A marked decrease in the activity of the amiloride-sensitive Na+/H+ exchanger has been demonstrated in hearts from streptozotocin (STZ)-induced diabetic rats. The aim of this study was to investigate the contribution of other specific sarcolemmal transport mechanisms to intracellular pH (pHi) recovery upon reperfusion in STZ-induced diabetic rat hearts and their relation to recovery of ventricular function. Isovolumic rat hearts were submitted to a zero-flow ischemie period of 28 min at 37°C and then reperfused for 28 min. The time course of pHi decline during ischemia and of recovery on reperfusion was followed by means of 31P-labeled NMR. The perfusion buffers used were either HEPES or CO2/HCO3−. An HCO3−-dependent (amiloride-insensitive) mechanism contributed to pHi recovery after ischemia in the diabetic rat hearts. Even when the Na+/H+ exchanger was blocked by amiloride in nominally HCO3−-free solution, a rapid rise in pHi occurred during the first 3 min of reperfusion. The early rise in pHi was reduced by external lactate and inhibited by α-cyano-4-hydroxycinnamate. This suggested that a coupled H+-lactate efflux may be a major mechanism for acid extrusion in the initial stage of reperfusion. The observation of a higher functional recovery on reperfusion in diabetic hearts is in accordance with previous studies using HCO3− buffer. However, this study shows that a good recovery of function occurred even more rapidly in diabetic hearts receiving HEPES-buffered solution than in those receiving HCO3−-buffered solution. This suggests that the HCO3−-dependent mechanism of regulation may be depressed in diabetic rat hearts.
Mechanisms of Intracellular pH Regulation During Postischemic Reperfusion of Diabetic Rat Hearts
Nassirah Khandoudi, Monique Bernard, Patrick Cozzone, Danielle Feuvray; Mechanisms of Intracellular pH Regulation During Postischemic Reperfusion of Diabetic Rat Hearts. Diabetes 1 February 1995; 44 (2): 196–202. https://doi.org/10.2337/diab.44.2.196
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