Postischemic recovery in the stunned myocardium after reperfusion in the presence or absence of a flow-limiting coronary artery stenosis.
Hyperemic flow occurs after release of a transient coronary artery occlusion in excess of the acquired oxygen debt if the vessel has sufficient vasodilator reserve. The purpose of this study was to determine whether differences exist in the degree of postischemic functional and metabolic recovery in the stunned myocardium when a reactive hyperemia is allowed to occur as opposed to reperfusion in the presence of a flow-limiting coronary artery stenosis. Anesthetized dogs were subjected to 15-minute episodes of coronary artery occlusion, followed by either 10 minutes (short reperfusion) or 3 hours (long reperfusion) of reperfusion to investigate early and late differences in tissue blood flow. At reperfusion a micrometer-driven occluder was either released fully within 1 minute (full-reactive [FR] group) or the occluder was slowly released to return coronary blood flow to preocclusion levels (no-reactive [NR] group). Areas at risk, myocardial blood flow (radioactive microspheres), hemodynamics, myocardial segment shortening (sonomicrometry) during occlusion, and high-energy phosphate levels (tissue biopsies) at 3 hours of reperfusion were similar in both groups. Recovery of function in the short-reperfusion group was significantly greater in the FR than the NR group until 3 minutes of reperfusion, which corresponded to the peak reactive hyperemic response. After this time there were no differences between the two groups in functional recovery until 2 and 3 hours after reperfusion when the percentage of segment shortening had deteriorated to a significantly greater extent (p less than 0.05) in the NR group than in the FR group. The reason for this finding may involve prolonged subendocardial ischemia if reperfusion is introduced into a flow-limiting stenosis, as suggested by the greater tissue blood flows in the ischemic reperfused region during early reperfusion in the FR versus NR group. These data suggest that coronary artery patency, in part, determines functional recovery in the stunned myocardium.
Farber
N E
NE
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226.
Pieper
G M
GM
Gross
G J
GJ
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology*; D004285:Dogs; D006339:Heart Rate; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010725:Phosphocreatine / Q000378:metabolism; D013997:Time Factors
D000227:Adenine Nucleotides; D010725:Phosphocreatine