title: A new model of myocardial infarction in Yucatan minipigs.
abstract: Myocardial infarction studies in pigs have been complicated by the use of antiarrhythmic drugs or the high incidence of ventricular fibrillation. We report on a new model of experimental myocardial infarction in thiamylal-anesthetized Yucatan minipigs. These studies were performed in the absence of intravenous antiarrhythmic drugs. No animals required resuscitation during either surgery or reperfusion and only 19% were resuscitated during occlusion. Extensive systemic hemodynamic, regional contractility and coronary blood flow measurements were continuously obtained during left anterior descending coronary artery (LAD) occlusion (45 min) and reperfusion (240 min). Mean arterial blood pressure and left ventricular + dP/dt decreased during occlusion, and both declined further upon reperfusion. Persistent dysfunction (segmental shortening from 24.8 +/- 1.3 to 3.9 +/- 0.9% (p less than 0.001); pre-occlusion and 5 min post-occlusion, respectively) occurred immediately after occlusion in the myocardium perfused by the LAD, while late declines in segmental shortening (19.6 +/- 0.9 to 17.2 +/- 1.2%; pre-occlusion and 240 min post-reperfusion, respectively) were observed in myocardium perfused by the left circumflex coronary artery. While heart rate did not change during occlusion, tachycardia occurred at the onset of reperfusion. Although initial reactive hyperemia following reperfusion was manually inhibited, high LAD blood flow following reperfusion occurred early (0 to 60 min) but returned below pre-occlusion values late (180 to 240 min). The area at risk represented 23.1 +/- 0.9% (n = 34) of the left ventricle and 39.0 +/- 3.2% of this area was infarcted. Therefore, 9.2 +/- 0.9% of the left ventricle was infarcted. These data suggest that myocardical infarction in anesthetized minipigs can be achieved without the aid of intravenous antiarrhythmic drugs and reduced cardioversion. Therefore, this new model can be utilized in the evaluation of therapeutic compounds focused on altering the detrimental consequences of myocardical infarction.
authors.affiliation: SmithKline Beecham Pharmaceuticals, Department of Pharmacology, King of Prussia, PA 19406.
authors.forename: S A
authors.initials: SA
authors.lastname: Hamburger
authors.forename: L J
authors.initials: LJ
authors.lastname: Kopaciewicz
authors.forename: R E
authors.initials: RE
authors.lastname: Valocik
mesh_terms: D000758:Anesthesia; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000502:physiology; D004195:Disease Models, Animal; D004554:Electric Countershock; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D013552:Swine; D013556:Swine, Miniature / Q000502:physiology*