Ischemic preconditioning reduces infarct size in swine myocardium.

Abstract

We evaluated the hypothesis that stunning swine myocardium with brief ischemia reduces oxygen demand in the stunned region and increases tolerance of myocardium to longer periods of ischemia. Wall function was quantified with ultrasonic crystals aligned to measure wall thickening, and stunning was achieved with two cycles of left anterior descending coronary artery (LAD) occlusion (10 minutes) and reperfusion (30 minutes), after which the LAD was occluded for 60 minutes and reperfused for 90 minutes. Infarct size (as a percent of risk region) was then determined by incubating myocardium with para-nitro blue tetrazolium. Regional oxygen demand was measured as myocardial oxygen consumption before the 60-minute LAD occlusion in the stunned region; tracer microspheres were used to determine blood flow, and blood from the anterior interventricular vein and left atrium was used to calculate oxygen saturations. After the second reperfusion period, wall thickening in the stunned region was reduced to 1.4 +/- 2.4% compared with 36.7 +/- 2.5% (mean +/- SEM) before ischemia (p less than 0.001). Regional myocardial oxygen consumption after stunning (3.1 +/- 0.7 ml O2/min/100 g) was no different from regional myocardial oxygen consumption before stunning (3.7 +/- 0.6 ml O2/min/100 g). In the nine pigs "preconditioned" by stunning, infarct size was 10.4 +/- 6.3% of the risk region compared with 48.0 +/- 12.7% in the six control pigs subjected to 60 minutes of ischemia without prior stunning (p less than 0.005). The risk regions were similar (14.4 +/- 1.5% vs. 14.6 +/- 1.9% of the left ventricle, preconditioned vs. control pigs, respectively). We conclude that stunning swine myocardium with two cycles of a 10-minute LAD occlusion followed by reperfusion increases ischemic tolerance but that changes in regional demand in stunned myocardium do not predict the marked reduction in infarct size that follows a subsequent 60-minute period of ischemia.

Reduction by prostaglandin E1 or prostaglandin E0 of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

“…The opening of KATP channels may also cause a decrease in ATP depletion, glycogen breakdown, and anaerobic glycolysis, thus preserving energy substrate (Grover et al, 1989;. Pronounced cardioprotective effects by ischaemic preconditioning have been demonstrated in models of myocardial ischaemia and reperfusion in the rat (Li & Kloner, 1992), rabbit (Cohen et al, 1991), dog (Li et al, 1990) and pig (Scott et al, 1990).…”

Ischemic preconditioning triggers the activation of MAP kinases and MAPKAP kinase 2 in rat hearts

“…This transient adaptive response has been demonstrated to be associated with decreased reperfusion-induced arrhythmias [2], increased recovery of postischemic contraction functions [3], and reduction of the infarct size [4]. The adaptive protection has been found to be mediated by gene expression and their transcriptional regulation [5].…”

Inducible Nitric-oxide Synthase Is an Important Contributor to Prolonged Protective Effects of Ischemic Preconditioning in the Mouse Kidney

“…Ischemic preconditioning is the phenomenon whereby a prior ischemic stress renders the organ resistant to a subsequent ischemic insult (1)(2)(3)(4). In the heart preconditioning, induced by short episodes of ischemia and reperfusion treatment, has two distinct phases: an early phase that lasts from a few minutes to 2 or 3 h and a late phase that is sustained for 2-4 days (5).…”