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Platelet deposition after surgically induced myocardial ischemia. An etiologic factor for reperfusion injury
Insights
Platelet deposition in heart vessels increases after ischemia and reperfusion, contributing to injury. Antiplatelet drugs like dipyridamole may prevent this damage.
Area of Science:
- Cardiovascular Science
- Surgical Research
- Hematology
Background:
- Myocardial preservation during surgery can be compromised by reperfusion injury.
- Reperfusion injury is characterized by reduced high-energy phosphates and increased coronary resistance.
- Platelet deposition in the coronary microvasculature is a hypothesized contributor to this injury.
Purpose of the Study:
- To investigate the role of platelet deposition in myocardial reperfusion injury following aortic cross-clamping.
- To differentiate platelet deposition from hemorrhage versus vascular entrapment.
- To assess the effect of an antiplatelet agent on platelet deposition during ischemia-reperfusion.
Main Methods:
- 15 dogs underwent normothermic bypass, 60 minutes of global ischemia, and 30 minutes of reperfusion.
- 111In-labeled platelets and 51Cr-labeled erythrocytes were infused to quantify deposition.
- Myocardial biopsy specimens were analyzed for platelet-to-erythrocyte ratios.
- Dipyridamole, an antiplatelet agent, was administered to a subset of dogs.
Main Results:
- Normothermic ischemia followed by reperfusion significantly increased platelet deposition (over twofold) compared to controls.
- Prolonged bypass alone caused only minimal platelet deposition.
- Pretreatment with dipyridamole appeared to prevent significant platelet deposition.
Conclusions:
- Platelet deposition in the coronary microcirculation is associated with surgically induced myocardial ischemia and reperfusion injury.
- Antiplatelet therapy may be beneficial in mitigating reperfusion injury after cardiac surgery.
Abstract:
Despite meticulous adherence to presently known principles of myocardial preservation, reperfusion after aortic cross-clamping results in a unique injury manifested by decreasing high-energy phosphate levels and increased coronary resistance. We hypothesize that platelet deposition into the coronary microvasculature is a major factor in reperfusion injury. To differentiate platelet deposition due to subendocardial hemorrhage from deposition due to vascular entrapment, we infused 111In-labeled platelets together with 51Cr-labeled erythrocytes into 15 dogs that were on normothermic bypass and subjected to 60 minutes of global ischemia followed by 30 minutes of reperfusion. Platelet deposition is indicated only when the proportion of platelets to erythrocytes in tissue exceeds that measured by peripheral blood. Myocardial biopsy specimens were obtained after 10 minutes of bypass, 120 minutes of continuous bypass (Group I), and at the end of reperfusion after global ischemia (Group II). In five dogs (Group III), dipyridamole (1 mg/kg), an antiplatelet activation agent, was administered in the preischemic period. Platelet deposition was expressed as the number of radioactive-labeled platelets deposited per gram of tissue. Bypass for 120 minutes resulted in only a minimal increase in platelet deposition. However, normothermic ischemia followed by reperfusion resulted in over a twofold increase in platelet deposition compared to controls. Pretreatment with dipyridamole appeared to avoid platelet deposition. These data indicate that platelet deposition in the coronary microcirculation following surgically induced myocardial ischemia may be associated with reperfusion injury and that antiplatelet drugs after this sequence.