Rose C E, Althaus J A, Kaiser D L, Miller E D, Carey R M
Am J Physiol. 1983 Dec;245(6):H924-9. doi: 10.1152/ajpheart.1983.245.6.H924.
To systemically evaluate the effects of acute hypoxemia and hypercapnic acidosis on the sympathetic nervous system, five unanesthetized mongrel dogs were studied during acute hypoxemia [arterial O2 tension (PaO2) 33 +/- 2 Torr], acute hypercapnic acidosis [arterial CO2 tension (PaCO2) 53 +/- 1 Torr; pH, 7.19 +/- 0.02], and combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 Torr; PaCO2, 52 +/- 1 Torr; pH, 7.18 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis resulted in increased mean arterial pressure, cardiac output, and heart rate. Moreover, combining acute hypoxemia and hypercapnic acidosis acted synergistically to increase circulating norepinephrine and epinephrine. Acute hypoxemia alone and acute hypercapnic acidosis alone resulted in reversible increases in mean arterial pressure, cardiac output, heart rate, and circulating norepinephrine. Although plasma epinephrine concentrations increased during acute hypoxemia, circulating epinephrine was unchanged during acute hypercapnic acidosis. These data indicate that acute hypoxemia and hypercapnic acidosis result in synergistic increase in circulating catecholamines.
为了系统评估急性低氧血症和高碳酸性酸中毒对交感神经系统的影响，我们对5只未麻醉的杂种犬在急性低氧血症[动脉血氧分压(PaO2) 33±2 Torr]、急性高碳酸性酸中毒[动脉血二氧化碳分压(PaCO2) 53±1 Torr；pH值，7.19±0.02]以及急性低氧血症合并高碳酸性酸中毒(PaO2，36±1 Torr；PaCO2，52±1 Torr；pH值，7.18±0.02)期间进行了研究。急性低氧血症合并高碳酸性酸中毒导致平均动脉压、心输出量和心率增加。此外，急性低氧血症与高碳酸性酸中毒联合作用可协同增加循环中的去甲肾上腺素和肾上腺素。单独的急性低氧血症和单独的急性高碳酸性酸中毒均导致平均动脉压、心输出量、心率和循环中的去甲肾上腺素出现可逆性增加。虽然在急性低氧血症期间血浆肾上腺素浓度升高，但在急性高碳酸性酸中毒期间循环中的肾上腺素未发生变化。这些数据表明，急性低氧血症和高碳酸性酸中毒可协同增加循环中的儿茶酚胺。
