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

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 the normal myocardium.Subepicardial transmembrane potentials were recorded with floating microelectrodes.Transmural tissue biopsies were obtained with a drill from the sites of extracellular potential measurements at various times after coronary occlusion.Tissue levels of adenosine triphosphate (ATP), creatine phosphate (CP), and lactate were determined in this tissue.Glycogen distribution was assessed histochemically.Early ischemic changes are T-Q depression (1.5 minutes), S-T elevation (4 minutes), unresponsivene88 (8 minutes), fall of CP (low and stable after 4 minutes), and rise in lactate (doubled within 10 minutes).Electrical activity temporarily returns between 30 and 50 minutes, while CP further decreases and lactate increases.After 2 hours, T-Q and S-T potentials have decreased, and cells have become unresponsive in the central ischemic zone; levels (in /unoles per gram dry weight) for CP and ATP are <1, for lactate circa 240.In the electrical border zone, intermediate metabolic values are found.No transmural electrical or metabolic gradients are present.In the border, zones with normal glycogen content interdigitate with zones depleted of glycogen.If occlusion is released after 2 hours, ATP, CP, and lactate levels do not change in central and border sites.In the border during reperfuaion, cells with nearly normal transmembrane action potentials are in close proximity to unresponsive cells with low resting membrane potentials.These findings suggest that the ischemic border is composed of interdigitating normal and ischemic zones sharply demarcated from each other.