Barnes R J, Bower E A, Rink T J
J Physiol. 1986 Sep;378:417-36. doi: 10.1113/jphysiol.1986.sp016228.
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. 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. 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. 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. 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 and output resistances of the portal vein and it is concluded that displacement blood from the peripheral to the central vasculature was induced by contraction capacitance vessels.
在氯醛糖麻醉下，对未开胸、自主呼吸且具有活跃血管反射的去肾上腺猫进行研究，观察在不同循环血量时，刺激内脏交感神经所引起的心输出量和平均右心房压力（R.A.P.）的变化。心脏自主神经被切断或用药物阻断。以4Hz刺激内脏神经远端，可使主动脉压力和R.A.P.在2分钟时升至最大值，随后缓慢下降。心输出量上升较慢，在3分钟时达到稳定状态；在循环血量较高时，心输出量起初会下降。尽管心输出量的增加在发展过程中较为缓慢，但比总外周阻力的增加维持得更好。在低循环血量时，心输出量的增加比例最大，R.A.P.的增加最小；而在高循环血量时，R.A.P.的增加较大，但心输出量的变化较小或为负值；这种变化模式类似于输血所导致的情况。刺激心脏交感神经会引起心输出量增加和R.A.P.下降，其幅度与R.A.P.的初始值相关。同时刺激内脏和心脏交感神经时，心输出量的变化叠加，而R.A.P.的变化相互抵消，在所有循环血量下，心输出量增加25% - 50%，而R.A.P.变化很小。在高循环血量时，输血通常不会改变心输出量或主动脉压力，但刺激内脏神经会增加外周阻力和主动脉压力，并且通常会引起左心室搏功增加，这无法用已知的肾上腺素能机制或左心室舒张末期压力升高来解释。刺激内脏神经会持续升高门静脉压力；其上升速度比主动脉压力或R.A.P.慢，并且与中心静脉压力的变化无关，前提是中心静脉压力不超过 +5 mmHg。心输出量的增加与门静脉输入和输出阻力之比的变化无关，得出的结论是，收缩容量血管可导致血液从外周血管向中心血管转移。
