Cell death in ischemic, reperfused porcine hearts: a histochemical and functional study.
The temporal development of infarcts was histochemically and functionally determined in porcine hearts. In one series of experiments (22 pigs), the distal third of the left anterior descending coronary artery (LAD) was transiently occluded for periods between 20 and 90 min and was reperfused for another 24 h. At the end of the experiments, the infarcted myocardium of four tissue slices was determined with a tetrazolium stain and related to the risk region which was delineated by a fluorescent dye. Infarcts started to develop in the ischemic septum and the subendocardial layer of the free anterior wall between 20 and 35 min of ischemia. Thereafter, infarctions progressed rapidly from the inner towards the outer layer at risk. The jeopardized anterior left ventricular wall became almost completely infarcted within 60 min of ischemia. In a second series of experiments (10 pigs) recovery of systolic shortening was studied with implanted ultrasonic crystals over 3 weeks of reperfusion. At the end of the experiments, systolic shortening was about 75% of baseline level when ischemia had lasted between 20 and 35 min. Almost no recovery was observed when the occlusion time lasted 45 to 60 min. This study suggests that the assessment of myocardial infarction with a tetrazolium stain after 24 h of reperfusion corresponds very well with functional recovery after 3 weeks of reperfusion. Furthermore, determination of regional myocardial function of the ischemic, reperfused segment in the chronic stage may be considered an additional tool to evaluate therapeutic effects on infarct size in this model.
Pich
S
S
Department of Cardiology, University of Göttingen, F.R.G.
Klein
H H
HH
Lindert
S
S
Nebendahl
K
K
Kreuzer
H
H
D000818:Animals; D002470:Cell Survival / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology*; D006439:Hemodynamics; D015425:Myocardial Reperfusion; D051381:Rats; D013552:Swine; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000209:etiology