Halperin M L, Fields A L
Am J Med Sci. 1985 Apr;289(4):154-9. doi: 10.1097/00000441-198504000-00005.
We have compared the capacity of major organs to produce lactic acid from endogenous sources relative to their ability to buffer that proton load. We deduced that the ultimate source for the rapid production of a very large amount of lactic acid must be hepatic and/or muscle glycogen or exogenous glucose, because the quantity of endogenous glucose is quite small and the rate of net protein catabolism is too slow. Of the organs examined, only the liver of fed persons can produce sufficient lactic acid to markedly overwhelm its own buffer capacity plus that of the ECF and other tissues. Moreover, it is important to realize that a fasted (low hepatic glycogen) subject who lacks the stimulus for muscle glycogenolysis can only develop a modest degree of acute lactic acidosis owing to a limited precursor availability; under these circumstances, hypoglycemia and/or localized tissue necrosis could be the major threats to that patient. We present two examples with more chronic lactic acidosis without hypoxia emphasizing that tissue catabolism may be necessary to support high rates of lactic acid production, and we suggest that a high plasma lactate concentration need not be present to observe a large turnover of this metabolite.
我们比较了主要器官从内源性来源产生乳酸的能力与其缓冲质子负荷的能力。我们推断，快速产生大量乳酸的最终来源必定是肝脏和/或肌肉糖原或外源性葡萄糖，因为内源性葡萄糖的量相当少，且净蛋白分解代谢的速率太慢。在所检查的器官中，只有进食者的肝脏能够产生足够的乳酸，从而明显超过其自身的缓冲能力以及细胞外液和其他组织的缓冲能力。此外，必须认识到，缺乏肌肉糖原分解刺激的禁食（肝糖原含量低）受试者，由于前体物质供应有限，只会出现适度的急性乳酸酸中毒；在这种情况下，低血糖和/或局部组织坏死可能是该患者面临的主要威胁。我们给出两个无缺氧的更慢性乳酸酸中毒的例子，强调组织分解代谢可能是支持高乳酸产生率所必需的，并且我们认为，观察到这种代谢物的大量周转不一定需要血浆乳酸浓度升高。
