Capsazepine abolishes pulmonary chemoreflexes induced by capsaicin in anesthetized rats.
Capsazepine abolishes pulmonary chemoreflexes induced by capsaicin in anesthetized rats.
复制标题
辣椒素消除麻醉大鼠中辣椒素诱导的肺化学反射。
DOI：
10.1152/jappl.1994.76.5.1848
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Lundberg,JM
中科院分区：
文献类型：
--
作者：
Lee,LY;Lundberg,JM
辣椒素刺激迷走肺c纤维传入，引起肺化学反射，以呼吸暂停、心动过缓和低血压为特征。苯基双胍（PBG）也可以引起类似的反射反应，这是另一种有效且常用的这些传入事件的兴奋剂。本研究旨在研究辣椒素竞争拮抗剂辣椒平对麻醉大鼠辣椒素和PBG引起的反射反应和c -纤维传入活性的影响。静脉输注辣椒素没有引起基线呼吸方式的明显改变，但完全消除了由静脉注射辣椒素引起的肺化学反射（1-2微克/千克静脉注射），其阻断作用迅速可逆。相比之下，对PBG（1-4微克/千克）的反射反应并没有被辣椒素改变，尽管辣椒素可以有效地阻止先前辣椒素处理导致的c纤维传入的脱敏。事实上，尽管辣椒素和PBG都引起了肺部迷走神经c纤维传入末梢突然而强烈的放电，但辣椒平在相同纤维中消除了前者的刺激作用，而不是后者。综上所述，辣椒素选择性地阻断辣椒素对迷走神经c纤维传入肺的刺激作用和随之而来的肺化学反射，可能是通过阻断位于这些传入末梢膜上的假定的“辣椒素受体”。
Capsaicin stimulates vagal pulmonary C-fiber afferents and elicits pulmonary chemoreflex, characterized by apnea, bradycardia, and hypotension. Similar reflex responses can be also evoked by phenylbiguanide (PBG), another potent and commonly used stimulant of these afferents. This study was carried out to determine the effect of capsazepine, a competitive antagonist of capsaicin, on the reflex responses and C-fiber afferent activity evoked by capsaicin and PBG in anesthetized rats. Intravenous infusion of capsazepine did not cause any significant change in the baseline breathing pattern, but it completely abolished the pulmonary chemoreflex elicited by bolus injection of capsaicin (1–2 micrograms/kg iv) and its blocking effect was rapidly reversible. In contrast, the reflex responses to PBG (1–4 micrograms/kg iv) were not altered by capsazepine despite the fact that they could be effectively prevented by the desensitization of C-fiber afferents resulting from a prior capsaicin treatment. Indeed, although both capsaicin and PBG evoked an abrupt and intense burst of discharge from the vagal C-fiber afferent endings in the lungs, the stimulatory effect of the former, but not the latter, was abolished in the same fibers by capsazepine. In summary, capsazepine selectively blocks the stimulatory effect of capsaicin on the vagal C-fiber afferents in the lungs and the consequent pulmonary chemoreflex, presumably by blocking the putative “capsaicin receptors” located in the membrane of these afferent endings.