EFFECT OF HALOTHANE AND ISOFLURANE ON IN-SITU DIAMETER RESPONSES OF SMALL MESENTERIC VEINS TO ACUTE GRADED HYPERCAPNIA

The purpose of the present study was to quantify the inhibitory effect of inhaled halothane and isoflurane on acute hypercapnia-induced resp onses of capacitance-regulating veins and related cardiovascular varia bles in response to sequential 40-s periods of 5%, 10%, 15%, and 20% i nspired CO2 (FICO2). Measurements were made in normoxic alpha-chloralo se-anesthetized rabbits before, during, and after either 0.75 minimum alveolar anesthetic concentration inhaled halothane or isoflurane. The graded hypercapnia caused graded venoconstriction and bradycardia but minimal presser responses. Hypercapnia-induced venoconstriction was b locked by prior local superfusion of the exposed veins with 3 x 10(-6) M tetrodotoxin. Both the hypercapnia-induced venoconstriction and bra dycardia responses were significantly attenuated by halothane or isofl urane and did not fully recover af ter removal of the anesthetics from the circulation. Both anesthetics produced a significant baseline (i. e., prehypercapnia) hypotension and a tendency toward a resultant tach ycardia. The baseline hypotension did not recover completely after eli mination of the anesthetic. Neither anesthetic altered baseline vein d iameter. These results agree with previous studies demonstrating that hypercapnic acidosis :produces mesenteric venoconstriction by elevatin g excitatory sympathetic efferent neural input via activation of perip heral and central chemoreceptors and that bradycardia results from act ivation of compensatory baroreflexes. The neural components of these r eflexes are possible primary sites for attenuation of these cardiovasc ular responses by halothane and isoflurane.