Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
