Ketoacid production in acute respiratory and metabolic acidosis and alkalosis in rats.

Ketoacid production in acute respiratory and metabolic acidosis and alkalosis in rats.
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大鼠急性呼吸性和代谢性酸中毒和碱中毒中酮酸的产生。

DOI:
10.1152/ajprenal.1989.256.3.f437
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发表时间:
1989
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Hood,VL
Hood,VL
中科院分区:
--
文献类型:
--
作者:
LaGrange,BM;Hood,VL

文献摘要

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代谢性酸中毒抑制酮症人和动物的酮酸生成,碱中毒则促进酮酸的产生。为了将这些影响与叠加呼吸性酸碱紊乱的影响进行比较,我们评估了清醒的酮症大鼠在代谢紊乱(静脉注射HCl或NaHCO3)或呼吸系统(高或低碳酸血症)紊乱时的酮输出。血pH值在3 h内下降0.1-0.2个单位,血酮浓度显著降低1.9 mm(代谢物)和1.1 mm(呼吸系统),尿酮排泄率显著降低1.3 mumol/min(代谢物)。随着全身pH值的升高,血酮浓度和尿酮排泄率显著增加。在代谢性酸碱紊乱(r=0.87)和呼吸性酸碱紊乱(r=0.67)中,血液pH值的变化与尿酮排泄率的变化相关。这些变化发生得很快,而且很快就可以逆转。这些发现表明,代谢或呼吸性酸碱紊乱引起的系统pH的轻微变化改变了酮症大鼠的净酮酸产生,证实了内源性酸输出的pH控制是酸碱调节,并表明介导这一过程的是系统pH,而不是重碳酸盐浓度。
Metabolic acidosis inhibits and alkalosis enhances ketoacid production in ketotic humans and animals. To compare these effects with those of superimposed respiratory acid-base disturbances, ketone output was evaluated in awake ketotic rats during metabolic (intravenous infusions of HCl or NaHCO3) or respiratory (hyper or hypocapnia) disorders. With decreases in blood pH of 0.1-0.2 units over 3 h, blood ketone concentrations significantly decreased an average of 1.9 mM (metabolic) and 1.1 mM (respiratory) and urinary ketone excretion rates significantly decreased by 1.3 mumol/min (metabolic). With increases in systemic pH, blood ketone concentrations and urinary ketone excretion rates were significantly increased. Changes in blood pH correlated with changes in urinary ketone excretion rates in both metabolic (r = 0.87) and respiratory (r = 0.67) acid-base disturbances. The alterations occurred promptly and were rapidly reversible. These findings indicate that modest changes in systemic pH from metabolic or respiratory acid-base disturbances modify net ketoacid production in ketotic rats, confirm pH control of endogenous acid output as an acid-base regulator, and show that systemic pH, not bicarbonate concentration, mediates the process.