刺激清醒大鼠躯体神经对失血性低血压的升压效应

在清醒雄性大鼠中经静脉抽出血液总量的约50%,造成失血性低血压。对照组大鼠在失血后不予处理。刺激组大鼠在失血后半小时用低频电脉冲刺激坐骨神经30min。刺激组动物的平均动脉压在刺激肘和刺激停止后2小时内均显著高于对照组。在同时记录内脏神经放电的动物中还看到,刺激坐骨神经时交感神经活动显著加强。这可能和血压、心率的恢复有关。在失血动物中刺激坐骨神经引起的升压效应不能被静脉内注射纳洛酮(8mg/kg)翻转;预先注射纳洛酮也不能阻断这种升压效应。在用水合氯醛麻醉的大鼠中,失血后刺激坐骨神经仍能引起升压反应。但如在刺激坐骨神经前静脉注射东莨菪碱(8—20mg/kg),则在多数动物中上述升压反应的幅度显著减小,甚至消失。实验结果表明,在失血性低血压的大鼠中,刺激坐骨神经可促进机体代偿反应,进一步加强交感神经活动,有利于血压的恢复。这一效应可能需要胆硷能递质参与,而内啡肽系统似乎不起重要作用。

PRESSOR EFFECT PRODUCED BY STIMULATION OF SOMATIC NERVE ON HEMORRHAGIC HYPOTENSION IN CONSCIOUS RATS

Experiments were carried out on male conscious rats.Hemorrhagic hypo-tension was produced by withdrawing blood 50% of the total blood volume)fromthe venous catheter.The animals were divided into two groups.In controlgroup,no treatment was given following hemorrhage.One hour after bleeding,the mean arterial pressure was maintained at a low level of 66% of the control value.In stimulation group,the sciatic nerve was stimulated with low frequency elec-trical pulses.The stimulation was lasted for 30 min.During stimulation,themean arterial pressure was 81% of the control level.The splanchnic nerve dis-charge was also increased.After the cessation of sciatic stimulation,the meanarterial pressure level was still significantly higher than that of the control group.This pressor response upon sciatic nerve stimulation was neither reversed norprevented by naloxone(8 mg/kg,i.v.).In chloral hydrate(400 mg/kg,i.p.)anaesthetized rats,stimulation of the sciatic nerve during hemorrhagic hypotensionstill produced an increase in arterial pressure.However,the pressor response wassignificantly decreased or even abolished by pretreatment of scopolamine(8 mg/kg,i.v.).The results obtained indicate that stimulation of the somatic nerve in animalswith hemorrhagic hypotension can further enhance the sympathetic activity andthus facilitate the recovery of blood pressure.The mechanism underlying thesomatic stimulation-induced pressor response in hypotensive animals is discussed.