Chapman R W
Can J Physiol Pharmacol. 1985 Dec;63(12):1608-11. doi: 10.1139/y85-265.
The calcium channel blocker, verapamil (0.1-1.0 mg/kg, i.v.) was administered to anesthetized rats to determine its effects on ventilation and on ventilatory responses to hypoxia and CO2. Verapamil produced a dose-dependent increase in tidal volume (VT) and a decrease in respiration rate (f). The bradypnea due to verapamil was characterized by an increase in expiratory duration (TE) and no change of inspiratory duration (TI). Verapamil produced similar changes in VT and f in vagotomized rats. The increase in respiration rate and minute volume due to hypoxia were inhibited by verapamil (0.5 and 1.0 mg/kg) but the increase in tidal volume due to hypoxia was depressed only with the 1.0 mg/kg dose. On the other hand, the increase in VT due to breathing CO2 was not changed by verapamil (0.1-1.0 mg/kg), but depression of the respiratory frequency response to CO2 occurred with 1.0 mg/kg of verapamil. These results indicate that verapamil produced slow, deep breathing and these responses were not mediated by vagal mechanisms. Ventilatory responses to hypoxia were depressed by verapamil. However, since the calcium blocker demonstrated no effect on the VT-CO2 relationship, verapamil did not change ventilatory chemosensitivity to CO2. The data also suggest that mechanisms governing the control of respiratory frequency are more sensitive to verapamil than tidal volume responses.
将钙通道阻滞剂维拉帕米（0.1 - 1.0毫克/千克，静脉注射）给予麻醉大鼠，以确定其对通气以及对低氧和二氧化碳通气反应的影响。维拉帕米使潮气量（VT）呈剂量依赖性增加，呼吸频率（f）降低。维拉帕米引起的呼吸减慢表现为呼气持续时间（TE）增加，吸气持续时间（TI）无变化。维拉帕米在迷走神经切断的大鼠中对VT和f产生类似变化。维拉帕米（0.5和1.0毫克/千克）抑制了低氧引起的呼吸频率和分钟通气量增加，但仅1.0毫克/千克剂量时低氧引起的潮气量增加才受到抑制。另一方面，维拉帕米（0.1 - 1.0毫克/千克）未改变二氧化碳引起的VT增加，但1.0毫克/千克维拉帕米会使对二氧化碳的呼吸频率反应降低。这些结果表明，维拉帕米产生缓慢、深沉的呼吸，且这些反应不是由迷走神经机制介导的。维拉帕米抑制了对低氧的通气反应。然而，由于钙通道阻滞剂对VT - 二氧化碳关系无影响，维拉帕米并未改变对二氧化碳的通气化学敏感性。数据还表明，控制呼吸频率的机制比潮气量反应对维拉帕米更敏感。
