In the present study the cl lect Cl left coronaly artery occlusion for 6 hours on the Twave voltage (mv), T wave area (mm2), sennn CPK ((J/t.) and infarction size (% fv) were studied ;n normal rats pretreated with calcium channel Mocker (Verapamil) and calcium gluconaic. The results showed that coronary artery occlusion in normal rats causes an increase in T wave voltage, T wave area, SCPK and infarction size was 62.92± 5.116% of left ventricle. Pretreated with verapami1 exerted a significant effects on T wave. Its Amplitude return to the prcligation value after 6 hours. However, the T wave area was increased and there was no effect on SCPK and infarction size.
Pretreatment with calcium gluconate excited an opposite effect on T wave voltage and T wave area where the ischemia induced changes were potentiated. Calcium gluconate pretreat¬ment was without effect on SCPK and infarction size.
Myocardial injury induced by ische¬mia is associated (I with complexes of calcium in the tissue which are detecta¬ble by electron microscope . The reac¬tion hetween myocardial ischcmia and myoplasmic calcium ions is complex. However ischemia is characterized by a reduction of myocardial ATP stores, which interferes with Irut.esarcolcmmal Na + - K + exchange, which intern el-evates intracellular Na + . Through an enhanced Na+ - Ca+ + exchange . in
IracelIul;trCa++increases ( Corr et al 1982 & Sedlis et al 1983). Lowered ATP stores also reduce Ca+ + uptake by the sarcoplasmic reticuIum and re¬duced the extrusions of Ca+ + from cells.
The resultant raised intracellulalr¬Ca + + causes mitochondrial Ca + + overhood which depresses ATP usage and activate sarcolcmmal phospholi¬pases. Membrane phospholipid degra¬dation products are released, they have