Lyrene R K, Welch K A, Godoy G, Philips J B
Pediatr Res. 1985 Dec;19(12):1268-71. doi: 10.1203/00006450-198512000-00009.
Hyperventilation (respiratory alkalosis) is an important treatment for persistent pulmonary hypertension in neonates. The precise way that hyperventilation attenuates hypoxic pulmonary vasoconstriction is unclear. We studied the effect of alkalosis on hypoxia-induced pulmonary vasoconstriction in 13 acutely instrumented, pentobarbital anesthetized, neonatal lambs. We specifically examined the relative effects of a metabolic alkalosis versus a respiratory alkalosis on hypoxic pulmonary vasoconstriction and compared these results to the control response to hypoxia without alkalosis. Hypoxic pulmonary vasoconstriction was significantly milder whenever the animal was alkalotic, regardless of whether the alkalosis was respiratory of metabolic. Thus, the elevated pHa rather than decreased PaCO2 during hyperventilation appears to be the major factor in moderating the response of the pulmonary vessels to acute hypoxia in this neonatal lamb model.
过度通气(呼吸性碱中毒)是治疗新生儿持续性肺动脉高压的重要方法。过度通气减轻缺氧性肺血管收缩的确切机制尚不清楚。我们对13只急性插管、戊巴比妥麻醉的新生羔羊进行研究,观察碱中毒对缺氧诱导的肺血管收缩的影响。我们特别研究了代谢性碱中毒与呼吸性碱中毒对缺氧性肺血管收缩的相对影响,并将这些结果与无碱中毒时缺氧的对照反应进行比较。无论碱中毒是呼吸性还是代谢性的,只要动物处于碱中毒状态,缺氧性肺血管收缩就明显较轻。因此,在这个新生羔羊模型中,过度通气期间升高的动脉血pH值而非降低的动脉血二氧化碳分压似乎是调节肺血管对急性缺氧反应的主要因素。