Lauzon A M, Dechman G, Martin J G, Bates J H
Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
Respir Physiol. 1995 Jan;99(1):127-38. doi: 10.1016/0034-5687(94)00075-b.
We characterized the complete time course of histamine-induced bronchoconstriction and its modulation via the release of endogenous catecholamines and by its actions on H2-receptors in anesthetized, tracheostomized, paralyzed, and artificially ventilated mongrel dogs. Respiratory resistance (R) and elastance (E) were estimated continuously with a recursive least squares estimator. Three protocols were followed in which multiple histamine bolus injections were given 1 h apart. We found that the time courses of E and R had consistent patterns (transient peak that returned to baseline within 1000 sec) even in cases of low mean arterial pressure (MAP). Indomethacin pre-treatments prevented tachyphylaxis to repeated i.v. challenges. beta-blockade produced a mild increase in baseline and a potentiation of the histamine-induced response in E and these effects were not altered with further alpha-or H2-blockade. Blockade of alpha-receptors increased the time to recovery in both E and MAP presumably by decreasing blood flow. Finally, we suggest that preventing the H2-receptor induced increase in bronchial blood flow may have increased the time to maximal E without affecting the recovery time.
我们在麻醉、气管切开、麻痹并人工通气的杂种犬中，描绘了组胺诱导的支气管收缩的完整时程，以及内源性儿茶酚胺释放和组胺对H2受体的作用对其的调节。使用递推最小二乘估计器连续估计呼吸阻力（R）和弹性（E）。遵循了三个方案，其中每隔1小时进行多次组胺推注。我们发现，即使在平均动脉压（MAP）较低的情况下，E和R的时程也具有一致的模式（短暂峰值，在1000秒内恢复到基线）。吲哚美辛预处理可防止对重复静脉注射刺激产生快速耐受。β受体阻滞剂使基线轻度升高，并增强了组胺诱导的E反应，且这些效应不会因进一步的α或H2受体阻滞剂而改变。α受体阻滞剂可能通过减少血流量而增加了E和MAP的恢复时间。最后，我们认为，阻止H2受体诱导的支气管血流量增加可能增加了达到最大E的时间，而不影响恢复时间。
