Halothane anesthesia causes active flow-independent pulmonary vasoconstriction

B. B. Chen, D. P. Nyhan, David Fehr, H. M. Goll, P. A. Murray

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

We utilized multipoint pulmonary vascular pressure-flow (P/Q̇) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q̇ relationship measured in conscious dogs is altered during halothane anesthesia. P/Q̇ plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q̇. Compared with conscious dogs, halothane (~ 1.2% end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P < 0.01) at all levels of Q̇. Halothane also decreased (P < 0.01) systemic arterial pressure and Q̇. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic α-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V1 + V2 receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P < 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume259
Issue number1 28-1
StatePublished - 1990

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Halothane
Vasoconstriction
Anesthesia
Lung
Prostaglandin-Endoperoxide Synthases
Vasopressin Receptors
Dogs
Ventilation
Reflex
Pulmonary Circulation
Arginine Vasopressin
Inferior Vena Cava
Peptidyl-Dipeptidase A
Pentobarbital
Constriction
General Anesthesia
Blood Vessels
Arterial Pressure
Thorax
Pressure

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

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abstract = "We utilized multipoint pulmonary vascular pressure-flow (P/Q̇) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q̇ relationship measured in conscious dogs is altered during halothane anesthesia. P/Q̇ plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q̇. Compared with conscious dogs, halothane (~ 1.2{\%} end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P < 0.01) at all levels of Q̇. Halothane also decreased (P < 0.01) systemic arterial pressure and Q̇. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic α-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V1 + V2 receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P < 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.",
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Halothane anesthesia causes active flow-independent pulmonary vasoconstriction. / Chen, B. B.; Nyhan, D. P.; Fehr, David; Goll, H. M.; Murray, P. A.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 259, No. 1 28-1, 1990.

Research output: Contribution to journalArticle

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AU - Chen, B. B.

AU - Nyhan, D. P.

AU - Fehr, David

AU - Goll, H. M.

AU - Murray, P. A.

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N2 - We utilized multipoint pulmonary vascular pressure-flow (P/Q̇) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q̇ relationship measured in conscious dogs is altered during halothane anesthesia. P/Q̇ plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q̇. Compared with conscious dogs, halothane (~ 1.2% end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P < 0.01) at all levels of Q̇. Halothane also decreased (P < 0.01) systemic arterial pressure and Q̇. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic α-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V1 + V2 receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P < 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.

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