Sympathoadrenal activation in sinoaortic-denervated rats following endotoxin.
Sympathoadrenal activation in sinoaortic-denervated rats following endotoxin.
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内毒素后窦主动脉去神经大鼠的交感肾上腺激活。
DOI：
10.1152/ajpregu.1991.260.4.r739
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Jones,SB
中科院分区：
文献类型：
--
作者：
Zhou,ZZ;Wurster,RD;Qi,M;Jones,SB
我们评估的作用，压力感受性反射介导的交感肾上腺激活内毒素中毒，急性以及慢性失神经大鼠。进行了三组实验。在第一个实验中，血液动力学和血浆儿茶酚胺反应后，内毒素（5毫克/公斤静脉注射）的α-氯醛糖麻醉大鼠急性窦主动脉压力感受器去神经（SAD）或假手术。在第二个实验中，使用慢性sinoacetic-denervated大鼠和假手术对照，并在急性制剂中进行实验。在第三个实验中，肼屈嗪（1毫克/公斤静脉注射）给予慢性失神经大鼠和假手术对照，以评估单一的贡献，在没有内毒素的情况下，压迫诱发的压力感受性反射解除抑制。在急性和慢性制剂中，内毒素在存在和不存在动脉压力感受器的情况下诱导血浆去甲肾上腺素和肾上腺素显著升高（P> 0.05）。肼苯哒嗪降压可使假手术组血浆中的儿茶酚胺含量明显升高，但其升高幅度远小于内毒素降压。单纯低血压并没有显著增加SAD大鼠血浆中的儿茶酚胺。这些结果表明，压力反射是不是在介导交感肾上腺激活的主要因素，在内毒素中毒和非压力反射机制可能参与刺激这种激活。
We evaluated the role of the baroreceptor reflex in mediating the sympathoadrenal activation during endotoxicosis, using acutely as well as chronically denervated rats. Three groups of experiments were conducted. In the first experiment, hemodynamic and plasma catecholamine responses following endotoxin (5 mg/kg iv) were measured in alpha-chloralose-anesthetized rats with acute sinoaortic baroreceptor denervation (SAD) or sham operation. In the second experiment, chronically sinoaortic-denervated rats and sham controls were used and experiments were conducted as in acute preparations. In the third experiment hydralazine (1 mg/kg iv) was given to chronically denervated rats and sham controls to evaluate the singular contribution of hypotension-evoked baroreflex disinhibition in the absence of endotoxin. In both acute and chronic preparations, endotoxin induced marked elevation of plasma norepinephrine and epinephrine in the presence as well as the absence of arterial baroreceptors (P greater than 0.05). Plasma catecholamines were significantly increased by hydralazine-induced hypotension in the sham group, but this elevation was far less than that induced by endotoxin. Hypotension alone did not significantly increase plasma catecholamines in SAD rats. These results suggest that the baroreflex is not the major factor in mediating sympathoadrenal activation during endotoxicosis and that non-baroreflex mechanisms may be involved in stimulating such activation.