AJP - Heart and Circulatory Physiology, Vol 259, Issue 1 74-H83, Copyright © 1990 by American Physiological Society
Halothane anesthesia causes active flow-independent pulmonary vasoconstriction
B. B. Chen, D. P. Nyhan, D. M. Fehr, H. M. Goll and P. A. Murray
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
We utilized multipoint pulmonary vascular pressure-flow (P/Q) plots to
investigate the effects of halothane anesthesia on the pulmonary
circulation. Our first objective was to assess the extent to which the P/Q
relationship measured in conscious dogs is altered during halothane
anesthesia. P/Q plots were constructed by stepwise constriction of the
thoracic inferior vena cava to decrease venous return and Q. Compared with
conscious dogs, halothane (approximately 1.2% end-tidal) resulted in
active, flow-independent pulmonary vasoconstriction (P less than 0.01) at
all levels of Q. Halothane also decreased (P less than 0.01) systemic
arterial pressure and Q. 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 alpha-adrenoreceptor block,
angiotensin converting-enzyme inhibition, combined arginine vasopressin V1
+ V2 receptor block, or by cyclooxygenase inhibition. Finally,
halothane-induced pulmonary vasoconstriction (P less than 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.
