Objective: To study the changes in tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) in a model of acute myocardial infarction reproduced in the dog with administration of nitroglycerin into internal thoracic artery under pressure.

Methods: Sixty healthy cross-breed dogs were randomly divided into experimental and control group with 30 dogs in each group. The animal model of acute myocardial ischemia was reproduced by ligating the left anterior descending coronary artery. Internal thoracic artery in the experimental group was ligated, and a tube was introduced into the proximal end. Nitroglycerine was infused under pressure into the internal thoracic artery in experimental group. The drug was given intravenously in control group. t-PA and PAI were measured before anterior coronary artery ligation and at 0.5, 2 and 6 hours after coronary artery ligation.

Results: The t-PA levels in two groups were increased at 0.5 hour after coronary artery ligation, and gradually declined in control group, while no obvious change was found in experimental group. There was significant difference between experimental group and control group at 6 hours after coronary artery ligation(P<0.05). PAI levels were increased after coronary artery ligation, peaking at 6 and 2 hours after coronary artery ligation in both groups. Significant difference in PAI level was observed between two groups at 6 hours after coronary artery ligation(P<0.05).

Conclusion: Introduction of nitroglycerine through internal thoracic artery under pressure is effective to accelerate release of t-PA from the endothelium while inhibit secretion of PAI, therefore it is useful to modulate the balance of fibrinolysis.

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