenuated partially by converting-enzyme inhibition. These results indicate that cyclooxygenase metabolites and angiotensin II exert opposing vasodilator and vasoconstrictor effects, respectively, on the pulmonary circulation of conscious dogs posthypoperfusion. These competing mechanisms are active during halothane anesthesia but are abolished during pentobarbital anesthesia.

Original languageEnglish (US)
Pages (from-to)257-267
Number of pages11
JournalAnesthesiology
Volume75
Issue number2
DOIs
StatePublished - Jan 1 1991

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Halothane
Pentobarbital
Prostaglandin-Endoperoxide Synthases
Angiotensin II
Dogs
Lung
Vasoconstriction
Anesthesia
Blood Vessels
Vasoconstrictor Agents
Vasodilator Agents
Pharmaceutical Preparations
Pulmonary Circulation
Economic Inflation
Inferior Vena Cava
Peptidyl-Dipeptidase A
Enzymes
Hypotension
Pressure

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

@article{5ded071d3fe44f5d8140a5df8acc5a1a,
title = "Pulmonary vasoregulation by cyclooxygenase metabolites and angiotensin II after hypoperfusion in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs",
abstract = "The authors investigated the extent to which endogenously produced metabolites of the cyclooxygenase pathway and angiotensin II modulate the pulmonary vascular response to increasing pulmonary blood flow after a period of systemic and pulmonary hypotension and hypoperfusion (defined as posthypoperfusion) in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs. The authors tested the hypothesis that vasodilator metabolites of the cyclooxygenase pathway offset the vasoconstrictor influence of angiotensin II to prevent pulmonary vasconstriction posthypoperfusion. Baseline and posthypoperfusion pulmonary vascular pressure-cardiac index (P/Q̇) plots were constructed by stepwise inflation and deflation, respectively, of a hydraulic occluder implanted around the inferior vena cava to vary Q̇. In intact (no drug), conscious dogs, the pulmonary vascular P/Q̇ relationship posthypoperfusion was not altered significantly compared with baseline. In contrast, after cyclooxygenase inhibition, active flow-independent pulmonary vasoconstriction (12-17{\%}; P < 0.01) was observed posthypoperfusion, and this response was abolished entirely by angiotensin converting-enzyme inhibition. During pentobarbital anesthesia, significant pulmonary vasoconstriction (27{\%}; P < 0.01) occurred posthypoperfusion in the no-drug condition. However, the magnitude of the posthypoperfusion vasoconstriction was not increased by cyclooxygenase inhibition, nor was it reduced by converting-enzyme inhibition. During halothane anesthesia, pulmonary vasoconstriction was not observed posthypoperfusion in the no-drug condition, but it was unmasked (8-13{\%}; P < 0.05) by cyclooxygenase inhibition and attenuated partially by converting-enzyme inhibition. These results indicate that cyclooxygenase metabolites and angiotensin II exert opposing vasodilator and vasoconstrictor effects, respectively, on the pulmonary circulation of conscious dogs posthypoperfusion. These competing mechanisms are active during halothane anesthesia but are abolished during pentobarbital anesthesia.",
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Pulmonary vasoregulation by cyclooxygenase metabolites and angiotensin II after hypoperfusion in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs. / Fehr, David; Nyhan, D. P.; Chen, B. B.; Murray, P. A.

In: Anesthesiology, Vol. 75, No. 2, 01.01.1991, p. 257-267.

Research output: Contribution to journalArticle

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T1 - Pulmonary vasoregulation by cyclooxygenase metabolites and angiotensin II after hypoperfusion in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs

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N2 - The authors investigated the extent to which endogenously produced metabolites of the cyclooxygenase pathway and angiotensin II modulate the pulmonary vascular response to increasing pulmonary blood flow after a period of systemic and pulmonary hypotension and hypoperfusion (defined as posthypoperfusion) in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs. The authors tested the hypothesis that vasodilator metabolites of the cyclooxygenase pathway offset the vasoconstrictor influence of angiotensin II to prevent pulmonary vasconstriction posthypoperfusion. Baseline and posthypoperfusion pulmonary vascular pressure-cardiac index (P/Q̇) plots were constructed by stepwise inflation and deflation, respectively, of a hydraulic occluder implanted around the inferior vena cava to vary Q̇. In intact (no drug), conscious dogs, the pulmonary vascular P/Q̇ relationship posthypoperfusion was not altered significantly compared with baseline. In contrast, after cyclooxygenase inhibition, active flow-independent pulmonary vasoconstriction (12-17%; P < 0.01) was observed posthypoperfusion, and this response was abolished entirely by angiotensin converting-enzyme inhibition. During pentobarbital anesthesia, significant pulmonary vasoconstriction (27%; P < 0.01) occurred posthypoperfusion in the no-drug condition. However, the magnitude of the posthypoperfusion vasoconstriction was not increased by cyclooxygenase inhibition, nor was it reduced by converting-enzyme inhibition. During halothane anesthesia, pulmonary vasoconstriction was not observed posthypoperfusion in the no-drug condition, but it was unmasked (8-13%; P < 0.05) by cyclooxygenase inhibition and attenuated partially by converting-enzyme inhibition. These results indicate that cyclooxygenase metabolites and angiotensin II exert opposing vasodilator and vasoconstrictor effects, respectively, on the pulmonary circulation of conscious dogs posthypoperfusion. These competing mechanisms are active during halothane anesthesia but are abolished during pentobarbital anesthesia.

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