Objective: Platelet activation and subsequent release of granules containing a variety of growth factors, at the site of injury, is crucial for the wound healing process. We postulated that a platelet-mediated paracrine effect may accelerate the healing process after myocardial infarction.
Methods: Allogenic platelet-rich and platelet-poor plasma (PRP and PPP) were collected from 15 healthy male Wistar rats. After thrombin activation, the level of vascular endothelial growth factor (VEGF) in PRP and PPP was measured by enzyme-linked immunosorbent assay. A rat model of myocardial infarction was induced by permanent ligation of the left anterior descending artery, and thrombin-activated PRP and PPP, respectively, were injected into the ischemic region. Seven days and 28 days after operation, surviving rats were killed. Ex-vivo left ventricular pressure-volume relationship was performed to evaluate passive diastolic function. Collagen analysis was performed by picrosirius red staining plus polarized microscopy. Angiogenesis and arteriogenesis were evaluated by immunofluorescent staining.
Results: After thrombin activation, VEGF level in PRP was significantly higher than that in PPP (187.5+/-45.5 vs. 30.1+/-7.8 pg/ml, P<0.01). Injection of thrombin-activated PRP into the infarcted area resulted in improvement of ventricular remodeling and accelerated healing, as demonstrated by limitation of ventricular expansion, attenuation of myocardial hypertrophy in the noninfarct region, facilitation of angiogenesis and arteriogenesis in the infarct.
Conclusion: Injection of thrombin-activated PRP could modulate favorably the postinfarction remodeling process. Platelet-released VEGF may participate in this protective effect.