Early disappearance of lymphatics draining ischemic myocardium in the dog.

To assess myocardial lymphatics during the evolution of myocardial infarction we performed lymphangiographic studies thirty and three hundred sixty minutes after occlusion of the left anterior descending coronary artery in 92 dogs. A morphometric index was employed on a coded basis to assess the lymphangiograms. Well before myocardial necrosis was evident, at thirty minutes, a striking reduction was evident in lymphatic filling in the ischemic zone: similar changes were seen three hundred sixty minutes after occlusion. Heparin in doses that rendered blood incoagulable did not prevent the lymphatic occlusion or collapse, but they were prevented by two agents that act as cardiac lymphagogues, hyaluronidase and CLS 2210. Lymph flow from the heart was assessed in another 23 dogs. Lymph flow fell sharply after coronary artery occlusion in placebo-treated dogs but was well maintained in dogs treated with hyaluronidase and with CLS 2210. The reduction in cardiac lymphatic filling and lymph flow occurred too early to be a consequence of myocardial necrosis. To the extent that reduced lymphatic drainage allows the local accumulation of potentially toxic products, it could contribute to the local damage. Treatment with the lymphagogues not only maintained lymphatic patency but also reduced evidence of myocardial damage evident on examination by light and electron microscopy. These studies provide an alternative to commonly held concepts on how hyaluronidase reduces myocardial infarction after coronary artery occlusion and support the concept that lymphatic occlusion or collapse plays a role in myocardial infarction.