Platelet depletion and infarct size in an occlusion-reperfusion model of myocardial ischemia in anesthetized dogs.
The formation of platelet aggregates and release of platelet-derived vasoactive mediators have been suggested to aggravate ischemic myocardium. The contribution of platelets to myocardial damage induced by 90-min occlusion and 5-h reperfusion in chloralose-anesthetized dogs was assessed after depletion of platelets with specific antidog platelet antiserum. Dogs treated with antiplatelet antiserum showed greater than 90% reduction in circulating platelets and serum TxB2 levels, but showed no reduction in infarct size (58 +/- 3 vs. 51 +/- 3% of risk area for control and thrombocytopenic dogs, respectively). Platelet depletion had no hemodynamic effect during the occlusion or reperfusion phases, nor reduced the incidence of arrhythmias. These results indicate that platelet aggregates or platelet-derived mediators do not contribute directly to the extent of damage in this occlusion-reperfusion model of myocardial ischemia.
Mullane
K M
KM
McGiff
J C
JC
D000758:Anesthesia; D000818:Animals; D001792:Blood Platelets / Q000276:immunology / Q000502:physiology*; D004195:Disease Models, Animal; D004285:Dogs; D007106:Immune Sera / Q000494:pharmacology; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology*; D010477:Perfusion; D010974:Platelet Aggregation; D010976:Platelet Count; D011863:Radioimmunoassay; D012306:Risk; D013921:Thrombocytopenia / Q000503:physiopathology; D013929:Thromboxane B2 / Q000097:blood
D007106:Immune Sera; D013929:Thromboxane B2