Effects of lymphatic transport of enzyme on plasma creatine kinase time-activity curves after myocardial infarction in dogs.

Abstract

Because creatine kinase (EC 2.7.3.2, CK) appears in cardiac lymph after myocardial infarction, determination of whether lymph inactivates CK in vitro and whether interruption of cardiac lymph flow influences estimation of infarct size based on plasma CK changes in conscious dogs was studied. After the effects of incubation of canine myocardial CK in native, deproteinized, or sulfhydryl-fortified lymph and dialysates were characterized, effects of interruption of cardiac lymph flow on plasma CK time-activity curves after coronary occlusion were assessed in 13 conscious dogs, 7 of which had exteriorized occlusive snares around cardiac lymphatics and the left anterior descending coronary artery. Native and deproteinized lymph as well as lymph dialysate markedly inactivated CK in vitro with associated nonenzymatically mediated proteolysis detectable on SDS [sodium dodecyl sulfate] gels. CK released into blood after coronary occlusion compared to myocardial CK depletion was 50% less in dogs with lymphatic occlusion (P < 0.01) although CK loss in the centers of infarcts (73% and 69%) and overall CK depletion (18% and 20%) were similar in the 2 groups. Based on comparison of observed to projected plasma CK values prior to lymphatic occlusion, significantly less CK appeared in blood when coronary occlusion was followed by lymphatic occlusion (P < 0.01), although the rate of disappearance of CK from the systemic circulation was not altered. Lymph inactivates CK in vitro, and plasma CK time-activity curves after coronary occlusion are influenced considerably by interruption of cardiac lymph flow, a factor that should be incorporated to refine enzymatic estimates of infarct size.