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阐明肾交感神经在抗利尿效应中所起的作用。对乌拉坦和氯醛糠混合液麻醉的Wistar 大鼠和猫,用3.2%氯化钠高渗盐水灌流小肠,观察到肾交感神经传出冲动显著增加,与灌流前的冲动频率相比,差异有非常显著意义(P<0.001);用等量生理盐水灌流前后,肾神经传出冲动则无显著变化,可是,先在隔下切断两侧迷走神经后再进行高渗盐水灌流,上述反射作用即不再出现。实验结果提示,小肠渗透压感受器兴奋,可反射性地增加肾交感神经的传出冲功。实际上,早已有文献报道,肾交感神经可直接作用于肾小管,促进钠和水的重吸收;因此,肾交感神经可能是上述抗利尿反射效应的传出途径。
To clarify the role of renal sympathetic nerve in anti-diuretic effect. In Wistar rats and cats anesthetized with a mixture of urethane and chloral hydrate, the afferent impulse of renal sympathetic nerve was significantly increased by perfusing the small intestine with 3.2% sodium chloride hypertonic saline. Compared with the impulsive frequency before perfusion, the difference (P <0.001). Before and after perfusion with equal volume of saline, there was no significant change in the afferent impulse of the renal nerves, however, perfusion of hypertonic saline followed by severance of the vagus nerve at both sides was performed. The above-mentioned reflex action No longer appear. Experimental results suggest that the small intestine pressure receptor excitement, reflective reflex can increase the impact of renal sympathetic. In fact, it has long been reported in the literature that the renal sympathetic nerve can act directly on the renal tubules and promote the reabsorption of sodium and water; therefore, the renal sympathetic nerve may be the efferent route to the antidiuretic reflex effect described above.