Investigators have produced arteriosclerosis in experimental animals by dietary means for almost half a century. In contrast to the situation in man, however, all previous reports indicate that complicating thrombosis and infarction have been extremely rare in experimental animals. The current report presents dietary regimens by means of which the authors have produced significant numbers of myocardial and renal infarcts in rats (6 of 10 in one group and 4 of 10 in each of 2 others). It is notable that thrombosis occurred before the appearance of severe structural changes in the arterial walls, although abundant fat could often be demonstrated histochemically.

Myocardial iufnrct.s were produced in rats by ligating the anterior descending branch of the left coronaiy artery. After one hour, changes in the ultrastructure of niyofibers in the infarcts were readily demonstrated by ele.tran microscopy. These changes became progressively severe with time, and consisted primarily of swelling of mitochrondria and sarcoplasmic reticulum followed by increased lipid droplets and myolysis. Autolysis of myocardium was also .studied :ind the changes found to be similar to those of myocardial infarcts, but more uniform and slightly delayed in development. Perhaps the early ultrastruct'jirl changes are related to hyperosmolarity of mitochondria and sarcoplasmic reticulum, especially after cell death. It is hoped that definition of ischemic ultrastruetural change will be useful in defining electron microscopic lesions in other forms of myocardial damage. 6i»0Cirrtilation Ri-tfarrh. Valnmr VI, Norembrr

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