Neurohistochemical and electron microscopic investigations of pathological and age-related changes in the cardiovascular system.

Neurohistochemical and electron microscopic investigations of the autonomic nervous system (ANS) of man and animals suggest that its ontogenesis can be divided into the premediatory, mediatory and postmediatory periods of development. The postmediatory period begins heterochronically in various ganglia of the ANS. A normal process of early cardiac desympathization usually occurs at the age of 35 to 60 years. Specific changes of preceding sudden cardiac death are elicited in different parts of the ANS and adrenal glands. This is accompanied by focal myocardial desympathization. Coronary vessels and conducting system which may influence myocardial hypersensitivity zones to catecholamines are involved in the process of destabilization of the cardiac function. Moreover, relationships are demonstrated which exist between the atherosclerotic lesions of the aortic wall and the status of its nerve plexuses.

Changes in neural and humoral mechanisms of the heart in sudden death due to myocardial abnormalities.

Quantitative neurohistochemical study of adrenergic elements of the myocardium and the adrenal medulla in victims of sudden death revealed an unequal and focal depletion of catecholamines attributable to prior pathologic processes in the myocardium. The greatest changes in cardiac innervation were found in cases of acute myocardial infarction and alcoholic cardiomyopathy, and the adrenergic plexuses were better preserved in cases of coronary heart disease without focal myocardial changes. Ultrastructural study of cardiac innervation in patients who died suddenly showed more pronounced changes in the nerve plexuses of the sinus node than in the perinodal nerves of the working myocardium. The changes in coronary artery innervation were usually related to the severity of stenosis due to fibrous plaque; desympathization of the vessels and the adjoining myocardial zone was also found in cases with 50% or greater occlusion of the lumen. The bulk of chromaffinocytes were depleted and weakly luminescent in the adrenal glands of patients with acute myocardial infarction who died suddenly. In contrast, chromaffinocytes with moderate and bright luminescence were prevalent in cases of sudden death with scarring from previous myocardial infarction and with alcoholic cardiomyopathy. Ultrastructural and histochemical examinations demonstrated that changes in the neurons of sympathetic ganglia increased with more severe atherosclerotic lesions of the aorta and with greater changes in the vessels supplying the ganglia. In experiments on rabbits and dogs, both coronary artery ligation and electrostimulation produced cardiac fibrillation followed by a local increase in luminescence intensity of the myocardial nerve plexuses when their density remained high. Chemoreceptors located along the coronary vessels and pulmonary artery in dogs included small cells with bright fluorescence and adrenergic nerve fibers.