Haemodynamic responses to stimulation of the splanchnic and cardiac sympathetic nerves in the anaesthetized cat.

Abstract

SUMMARY1. The changes in cardiac output and mean right atrial pressure (R.A.P.) evoked at different circulating blood volumes by stimulation of the splanchnic sympathetic nerves were investigated in adrenalectomized cats under chloralose anaesthesia, with unopened chests and spontaneous respiration and with active vascular reflexes. The cardiac autonomic nerves were cut or blocked pharmacologically.2. Stimulation of the distal ends of the splanchnic nerves at 4 Hz caused aortic pressure and R.A.P. to rise to maximum values at 2 min before declining slowly. Cardiac output rose more slowly to a steady state at 3 min; at higher circulating volumes it fell initially. Although the output increments were slower in development they were better sustained than those in total peripheral resistance. The proportionate output increments were largest and the R.A.P. increments least at low circulating volumes whereas at high volumes the R.A.P. increments were large but the output changes were small or negative; the pattern of changes resembled that resulting from infusion of blood.3. Stimulation of the cardiac sympathetic nerves evoked a rise in output and a fall in R.A.P. related in magnitude to the initial value of R.A.P. On simultaneous stimulation of the splanchnic and cardiac sympathetic nerves the changes in output combined whereas the R.A.P. changes cancelled, to give output increments of 25-50 % with little change in R.A.P. at all circulating volumes.4. At high circulating volumes infusion of blood did not usually alter output or aortic pressure, but splanchnic nerve stimulation increased peripheral resistance and aortic pressure and commonly evoked a rise in left ventricular stroke work which could not be accounted for by known adrenergic mechanisms or by elevation of left ventricular end-diastolic pressure.5. Portal venous pressure was consistently elevated by splanchnic nerve stimulation; it rose more slowly than did aortic pressure or R.A.P. and was independent of a changing central venous pressure provided this did not exceed +5 mmHg. The cardiac output increments were not related to changes in the ratio between the input

Role of Volume Redistribution in the Congestion of Heart Failure

“…In this study, changes in cardiac output and mean right atrial pressure were evoked at different circulating blood volumes by stimulation of the splanchnic sympathetic nerves. With high circulating volumes, infusion of more volume did not consistently alter output or aortic pressure, but splanchnic nerve stimulation increased peripheral resistance and aortic pressure and commonly evoked a rise in left ventricular stroke volume . The study by Barnes and colleagues suggests that constriction of the splanchnic vasculature is more effective in raising cardiac filling pressures than external volume loading alone and thus emphasizes the potential contribution of the splanchnic vascular compartment to cardiac decompensation.…”

Mean circulatory filling pressure during splanchnic nerve stimulation and whole‐body hypoxia in the anaesthetized cat.

“…The mean increase observed, from 7-1 to 11P2 mmHg, is more than sufficient to account for the cardiac output increments evoked by splanchnic nerve stimulation in adrenalectomized cats. The mean increases of 38 % in output and 04 mmHg in RAP at low blood volume reported by Barnes et al (1986) would have required MCFP to rise from 7-1 to 10-2 mmHg in the absence of a change in resistance to venous return.…”

“…Terminations of the hepatic portal vein collapse at pressures of 3-5 mmHg (Mitzner, 1974;Barnes et al 1986). The hepatic venous waterfall resistance was evident in the present experiments at MCFP values below 5 mmHg; portal venous pressure and RAP then failed to meet at the cross-over pressure.…”

“…Hepatic portal venous pressure was measured through a soft vinyl catheter (SV45; Dural Plastics and Engineering) inserted into a branch of the splenic vein exposed by a mid-line abdominal incision. If the splanchnic nerves were to be cut or stimulated they were exposed on each side by a retro-peritoneal approach through flank incisions, and after the greater and lesser splanchnic nerves had been cut their distal ends were placed on shielded stimulating electrodes (Barnes et al 1986). The nerves were stimulated by square-wave pulses of duration 1 ms and amplitude 20 V, usually at a frequency of 10 Hz.…”

Sepsis, venous return, and teleology

“…Experiments in anaesthetised cats show that directly stimulating the sympathetic innervation of the heart, without stimulating the sympathetic drive to the rest of the vasculature, results in profound increases in heart rate with little increase in cardiac output. If the venous return is low or limited, increasing the cardiac contractility and heart rate does not increase cardiac output significantly [14,15]. The observation that isolated cardiac sympathetic stimulation does not raise the cardiac output significantly has been made by many authors [16].…”