PURPOSE: The hemodynamic responses secondary to sympathetic suppression by esmolol may alter blood flow to splanchnic organs. We investigated whether esmolol might modify splanchnic organ blood flow responses during sodium nitroprusside (SNP)-induced hypotension in dogs anesthetized with sevoflurane. METHODS: The control group (n = 10) received SNP (SNP group). The ES25 and ES100 groups (n = 10, each) received SNP combined with esmolol infused at a constant rate of 25 and 100 micro g*kg(-1)*min(-1) during the hypotensive period after a mean arterial pressure (MAP) of 60 mmHg was attained by the infusion of a 0.03% SNP solution, respectively. The renal, hepatic, and pancreatic blood flows (RBF, HBF, and PBF) were measured by using the hydrogen clearance method. RESULTS: Cardiac index in the SNP group increased (P < 0.01), but in the ES groups it decreased (P < 0.01). Left ventricular dP/dtmax in the SNP group remained unchanged, but in the ES groups it decreased (P < 0.01, each) during the hypotensive period. Except for HBF in the SNP group, the splanchnic blood flow in all groups decreased (P < 0.01, each). The HBF in the ES groups was lower than that in the SNP group (SNP vs ES25, ES100; 70 +/- 1 vs 64 +/- 5, 6 3 +/- 3 mL*min(-1)*100 g(-1)). CONCLUSIONS: This study shows that the differences in HBF between SNP-induced hypotension with or without esmolol may be due to the changes in cardiac output caused by alterations of cardiac contractility. These findings suggest that a small dose of esmolol may impair the maintenance of HBF during SNP-induced hypotension.
PURPOSE: The hemodynamic responses secondary to sympathetic suppression by esmolol may alter blood flow to splanchnic organs. We investigated whether esmolol might modify splanchnic organ blood flow responses during sodium nitroprusside (SNP)-induced hypotension in dogs anesthetized with sevoflurane. METHODS: The control group (n = 10) received SNP (SNP group). The ES25 and ES100 groups (n = 10, each) received SNP combined with esmolol infused at a constant rate of 25 and 100 micro g*kg(-1)*min(-1) during the hypotensive period after a mean arterial pressure (MAP) of 60 mmHg was attained by the infusion of a 0.03% SNP solution, respectively. The renal, hepatic, and pancreatic blood flows (RBF, HBF, and PBF) were measured by using the hydrogen clearance method. RESULTS: Cardiac index in the SNP group increased (P < 0.01), but in the ES groups it decreased (P < 0.01). Left ventricular dP/dtmax in the SNP group remained unchanged, but in the ES groups it decreased (P < 0.01, each) during the hypotensive period. Except for HBF in the SNP group, the splanchnic blood flow in all groups decreased (P < 0.01, each). The HBF in the ES groups was lower than that in the SNP group (SNP vs ES25, ES100; 70 +/- 1 vs 64 +/- 5, 6 3 +/- 3 mL*min(-1)*100 g(-1)). CONCLUSIONS: This study shows that the differences in HBF between SNP-induced hypotension with or without esmolol may be due to the changes in cardiac output caused by alterations of cardiac contractility. These findings suggest that a small dose of esmolol may impair the maintenance of HBF during SNP-induced hypotension.