Cell death in ischemic, reperfused porcine hearts: A histochemical and functional study

Abstract

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.

The Coronary Circulation as a Target of Cardioprotection

“…12 Pigs have a negligible native collateral circulation, and infarction starts after 15 to 35-minute coronary occlusion and affects 80% of the area at risk after 60 to 180 minutes. 23,24 Primates have few innate collaterals but are relatively resistant to myocardial ischemia; there is no infarction after 40-to 60-minute coronary occlusion, and even after 90-minute coronary occlusion, infarct size is smaller than that in pigs. 25 Apart from such species differences in the native collateral circulation, coronary vasomotor mechanisms also differ between species.…”

Pentobarbital versus medetomidine-ketamine-fentanyl anaesthesia: effects on haemodynamics and the incidence of ischaemia-induced ventricular fibrillation in swine

“…Furthermore, they have few native collaterals (White & Bloor 1981) and it is therefore not necessary to incorporate collateral ow as a covariate in the analysis of ventricular brillation. The analysis of ventricular brillation was restricted to 10 min of ischaemia (the early phase of ischaemia [Verdouw & Hartog 1986, Sedlis 1992), because myocardium subjected to 10 min of ischaemia does not develop irreversible cell injury (Pich et al 1988). Accordingly, myocardial infarction as a confounder in the analysis of ventricular brillation was avoided.…”

Comparative study on the enhancement of ischemic tolerance by intracoronary pretreatment with three calcium antagonists in pig hearts

“…This method has been validated in several studies. The result of the nitroblue tetrazolium stain corresponds very well with histological [16], ultrastructural [17], and functional [18] criteria of cell death, provided ischemia or ischemia plus reperfusion last more than 6 hours. The risk region could accurately be delineated by an injected dye because porcine hearts lack significant collateral blood flow [19,20], warranting a clear and sharp border between ischemic and well-perfused myocardium.…”