Abstract
This study was undertaken to clarify mechanisms accounting for striking disparities in the rate of plasma creatine kinase (CK) disappearance after experimental myocardial infarction compared to the much more rapid disappearance after bolus injections. In addition, it was designed to better characterize parameters employed in enzymatic estimation of infarct size. A two compartment model was utilized to analyze plasma CK activity after bolus injections of purified myocardial CK in dogs, and was found to provide better fits to plasma CK time-activity curves than those available with previously used one compartment models. However, the new model did not explain the differences in disappearance rates after infarction compared to injection. These appear to depend on continuing release of CK from the ischemic heart relatively late after infarction and upon differences in the behavior of native circulating CK compared to CK extracted from myocardium even under mild conditions.