CARDIOMYOPATHY IN RATS WITH WALKER-256 TUMOR - THE POTENTIAL ROLE OF MICROVASCULAR DISEASE IN ITS GENESIS

Considering that diffuse abnormalities of myocardial microcirculation with transient ischemia have been suggested to play a role in the gene sis of myocytolytic necrosis, characteristic lesion of dilated or cong estive cardiomyopathies, and the bloodstream is the most common pathwa y for dissemination of cancer cells, which gain access to the microcir culation, the present study was undertaken to search for morphologic a nd electrocardiographic evidence of myocardial damage associated with microcirculatory disease in rats experimentally inoculated with the Wa lker 256 tumor. Young albino rats inoculated intramuscularly with the Walker 256 tumor developed a cardiomyopathy characterized by diffuse s mall foci of myocytolytic necrosis, decreased thickness of the mean le ft midventricular wall associated with reduced size of the minor diame ter of myocytes, and electrocardiographic abnormalities reflecting the myocardial damage, correlated with the presence of a microvascular di sease, characterized by intramyocardial microvessels (less than 50 mu m in diameter) partially or totally occluded because of entrapment of tumor cells and fibrin-platelet/tumor cell-cellular debris thrombi. Th e occlusive or subocclusive small vessel lesions preceded the developm ent of the myocytolytic necrosis, suggesting that the microvascular di sease would play an important role in the process of focal micronecros is and consequent electrocardiographic changes. However, it must be ta ken into account that the tumor thromboemboli can generate related fac tors that could promote cell injury and cell death. In conclusion, the hematogenic dissemination of Walker 256 cells promotes the developmen t of an experimental cardiomyopathy attributable, at least in part, to microvascular obliterative changes in the myocardium.