Effects of splanchnic nerve stimulation on cardiac preload, afterload, and output in cats.

Abstract

Splanchnic nerve stimulation (SNS) mobilizes up to 25% of the total blood volume from the splanchnic venous bed, constricts the splanchnic arterioles and releases catecholamines and renin. The effects of these changes on cardiac preload, afterload and output were examined in cats anesthetized with chloralose. Before adrenalectomy SNS caused increases in right atrial and arterial pressures and cardiac output, but total peripheral resistance did not change. After adrenalectomy SNS increased right atrial pressure, arterial pressure and peripheral resistance but cardiac output did not change. Adrenal catecholamines evidently are necessary for an increased cardiac output during SNS. After adrenalectomy and elimination of the baroreceptor reflexes SNS still caused no increase in cardiac output. When the increases in arterial pressure were prevented by nitroprusside infusions or by opening an arteriovenous (A-V) shunt, SNS caused an increase in cardiac output even though the increase in right atrial pressure was smaller than before. The results are quantitatively described by the Frank-Starling relationship between stroke work and right atrial pressure and are interpreted as follows. Venoconstriction alone causes an increase in cardiac output with a minimal rise in cardiac preload (right atrial pressure). If afterload (systemic and pulmonary arterial pressures) increases, this reduces the increase in cardiac output causing a further rise in preload. The rise in preload tends to restore cardiac output but is limited by pooling of blood elsewhere in the venous system (.apprx. 4 ml/kg for each 1-mm rise in right atrial pressure). A new equilibrium is then reached between preload, afterload and cardiac output. The interaction between preload and afterload in the control of cardiac output is demonstrated.