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In clinical cardiology, our attention is often directed toward the neurogenic type of myocardial infarction. First, the association between emotional stress and acute myocardial infarction, and second, the absence of demonstrable coronary occlusive disease in 15 to 20 per cent of fatal cases that are examined, suggest that rapid myocardial necrosis may be caused by factors other than coronary occlusion. This assumption is difficult to prove and indeed one is hard put to demonstrate neurogenic myocardial necrosis with the force and clarity of a well-developed coronary occlusion and the adjacent mass of necrotic myocardium.Earlier investigators have described myocardial necrosis in the absence of coronary artery disease. Josuel demonstrated the myocardial lesions produced by catecholamines. Selye2 described myocardial necrosis produced by various types of stress in animals previously treated with fluorohydrocortisone, and Raab and colleagues3 has shown that anti-adrenergic drugs protect rats from stress induced myocardial necrosis. Anichkov and Vedeneyeva4 have produced myocardial necrosis by stimulating sympathetic nerve trunks and by the intravenous administration of norepinephrine.On the other hand, Manning and associates5 very clearly demonstrated myocardial necrosis and peptic ulceration following vagus nerve stimulation in eserine-treated animals. They also demonstrated the protective effects of atropine in preventing both gastric ulceration and myocardial necrosis.Thus we have myocardial necrosis produced by stimulation of both vagus and sympathetic nervous systems, and prevented by both atropine and antiadrenergic drugs.Manning and associates5 employed electrical stimuli of sufficient intensity to give maximal physiologic response and applied it almost continously until the animals died. For this reason their work was thought to be so far beyond the realm of physiologic limits as to be of no clinical significance.Since myocardial necrosis can be produced by such widely diverse means, we wished to determine which of the methods would more closely parallel the clinical and physiologic changes seen in men in states of near rage with slow pulse and normal blood pressure preceding the onset of myocardial inf arction. We were curious to determine if more physiologic electrical stimulation of nerve trunks would produce myocardial necrosis. Since the primary purpose was to find a model which could be used in the study of the role of emotional factors in myocardial inf arction, a primate was selected.at MOUNT ALLISON UNIV on June 25, 2015 ang.sagepub.com Downloaded from

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While experimental atheromatous lesions have been produced by dietary manipulations 1-4 and by neurologic stimulation,5 one of the widely accepted theories of atherogenesis is that of thrombosis.Since Duguid6 explained that thrombi may become organized, leaving plaques that resemble atheroma, many investigators have studied the behavior of experimental intra-arterial lesions. The most recent of these papers were summarized by Henry7 in 1962. Poole8 emphasized the fact that a vein thrombus consists of a white cell-free head, attached to the vessel wall with a larger red tail trailing in the direction of blood flow. In arteries the lesion contains less cells and in extreme cases may consist entirely of platelets. The cell-rich thrombi are larger and when organized appear to contain more lipid and, in some respects, resemble atheroma. Small lesions composed entirely of platelets appear to become insignificant.The mechanism determining the cell-trapping tendency of an experimental intra-arterial thrombus is not completely understood. It has been assumed that the intima carried a negative charge9 and that platelets and cells are repelled until the intima is injured or altered in some manner, in which case the charge is reversed and passing platelets are attracted, adhering to the area in increasing numbers until the negative charge has been restored. The larger cells with resistance to blood flow greater than their electrical attraction are swept past the area, and presumably the difference between vein and arterial thrombi could be accounted for by the increased flow rate in the arteries. Since experimental thrombi in arteries do vary in size and cellular content, the possibility of other factors influencing viscosity and the physiochemical character of blood has not been ruled out.We have studied the microscopic appearance of the head or origin of intraarterial thrombi forming at the site of a fine silk thread placed in the artery wall parallel to the direction of blood flow in experimental animals, and have been interested in the influence of various agents that might change the physiochemical character of blood and alter these lesions.Among the many physiochemical characteristics of arterial and capillary blood studied, the electrophoretic mobility of lipoproteins and the packing character of red cells seem to correlate best with thrombus size and cellular content. The correlation with noncellular lipid content of the thrombus is less clear at this time and will be the subject of another report.