Acetylcholine and carotid body excitation during hypoxia in the cat.
Acetylcholine and carotid body excitation during hypoxia in the cat.
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猫缺氧时乙酰胆碱和颈动脉体兴奋。
DOI：
10.1152/jappl.1994.76.4.1566
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Shirahata,M
中科院分区：
文献类型：
--
作者：
Fitzgerald,RS;Shirahata,M
本研究的目的是检验乙酰胆碱（ACh）在颈动脉体缺氧刺激期间是一种兴奋性神经递质的假设。猫被麻醉、麻痹并进行人工通气。颈总动脉装有一个包含旋塞的环，用于选择性地灌注颈动脉体。记录整个颈动脉窦神经的神经活动。猫用10％O2通气3分钟，颈动脉体正常灌注其自身的低氧动脉血后，转动旋塞，用含有α-银环蛇毒素、美加明和阿托品的同等低氧的Krebs-Ringer碳酸氢盐溶液(KRB)或不含低氧阻滞剂的KRB灌注颈动脉体2分钟。将旋塞阀恢复到原来的位置，使无阻滞剂的低氧血液再次灌注颈动脉体。通过该方案，我们发现 1) 胆碱能阻滞剂以剂量依赖性方式降低了颈动脉体对缺氧 KRB 的反应； 2) 颈动脉压力感受器活性没有被阻滞剂降低，这表明阻滞剂的作用不是非特异性的（而利多卡因迅速降低化学感受器和压力感受器活性）； 3) 在灌注的低氧血液中加入阻滞剂也减少了颈动脉体的神经输出； 4) 阻滞剂降低了颈动脉体对含有 P 物质（20 微克/100 毫升）的缺氧 KRB 的神经反应，表明 P 物质可能与颈动脉体中的 ACh 相关。我们的结论是，这些数据提供了良好的证据支持乙酰胆碱在颈动脉体缺氧兴奋中的兴奋作用。
The purpose of this study was to test the hypothesis that acetylcholine (ACh) is an excitatory neurotransmitter during the hypoxic stimulation of the carotid body. Cats were anesthetized, paralyzed, and artificially ventilated. The common carotid artery was fitted with a loop containing a stopcock for selectively perfusing the carotid body. Neural activity was recorded from the whole carotid sinus nerve. After the cats had been ventilated on 10% O2 for 3 min with the carotid body being normally perfused with its own hypoxic arterial blood, the stopcock was turned, and either equally hypoxic Krebs-Ringer bicarbonate solution (KRB) containing alpha-bungarotoxin, mecamylamine, and atropine or hypoxic blocker-free KRB perfused the carotid body for 2 min. The stopcock was returned to its original position, allowing blocker-free hypoxic blood to perfuse the carotid body once again. With this protocol we found 1) the cholinergic blockers reduced the carotid body response to hypoxic KRB in a dose-dependent manner; 2) carotid baroreceptor activity was not reduced by the blockers, suggesting that the action of the blockers was not nonspecific (whereas lidocaine rapidly reduced both chemoreceptor and baroreceptor activity); 3) inclusion of the blockers in perfused hypoxic blood also reduced neural output from the carotid body; and 4) the blockers reduced the carotid body's neural response to hypoxic KRB containing substance P (20 micrograms/100 ml), suggesting that substance P may be linked to ACh in the carotid body. We conclude that these data provide good evidence supportive of an excitatory role for ACh in carotid body hypoxic excitation.