Morphine depression of myocardial function.

A modified Langendorff rat heart preparation with an isolated working rat heart was used to establish the presence of opiate receptors in the myocardium and to demonstrate the effects of an opiate agonist on myocardial function in the absence of neuronal and humoral factors. Twenty-five Sprague-Dawley rats weighing 400-500 gm were anesthetized and had their hearts excised and attached to the Langendorff perfusion apparatus. After a 30 min control period, the Krebs-Henseleit Buffer (KHB) perfusion solution was altered by the addition of 0.9% NaCl (S) or morphine sulfate (MS), which resulted in a final concentration of 2 X 10(-4) M or 3 X 10(-4) M MS in the KHB. Temperature, preload, and afterload were kept constant while heart rate (HR), cardiac output (CO), and aortic dP/dtmax were measured. Significant dose-related depression of HR, CO, and less significantly, aortic dP/dtmax were demonstrated. The data suggest that opiate receptors are present in the myocardium and that morphine sulfate directly effects the myocardium causing a significant decrease in HR, CO, and aortic dP/dtmax. These changes are a result of opiate receptor agonism, which seems to be primarily a negative chronotropic effect and might explain the mechanism for the role of endogenous opiates during shock.