Platelet depletion in experimental myocardial infarction.
Accumulation of platelets in the microvasculature after acute myocardial ischemia may exacerbate tissue injury through the formation of microthrombi and by the release of vasoactive substances. To assess the role of platelets in myocardial ischemic injury and infarction, circulating platelets were reduced by 94 +/- 2% (mean +/- S.E.M.) with sheep antiserum to canine platelets. Regional myocardial ischemia was produced by occlusion of the left circumflex coronary artery (LCCA) for 90 min followed by reperfusion for 5 hours. Infarct size did not differ significantly between antiplatelet serum and nonimmune serum groups: 36 +/- 8 vs. 43 +/- 4% of the area at risk, determined by a post-mortem dual staining technique (p greater than 0.05). A second occlusion-reperfusion control group, sacrificed at 24 hours, did not differ from 5 hr reperfused groups with regard to infarct size. Coronary sinus thromboxane B2 (TXB2) concentrations were not altered significantly by platelet depletion. Histopathologic examination confirmed the presence of necrosis in the infarcted myocardium and revealed substantial leukocytic infiltration in both groups. The results suggest that circulating platelets are not required for the full expression of myocardial ischemic injury resulting from temporary coronary artery occlusion followed by reperfusion.
D000818:Animals; D004285:Dogs; D006439:Hemodynamics; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D010974:Platelet Aggregation; D010976:Platelet Count; D013928:Thromboxane A2 / Q000378:metabolism; D013929:Thromboxane B2 / Q000378:metabolism
D013929:Thromboxane B2; D013928:Thromboxane A2