ABSTRACT
Controlled hypotension induced with sodium nitroprusside (SNP) has been most widely used to facilitate the surgical procedure and to reduce blood loss. However, major problem with its clinical use is cyanide toxicity, which is dose related. And resitance and tachyphylaxis, probably being mediated by sympathoadrenal response to lowered blood pressure, is known to increase dose requirements. Accordingly, several attempts have been made to attenuate sympathetic activity and therefore to reduce dose requirement of SNP. Verapamil, a representative calcium channel blocker, exerts inotropic and chronotropic effect, as well as vasodilation. And it is, also, known to impair pulmonary gas exchange. The purpose of these experiments was to evaluate hemodynamic and gas exchange effects of verapamil, and also its efficacy for reducing the amount of SNP during induced hypotension in patients anesthetized with isoflurane and N2O. Twenty five patients, scheduled to undergo general anesthesia with hypotension, were randomly assigned to two groups. Twelve patients were pretreated with verapamil (160mg, SOD: verapamil group) and the other thirteen were not (control group). The results were as follows: 1) Cardiac index remained unchanged in both groups and did not differ significantly between groups at all times. 2) Heart rate was significatly lower in verapamil group than in control group in the hypotensive period. (113+/- 3.3 vs 103+/- 2.7, p < 0.05) 3) Hypotension induced by SNP resulted from a marked decrease in systemic vascular resistance in both groups. 4) MPAP, PCWP, CVP, SVR and PVR significantly decreased after SNP infusion in both groups, but they did not differ significantly between the groups at all times. 5) SNP dose requirements to attain the same MAP reduction did not differ significantly between groups. (5.5+/-0.8vs 4.1+/-0.8mcg/kg/min, NS) 6) Verapamil pretreatment produced no significant change in intrapulmonary shunt fraction at all times. 7) SNP caused a signficant decrease in arterial oxygen tension in both group, but there were no significant difference between groups at all times. From the above results, it might be concluded 1) that verapamil, in clinical doses, does not blunt a reflex increase in sympathetic activity in response to SNP induced vasodilation, since it produced only a minor influence on SNP induced hemodynamics and the SNP dose requirements, and that verapamil does not inhibit hypoxic pulmonary vasoconstriction during isoflurane-N2O anesthesia. Thus, verapamil could not be a valuable adjunct of SNP in enhancing the hypotensive effect in spite of preserved arterial oxygenation.