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Am J Physiol Heart Circ Physiol 278: H1457-H1463, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 5, H1457-H1463, May 2000

Importance of bicarbonate transport for protection of cardiomyocytes against reoxygenation injury

C. Schäfer, Y. V. Ladilov, B. Siegmund, and H. M. Piper

Physiologisches Institut, Justus-Liebig-Universität Giessen, D-35392 Giessen, Germany

Isolated cardiomyocytes from adult rats were incubated in anoxic bicarbonate-buffered media at extracellular pH (pHo) 6.4 until a cytosolic Ca2+ overload and intracellular pH (pHi) of 6.4 were reached. On reoxygenation, the pH of the medium was changed to 7.4 to activate the Na+/H+exchanger (NHE) and the Na+-HCO-3 symporter (NBS). The reoxygenation was performed in the absence or presence of the NHE inhibitor HOE-642 (3 µmol/l) and/or the NBS inhibitor DIDS (0.5 mmol/l), as in bicarbonate-free media. In reoxygenated control cells pHi rapidly recovered to the preanoxic level, and a burst of spontaneous oscillations of cytosolic Ca2+ occurred, accompanied by the development of hypercontracture. When NBS and NHE were simultaneously inhibited during reoxygenation, pHi recovery was prevented, Ca2+ oscillations were attenuated, and hypercontracture was abolished. Sole inhibition of NBS or NHE showed no protection against hypercontracture. In the absence of cytosolic acidosis, HOE-642 or DIDS did not prevent hypercontracture induced by Ca2+ overload. The results demonstrate that simultaneous inhibition of NHE and NBS is needed to protect myocardial cells against reoxygenation-induced hypercontracture.

ischemia; reperfusion; myocytes


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