Lactic acidosis: effect of treatment on intracellular pH and energetics in living rat heart.

Lactic acidosis: effect of treatment on intracellular pH and energetics in living rat heart.
复制标题

乳酸性酸中毒:治疗对活体大鼠心脏细胞内 pH 值和能量学的影响。

DOI:
10.1152/ajpheart.1992.262.5.h1572
复制
发表时间:
1992
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Gore,JC
Gore,JC
中科院分区:
--
文献类型:
--
作者:
Zahler,R;Barrett,E;Majumdar,S;Greene,R;Gore,JC

文献摘要

被引文献

相似文献

全身性酸血症可能损害心脏的收缩能力,易发生心律失常。此外,碳酸氢盐治疗可能会进一步抑制心脏功能并增加死亡率。无论是心肌细胞内pH的变化还是能量代谢的变化是导致这种性能下降的原因,在活体环境中还没有得到澄清。因此,我们研究了乳酸酸中毒和两种建议的治疗方法对麻醉活体大鼠心肌能量和细胞内pH的影响。先前验证的31P标记核磁共振(31P-核磁共振)波谱技术使用饱和脉冲来跟踪心肌细胞内的pH、磷酸肌酸(PCR)、三磷酸腺苷(ATP)和无机磷(PI)。在获得基线值后,我们注入乳酸以达到大于5 mM的水平。然后我们加入小苏打(n=7)或生理盐水(n=5)的输液。在乳酸输注过程中,动脉pH下降(从7.27降至7.07,P<0.0001),但心肌细胞内pH无明显变化(7.13vs.7.07,P>0.05)。但Pcr/PI的比值随着酸血症的增加而降低(从3.13降至2.24,P=0.004),提示能量代谢受损。与生理盐水相比,小苏打输注可恢复全身pH值(从7.08降至7.29),但心肌pH值无明显变化。此外,在碳酸氢盐治疗后,Pcr/PI进一步下降(1.41比2.42,P=0.08),但在生理盐水治疗后没有下降。因此,尽管全身性酸血症逆转,但碳酸氢盐治疗较生理盐水更严重的能量代谢损害。这提示了以前报道的碳酸氢盐治疗心脏不良反应的机制。
Systemic acidemia may impair cardiac contractility and predispose to arrhythmias. Moreover, bicarbonate treatment may further depress cardiac performance and increase mortality. Whether changes in myocardial intracellular pH or energy metabolism underlie this diminished performance has not been clarified in the in vivo setting. Thus we investigated the effect of lactic acidosis and two proposed treatments on myocardial energetics and intracellular pH in anesthetized living rats. A previously validated 31P-labeled nuclear magnetic resonance (31P-NMR) spectroscopic technique using saturating pulses was used to follow myocardial intracellular pH, phosphocreatine (PCr), ATP, and inorganic phosphate (Pi). After obtaining baseline values, we infused lactic acid to achieve a level greater than 5 mM. We then added an infusion of either bicarbonate (n = 7) or saline (n = 5). During lactic acid infusion, arterial pH declined (from 7.27 to 7.07, P less than 0.0001), but myocardial intracellular pH did not change (7.13 vs. 7.07, P not significant). The ratio of PCr to Pi, however, decreased with acidemia (from 3.13 to 2.24, P = 0.004), suggesting impaired energy metabolism. Compared with saline, bicarbonate infusion restored systemic pH (from 7.08 to 7.29), but myocardial pH was unaltered. In addition, PCr/Pi declined further following bicarbonate treatment (1.41 vs. 2.42, P = 0.08) but not following saline. Thus, despite reversal of systemic acidemia, bicarbonate treatment was associated with more severe impairment of energy metabolism than saline. This suggests a mechanism for previously reported adverse cardiac effects of bicarbonate treatment.