The "border zone" in myocardial ischemia. An electrophysiological, metabolic, and histochemical correlation in the pig heart.

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Abstract
Regional ischemia was produced in isolated perfused pig hearts and in hearts in situ by clamping the left descending coronary artery. Intramural and epicardial DC electrograms were recorded from multiple, regularly spaced sites in the central ischemic and border zones and in normal myocardium. Subepicardial transmembrane potentials were recorded with floating microelectrodes. Transmural tissue biopsies were obtained from the sites of extracellular potential measurements at various times after coronary occlusion. Tissue levels of ATP, creatine phosphate (CP) and lactate were measured. Glycogen distribution was assessed histochemically. Early ischemic changes are T-Q depression (1.5 min), S-T elevation (4 min), unresponsiveness (8 min), fall of CP (low and stable after 4 min) and rise in lactate (double within 10 min). Electrical activity temporarily returned between 30 and 50 min, CP further decreased and lactate increased. After 2 h, T-Q and S-T potentials decreased, and cells became unresponsive in the central ischemic zone; levels (in .mu.mol/g dry weight) for CP and ATP were < 1, for lactate .apprx. 240. In the electrical border zone, intermediate metabolic values occurred. No transmural electrical or metabolic gradients were present. Border zones with normal glycogen content interdigitated with zones depleted of glycogen. If occlusion was released after 2 h, ATP, CP and lactate levels did not change in central and border sites. In the border during reperfusion, cells with nearly normal transmembrane action potentials were in close proximity to unresponsive cells with low resting membrane potentials. The ischemic border may be composed of sharply demarcated interdigitating normal and ischemic zones.

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