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Systemic hypoxia is a common abnormality encountered frequently in the clinical setting that produces compensatory cardiopulmonary changes affecting heart rate, blood pressure, peripheral vascular resistance, and respiratory drive. These changes are known to be inhibited or reversed by inhaled anesthetics. More recently, chemoreflex-mediated constriction of capacitance veins has been identified as a mechanism that contributes significantly to the hemodynamic adjustments during hypoxia. However, the effects of anesthetics on this response have not been clarified. The current study was designed to quantify sympathetically mediated mesenteric venoconstriction as well as heart rate and blood pressure responses to acute graded hypoxia; to identify the inhibitory effects of inhaled halothane on these responses; and to estimate the contribution of the peripheral chemoreceptors in mediating these changes. Changes in mesenteric vein diameter were measured in alpha-chloralose anesthetized rabbits in situ with simultaneous changes in heart rate and blood pressure during 40-s periods of 10%, 5%, 2.5%, and 0% inspired O2 administered sequentially before, during, and after 1% or 1.25% inhaled halothane. Sympathetic efferent nerve activity also was measured, and, in a separate group of animals, measurements were preceded by carotid chemoreceptor denervation. Hypoxia-mediated venoconstriction, bradycardia, and hypertension were attenuated almost equally by both 1% and 1.25% inhaled halothane (the higher dose produced only slightly greater inhibition). These responses were inhibited significantly in chemoreceptor-denervated animals, and the subsequent 1% inhaled halothane added only minimal additional attenuation. Increases in chemoreflex-mediated sympathetic efferent nerve activity also were reduced significantly by (1.25%) inhaled halothane. These results indicate that halothane impairs capacitance vein responses and other hemodynamic adjustments during hypoxia. Inhibition of these compensatory changes appears to be mediated, at least in part, via attenuation of peripheral chemoreflex responses and suppression of the resultant reflex increases in sympathetic efferent nerve activity.
Stekiel et al. (1992) studied this question.