Reduction by Hyaluronidase of Myocardial Necrosis following Coronary Artery Occlusion
Electrocardiographic, enzymatic, and morphologic signs of myocardial ischemic injury following coronary occlusion have previously been shown to be ameliorated by reducing myocardial oxygen requirements, and/or by increasing the availability of oxygen as well as of substrates for anaerobic ATP production. Since hyaluronidase increases diffusion through the extracellular space and may facilitate delivery of substrates to ischemic cells, the influence of its administration on the size of experimentally produced infarcts was studied. In 14 control dogs epicardial electrocardiograms were taken in 10-15 sites on the anterior surface of the left ventricle before and after occlusion of the left anterior descending coronary artery. Twenty-four hours later, transmural specimens were obtained from the same sites from which electrocardiograms had been recorded, and were analyzed for creatine phophokinase (CPK) activity, for histologic changes, and glycogen content. In control dogs, sites exhibiting S-T-segment elevation 15 min after occlusion showed early structural signs of necrosis and glycogen depletion in 97% of specimens taken after 24 hours. The relationship between S-T-segment elevation at 15 min (mv) and CPK activity 24 hours later (IU/mg protein) was log CPK = –0.061 S-T + 1.26. Hyaluronidase (225 u/kg) was given to 15 dogs; no hemodynamic changes occurred but the depression of CPK activity was reduced following occlusion; log CPK = –0.024 S-T + 1.28. Similarly, only 55% of sites that showed S-T-segment elevation prior to hyaluronidase administration exhibited histologic signs of early infarcts and glycogen depletion 24 hours later. It is concluded that hyaluronidase diminished myocardial necrosis following acute coronary occlusion.
- Myocardial ischemic injury
- Myocardial creatine phosphokinase
- Myocardial infarction
- Epicardial electrocardiography
- S-T-segment elevation
- Left ventricular function
- Received January 10, 1972.
- Accepted March 30, 1972.
- © 1972 American Heart Association, Inc.