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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。
Experiments were performed in anesthetized dogs. When sodium nitroprusside was infused intravenously, mean arterial pressure and left ventricular systolic pressure were significantly decreased, dp / dt max, - dp / dt max and annulus area of left ventricle were significantly decreased. Electrical stimulation of the deep peroneal nerve at this time can make arterial blood pressure and left ventricular systolic pressure increased significantly, dp / dt_ (max) and cardiac annulus area also increased significantly. After stopping the stimulation, arterial pressure and left ventricular systolic pressure gradually returned to the level before stimulation. Stop injection of sodium nitroprusside 5 to 15 minutes, the above indicators were restored to the level before injection. In dogs with endotoxin-induced shock, electrical stimulation of the deep peroneal nerve could also increase mean arterial pressure and left ventricular systolic pressure, while dp / dtmax, -dp / dtmax and Mesenteric vascular resistance was significantly increased, but no significant increase in renal vascular resistance. The results of this experiment together with previous experimental data show that when vasodilator is used to cause hypotension, the vasopressor effect caused by somatic nerve stimulation appears to be mainly due to an increase in myocardial contractility; whereas in endotoxic shock, somatic nerve stimulation can be induced Improve myocardial contractility and increase visceral vascular resistance caused by the role of step-up.