Mechanism of the cardiac output reduction by hexamethonium

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Abstract
The action of ganglionic blocking agents on the cardiac output has been studied in intact, closed-chested animals whose cardiac filling pressure was maintained constant by means of a pressure-stabilizer operating through a jugular catheter introduced into the right heart. Under these conditions cardiodynamic consequences of venous pooling are negated. Hexamethonium produces a fall in cardiac output and blood pressure comparable to that observed in animals without controlled venous pressure. In cardiac sympathectomized animals the cardiac output increases slightly following the administration of hexamethonium. These observations indicate that the ganglion blocking agents reduce cardiac output primarily by blocking tonic sympathetic activity to the heart. The decrease in cardiac output is brought about by a reduction in both stroke volume and heart rate. Sympathetic tone to the blood vessels is reduced by a low dose of hexamethonium before a significant depression in cardiac output occurs.