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Hemodialysis with Calcium-Free Dialysate Prevents Myocardial Creatine Kinase Depletion After Brief Coronary Artery Occlusion in Dogs

Department of Medicine, University of Athens and "Alexandra" State and University Hospital, Athens, Greece

Joan Karli

Department of Medicine, University of Athens and "Alexandra" State and University Hospital, Athens, Greece

Anastasios Pistevos

Department of Medicine, University of Athens and "Alexandra" State and University Hospital, Athens, Greece

Gabriel Levis

Department of Medicine, University of Athens and "Alexandra" State and University Hospital, Athens, Greece

Spyridon Moulopoulos

Department of Medicine, University of Athens and "Alexandra" State and University Hospital, Athens, Greece

To evaluate the effect of hypocalcemia on myocardial creatine kinase (CK) depletion after brief coronary artery occlusion and reperfusion, dogs were ren dered hypocalcemic via systemic hemodialysis for eighty minutes in the absence of Ca. Control animals were hemodialysed in the presence of Ca. The left ante rior descending coronary artery was then occluded for six minutes and reperfu sion for eighty minutes occurred at low flow of dialysate. A 50% decrease in serum Ca of the hypocalcemic animals during the eighty minutes of hemodialy sis resulted in a significant (about 35%) decrease of myocardial Ca. Comparison of the myocardial creatine kinase activity following reperfusion showed preser vation of the enzyme in the ischemic areas of the hypocalcemic animals, whereas the CK activities of the ischemic areas of the normocalcemic animals were much lower (p < 0.005). During the reperfusion period serum Ca of the hypocalcemic group increased to 75% of that of the normocalcemic group while myocardial Ca of both ischemic and nonischemic areas reequilibrated to normocalcemic values. Hemodynamic parameters during the various phases of the experiment were not altered significantly. It is concluded that transient decrease of myocar dial Ca produced by hypocalcemia prior to occlusion leads to protection against myocardial damage after brief coronary ligation.

Angiology, Vol. 39, No. 10, 865-872 (1988)
DOI: 10.1177/000331978803901003


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