Changes in the myocardial cell membrane calcium channel in myocardial ischemia-Relation to ventricular fibrillation.

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To explore possible roles of the calcium channel of myocardial cell membrane in the pathogenesis of ventricular fibrillation (Vf), we examined changes in the myocardial cell membrane 3H-nitrendipine (3H-N)-binding site in dogs with Vf in experimental myocardial ischemia. In animals which developed Vf 15±2 min after coronary ligation, the ischemic myocardium had a significantly larger number of 3H-N-binding sites (296±4 fmol/mg protein) compared to the nonischemic area (240±10). In animals in which Vf was elec trically induced 20min after coronary artery ligation, there was no increase of Bmax in ischemic (221±6) and nonischemic (227±5) area. Therefore, these results indicate that increase in Bmax in the ischemic area in Vf is not asecondary phenomenon caused by Vf. In animals without Vf, the number of binding sites (Bmax) did not increase significantly in the 15- and 30-min ischemic (216±3, 245±11) and nonischemic (227±, 213±7) area. No significant change was observed in the Kd for is chemia, nonischemia, or the ischemic period between the those groups. It is known that the myocardial cell membrane binding site of 3H-N is closely linked with voltage-de pendent Ca channel (VDCC). We concluded that the increase in the number of 3H-Nbinding sites that is VDCC, is one of the major factors responsible for development of Vf at about 15-min ischemia.
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