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Calcitonin gene-related peptide (CGRP) produces vasodilation, hypotension, and tachycardia. We compared the hemodynamic effects of CGRP-induced hypotension with the effects of prostaglandin E (PGE), which is currently used as a hypotensive agent during anesthesia. Eighteen mongrel dogs were anesthetized with pentobarbital (25 mg·kg), and 0.87% halothane in oxygen (1MAC). Measurements of hemodynamic variables were made before, during, and after induced hypotension. The mean arterial pressure (MAP) was lowered to 60 mmHg by the infusion of either CGRP ( n=10) or PGE ( n=8). This decrease in MAP was appoximately 50% of the baseline value. The CGRP- and PGE-induced hypotension resulted in 61% and 51% maximum reductions ( P<0.01, respectively) in systemic vascular resistance associated with a significant increase in stroke volume index; the two treatments, however produced inconsistent changes in cardiac index (CI). With CGRP, a maximum increase of 144% ( P< 0.01) in CI was observed during induced hypotension. In contrast, PGE-induced hypotension caused no significant changes in CI throughout the observation period. Left ventricular maximum dP/dt decreased ( P<0.01) during the hypotensive period with PGE, whereas it remained un-changes during CGRP-induced hypotension. The different results for changes in CI and cardiac contractility during the CGRP- and PGE-induced hypotension were probably due to differences in ventricular filling pressure. Hypotension induced by PGE was associated with a significant decrease in heart rate (HR), whereas CGRP did not affect HR. This study shows that both CGRP and PGE are effective in decreasing afterload and in inducing hypotension; the results suggest that CGRP is a useful vasodilator for inducing hypotension during halothane anesthesia. [ABSTRACT FROM AUTHOR]

Calcitonin gene-related peptide (CGRP) is known to produce vasodilation, hypotension, and tachycardia. To investigate the interaction between CGRP and anesthetics, the hemodynamic response to infusions of CGRP was studied in dogs anesthetized with halothane or pentobarbital. In halothane-anesthetized dogs given 0.4 μg·kg of CGRP, mean arterial pressure (MAP) did not change significantly. However, there was a significant reduction in systemic vascular resistance (SVR) associated with significant increases in cardiac index (CI) and stroke volume index (SVI). Higher doses (4 and 40 μg·kg) of CGRP produced dose-dependent decreases in MAP accompanied by a reduction in SVR. Further, both CI and SVI significantly increased at 4 μg·kg CGRP but remained unchanged at the 40 μg·kg infusion rate. Heart rate (HR) was not increased at all doses but was decreased at 40 μg·kg. In pentobarbital-anesthetized dogs, CGRP at doses of 4 μg·kg produced a qualitatively similar cardiovascular responses as that observed in halothane-anesthetized dogs, but with one exception: HR was significantly increased. The results show that the hemodynamic profiles induced by CGRP during halothane or pentobarbital anesthesia are a decrease in MAP accompanied by a reduction in SVR and no consistent alterations in CI. However, CGRP effects on HR showed in a different way. The results also show that HR response differs depending on the anesthetics used: HR increases during pentobarbital anesthesia, while it does not increase during halothane anesthesia. [ABSTRACT FROM AUTHOR]

The cardiovascular responses to an infusion of KRN2391, a potassium channel opener, was studied in halothane-anesthetized dogs. Intravenous administration of KRN2391 at 1.0 and 5.0 μg·kg·min for 60 min produced dose-dependent decreases in mean arterial pressure (MAP) and systemic vascular resistance (SVR) associated with dose-dependent increases in the cardiac index (CI) and stroke volume index (SVI) but was not accompanied by an increase in heart rate (HR). The maximum decrease in MAP during the infusion of KRN2391 at 1.0 and 5.0 μg·kg·min was −13±7% (P<0.01) and −37±10% (P<0.01), respectively. The maximum reduction in SVR after 1.0 and 5.0 μg·kg·min was −20±11% (P<0.01) and −60±16% ( P<0.01), respectively. A KRN2391 infusion of 1.0 and 5.0 μg·kg·min increased Cl a maximum of 11±13% ( P<0.05) and 65±33% (P<0.01), respectively. KRN2391 1.0 μg·kg·min showed a tendency to increase SVI but this change was not significant, KRN2391 5.0 μg·kg·min, however, produced a significant increase in SVI. The present results demonstrate that the decrease in MAP and the increases in CI and SVI caused by KRN2391 are due to a reduction in the afterload. Therefore, we conclude that these cardiovascular profiles of KRN2391 may be benificial in perioperative uses including the control of systemic blood pressure and the treatment of hypertension during halothane anesthesia in clinical practice. [ABSTRACT FROM AUTHOR]