Effect of Experimental Infarction, Manual Massage, and Electrical Defibrillation on Myocardial Lipoprotein Lipase Activity of Dogs*

Abstract

It has been demonstrated that heart muscle contains lipoprotein lipase (LPL) in high concentrations (1, 2). This enzyme, which appears to be identical with the post-heparin "clearing factor," specifically hydrolyzes the triglyceride component of chylomicrons and other low density lipoproteins (3).It is assumed that the enzyme is held on the cell surfaces by electrostatic forces (4) and is in equilibrium with small quantities of circulating LPL (5). Injection of heparin (6) and other substances with negatively charged polar groups (7-10) is followed by a prompt appearance of LPL activity in the circulation. These observations suggest that alteration of the electrostatic forces holding the enzyme to the binding sites on the cell surfaces may account for the immediate action of these substances.Ligation of the coronary artery produces immediate electrocardiographic (ECG) changes, which are assumed to reflect the disturbed equilibrium of the electrostatic forces over the infarcted area. Manual massage, by producing subepicardial damage, can also result in changes of the surface electrostatic forces. Infarction and massage affect the electrostatic forces of the damaged surfaces only. Electrical defibrillation, on the other hand, can disturb the electrostatic equilibrium of the entire myocardium.This study was undertaken in order to demonstrate the effect of myocardial infarction, manual massage, and electrical defibrillation on the level of myocardial LPL. It was assumed that these factors would release the enzyme from its binding sites by a possible effect on the electrostatic forces

Effect of Diabetes and Insulin on the Activity of Myocardial and Adipose Tissue Lipoprotein Lipase of Rats*

“…The ples of each incubation medium were taken for determination of the heparin-released lipase activity. The lipolytic activity was determined according to the procedure described before (8,9), and expressed in microequivalents of FFA liberated by 1 g wet weight of tissue during one hour of incubation.…”

Improved myocardial performance induced by dofibrate during reperfusion after acute myocardial infarction

“…Thus, the reduction of tissue oleic acid, arachidonic acid, and linoleic acid during ischemia and reperfusion could result from the increased peroxisomal p-oxidation of fatty acids (Lazarow and De duve 1975; MacDonald and Swam 29861, from the decreased lipolysis (Kessler and Senderoff 1962), or from the increased phospholipid synthesis through the increased activity of H -acylglycerophosphorylcholine acyltransferase (Kawashima et a&. 1986).…”