EFFECTS OF REGIONAL MYOCARDIAL LIDOCAINE INFUSION ON HIGH-ENERGY PHOSPHATES

High energy phosphates [phosphocreatine (PCr) and adenosine triphospha te (ATP)] are maintained in the heart under conditions of altered myoc ardial contractility and under certain conditions of myocardial ischem ia (such as hibernating myocardium). However, the metabolic consequenc es of reduced regional contractility have not been investigated. This study was designed to test the hypotheses that (1) under conditions of normal blood flow, reduction in regional contractility does not resul t in changes in PCr or ATP and (2) under conditions of reduced blood n ow, reduction in regional contractility prevents the expected decline in high energy phosphates usually seen in regional ischemia. An in sit u open chest. swine preparation was used in which regional contractili ty was reduced with the administration of intracoronary lidocaine. Hig h energy phosphates were measured using phosphorus-31 magnetic resonan ce spectroscopy (NMR) under conditions of normal flow and reduced flow . Intracoronary lidocaine infusion in 9 animals did not change blood f low from basal levels, but significantly reduced regional segment shor tening from 0.16+/-0.02 to 0.02+/-0.01. The ratio of PCr/ATP did not c hange with lidocaine infusion (control: 1.53+/-0.09; lidocaine: 1.59+/ -0.11), but oxygen content in the anterior interventricular vein incre ased from 8.25+/-0.69 to 9.83+/-0.91 ml/O-2/100 ml blood in parallel s tudies (P=0.04). While the lidocaine infusion was maintained, subseque nt coronary stenosis significantly reduced subendocardial blood flow f rom 0.91+/-0.06 to 0.41+/-0.06 ml/min/g without significantly altering high energy phosphates (PCr/ ATP=1.51+/-0.15). In contrast to the 29% decline in PCr previously seen with regional ischemia, PCr was unchan ged with this degree of flow reduction in the presence of lidocaine, T hus, PCr and ATP are unchanged under conditions of reduced contractili ty, consistent with equilibrium of energy synthesis and utilization. I n addition, factors which reduce myocardial contractility either pharm acologically or endogenously, protect against the metabolic consequenc es of reduced now by reducing MVO(2).