刺激腓深神经对低血压或休克狗心血管活动的影响

实验在麻醉狗中进行。静脉内匀速注射硝普钠时,平均动脉压和左心室收缩压明显降低,左心室dp/dt_(max)、-dp/dt_(max)和心力环面积均明显减小。此时电刺激一侧腓深神经可使动脉血压和左心室收缩压明显升高,dp/dt_(max)和心力环面积也显著增加。停止刺激后,动脉血压和左心室收缩压逐渐回向刺激前的水平。停止注射硝普钠5～15分钟后,上述各项观察指标基本恢复到注药前的水平。在用大肠杆菌内毒素造成休克的狗中,电刺激一侧腓深神经,也能使平均动脉压和左心室收缩压升高,同时dp/dt_(max)、-dp/dt_(max)和肠系膜血管阻力明显增高,但肾血管阻力增加不明显。本实验结果与以往的实验资料一起表明,在用扩血管药造成低血压时,躯体神经刺激引起的升压效应似乎以心肌收缩力增加为主;而在内毒素休克时,躯体神经刺激可通过改善心肌收缩功能和增加内脏血管阻力而引起升压作用。

CARDIOVASCULAR EFFECTS OF DEEP PERONEAL NERVE STIMULATION IN HYPOTENSIVE OR SHOCK DOGS

Experiments were performed on 15 anaesthetized dogs, mean arterial pressure, left intraventricular pressure, dp/dt max, -dp/dt max and the area of cardiac force loop ( CFL ) were reduced markedly by intravenous infusion of sodium nitroprusside ( NP) .During NP- induced hypotension,stimulation of the deep peroneal nerve ( DPN ) produced a pressor effect and increase in left ventricular systolic pressure ( LVSP ) , dp/dt max and the area of CFL. After cessation of DPN stimulation, blood pressure and LVSP gradually returned to their prestimulation values. All variables observed recovered to their control levels within 5 to 15 min after termination of NP infusion.In a separate group of dogs circulatory shock was produced by intravenous injection of E coli endotoxin ( 5 mg/kg) . One hour after endotoxin injection, electrical stimulation was applied to DPN, which resulted in increase in MAP, LVSP, dp/dt max and -dp/dt max. The mesenteric vascular resistance was also increased by DPN stimulation, but there was no significant change in renal vascular resistance. No such changes were observed in endotoxin shock dogs without DPN stimulation.The results obtained indicate that during NP hypotension, the pressor effect of DPN stimulation was mainly caused by increase in the cardiac contractile force, but in the animals with endotoxin shock, the pressor effect of DPN stimulation was probably mediated by the increase of both the cardiac contractile force and the resistance of mesenteric vessels.