Aaron E A, Forster H V, Lowry T F, Korducki M J, Ohtake P J
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226, USA.
J Appl Physiol (1985). 1996 Jan;80(1):176-81. doi: 10.1152/jappl.1996.80.1.176.
To gain insight into the role of cerebral lactic acidosis in the hypoxic ventilatory response, we administered dichloroacetate (DCA) intravenously to inhibit lactic acid production in 7 awake goats (40-70 kg) during 0.5 h of normoxia (inspired O2 fraction = 0.209) and 5 h of poikilocapnic hypoxia (inspired O2 fraction = 0.125). On separate days, these goats were also studied with a continuous saline infusion (18 ml/h iv) during 5 h of normoxia and hypoxia. Arterial PCO2 (PaCO2) did not change during the 5-h normoxic period. During hypoxia, arterial PO2 fell significantly (P < 0.05) with both saline (from 111.3 to 39.0 Torr) and DCA (from 111.8 to 42.0 Torr) infusions. PaCO2 decreased (P < 0.05) during the first 0.5 h of both the saline and DCA hypoxia protocols. The decrease was greater (P < 0.05) during DCA (from 36.5 to 33.5 Torr) than during saline infusion (from 37.7 to 36.3 Torr). With saline infusion, PaCO2 decreased (P < 0.05) by 4.9 Torr between 0.5 and 5.0 h of hypoxia. However, over this period of DCA hypoxia, PaCO2 did not significantly decrease (P > 0.05). We conclude that the enhanced hyperventilation with DCA during acute hypoxia is consistent with brain lactic acidosis depressing breathing. Absence of additional significant hyperventilation after 0.5 h of DCA hypoxia suggests that a time-dependent alleviation of brain lactic acidosis might normally contribute to ventilatory acclimatization to hypoxia.
为深入了解脑乳酸酸中毒在低氧通气反应中的作用，我们对7只清醒山羊（体重40 - 70千克）静脉注射二氯乙酸（DCA）以抑制乳酸生成，实验过程包括0.5小时的常氧（吸入氧分数 = 0.209）和5小时的变碳酸低氧（吸入氧分数 = 0.125）。在不同日期，这些山羊还接受了连续生理盐水输注（18毫升/小时，静脉注射），同样经历5小时的常氧和低氧过程。在5小时的常氧期，动脉血二氧化碳分压（PaCO₂）未发生变化。在低氧期间，生理盐水输注（从111.3降至39.0托）和DCA输注（从111.8降至42.0托）时，动脉血氧分压（PO₂）均显著下降（P < 0.05）。在生理盐水和DCA低氧实验方案的最初0.5小时内，PaCO₂均下降（P < 0.05）。DCA组下降幅度更大（P < 0.05）（从36.5降至33.5托），大于生理盐水输注组（从37.7降至36.3托）。生理盐水输注时，低氧0.5至5.0小时期间PaCO₂下降（P < 0.05）4.9托。然而，在DCA低氧的这段时间内，PaCO₂未显著下降（P > 0.05）。我们得出结论，急性低氧期间DCA引起的过度通气增强与脑乳酸酸中毒抑制呼吸一致。DCA低氧0.5小时后未出现额外显著的过度通气，表明脑乳酸酸中毒的时间依赖性缓解可能通常有助于通气适应低氧。
