Crie J S, Wildenthal K, Adcock R, Templeton G, Willerson J T
Am J Physiol. 1976 Oct;231(4):1209-13. doi: 10.1152/ajplegacy.1976.231.4.1209.
Isolated, isometrically contracting cat papillary muscles were used to evaluate the inotropic interactions of lactic acidosis, hypercarbic acidosis, and lactate ion with hypertonic mannitol. These studies have documented that both lactic acidosis (pH less than 7.0) and lactate ion at a normal pH inhibit the inotropic effect of hyperosmotic mannitol in vitro. In contrast, hypercarbic acidosis does not prevent the inotropic effect of mannitol. Inhibition by lactic acid of mannitol's effects on contractility persists in the presence of beta-receptor blockade. The results suggest that inhibition by severe lactic acidosis of the direct inotropic effect of hyperosmolality in isolated cardiac muscle is mediated by lactate ion rather than acidosis per se.
采用离体等长收缩的猫乳头肌来评估乳酸酸中毒、高碳酸血症性酸中毒以及乳酸根离子与高渗甘露醇之间的变力相互作用。这些研究已经证明,乳酸酸中毒(pH值小于7.0)以及正常pH值下的乳酸根离子在体外均会抑制高渗甘露醇的变力作用。相比之下,高碳酸血症性酸中毒并不会阻止甘露醇的变力作用。在存在β受体阻滞剂的情况下,乳酸对甘露醇收缩性作用的抑制依然存在。结果表明,在离体心肌中,严重乳酸酸中毒对高渗状态直接变力作用的抑制是由乳酸根离子介导的,而非酸中毒本身。