Supplementation of antihypertensive action of sodium nitroprusside (SNP) is almost standard practice and should obviate the need for potentially toxic doses to control blood pressure. Clonidine, an antihypertensive agent known to reduce sympathetic outfiow via alpha2-adrenergic receptor stimulation, has been shown to decrease MAC of halogenated agent, and to reduce the amount of SNP required to reduce the desired hypotension. To determine the effects of clonidine on the hemodynamics and intrapulmonary shunting during SNP infusion, clonidine and/or SNP were administered to 22 patients anesthetized with halothane-N2, O-O2 (FIO2:0.5) In one group of 11 patients, clonidine 1.5ug/kg was injected intravenously. In another group of 11 patients, clonidine 1.5 ug/kg was injected intravenously 30 minutes after starting the SNP infusion (3 ug/kg/min). The results were as follows. 1) Clonidine alone produced a small decrease in MAP (10%) and CI (8%) but other hemodynamic values remained unaltered. 2) Arterial oxygen tension and intrapulmonary shunting was not changed by clonidine. 3) Heart rate (15%) was increased , but MAP (29%), MPAP (24%), PCWP (25%), CVP (32% ), SVR (29%)and PVR(24%) were decreased significantly, and CI, SVI remained unchanged during SNP hypotension. 4) SNP caused a significant increase in intrapulmonary shunt fraction from 8.62% to 10.58% and a decrease in PaO2. 5) In group of clonidine under SNP infusion, conidine did not significantly affect the hemodynamic response to SNP except for 15% decrease in BP. 6) Clonidine caused no significant change on gas exchange effect of SNP. These results indicate that clonidine did not significantly affect the hemodynamics and intrapul-monary shunting during SNP hypotension. Therefore, clonidine could be used as a valuable adjuvant for reducing the amount of SNP and decreasing MAC of halothane.