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Adrenergic plexuses in the myocardium and adrenal medulla were studied histochemically under conditions of increased left or right ventricular afterload. Under conditions of high afterload not accompanied by heart failure the density of sympathetic myocardial innervation remained unchanged in the loaded ventricle, but increased in the intact ventricle. Comparison of the state of the sympathoadrenal system under conditions of increased afterload complicated or uncomplicated by heart failure revealed common prognostically unfavorable changes: sharp decrease in the density of adrenergic nerve plexuses in the ventricular myocardium and activation of adrenal chromaffin cells.

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The production of massive pulmonary embolism in dogs initially results in elevated norepinephrine levels in the stellate ganglion and ventricular myocardia. Six hours after its onset, destructive changes in the stellate ganglion nerve cells are more pronounced than at 1 h and their functional activity is decreased, as are norepinephrine levels in the adrenergic neurons and their terminals. A characteristic feature of compensated massive pulmonary embolism is the presence of many neurons showing pronounced hyperchromatosis and pyknomorphic shrinkage. Key Words: experimental massive pulmonary embolism; sympathetic nervous system; stellate ganglionAlterations in the state of the sympathetic nervous system (SNS) and in cardiac work are closely interrelated and interdependent. We have shown previously that acute massive pulmonary embolism (MPE) is accompanied by considerable hemodynamic shifts in the pulmonary and systemic circulations [1] and by structural and metabolic changes in the ventricular myocardia, and that these changes are most strongly marked when cardiac insufficiency has developed [4,5]. The purpose of the present work was to study the state of stellate ganglion (SG) neurons and of adrenergic nerve plexuses of the ventricular myocardia in experimental MPE complicated or uncomplicated by cardiac insufficiency. MATERIALS AND METHODSThe experiments were conducted on a total of 59 mon~el dogs (body weight 15-20 kg) under natuRussian State Medical University, Moscow. (Presented by V. S. Saverev, Member of the Russian Academy of Medical Sciences} ral ventilation (their chest was not opened) and general anesthesia achieved by fractional intravenous administration of thiopental sodium (20 mg/kg) following premedication with Promedol (10 mg/kg) injected intramuscularly. The procedures used to catheterize the heart and vessels, record hemodynamic parameters, and produce acute MPE were described in our earlier article [1].The dogs with MPE were divided into three groups. The In'st two groups consisted of dogs without detectable signs of circulatory insufficiency (animals with compensated MPE). In these groups, material for neurohistological study was taken after euthanasia with a lethal dose of thiopental sodium 1 h or 6 h after MPE production. The third group comprised dogs in which the onset of MPE was followed by the rapid development of fatal cardiac failure (animals with decompensated MPE); after their death tissue samples were taken for morphological study. Control dogs were also divided into three groups. After catheterization (without embolization) they were immobilized on the oper-

Comparative study of pathomorphology of myocardial circulation under conditions of increased afterload of the left or right ventricles showed similar changes. All compartments of the coronary bed were plethoric, capillary blood stasis and perivascular edema, more pronounced in arterial vessels, were detected in both cases. These changes equally involved both ventricles and the ventricular septum. Significant differences consisted in local increase in the density of functioning capillaries. The increase was the maximum in hemodynamically overloaded ventricle and ventricular septum, presumably due to increase of their contractile activity. The density of functioning capillaries in the intact (vs. pressure overloaded) ventricle also increased, but to a lesser degree, which could be due to systemic neurohumoral effects. If increased afterload was complicated by the development of heart failure, circulatory disorders in the myocardium progressed. Significant increase in the density of functioning capillaries in all cardiac compartments indicated decreased vascular tone and exhaustion of coronary reserve. This was paralleled by a sharp arterial plethora in case of increased afterload of the left ventricle and sharp blood stasis in the microcirculatory bed in case of increased right ventricle afterload. Reduction of effective perfusion pressure in the presence of coronary dystonia can cause coronary insufficiency and myocardial ischemia in case of increased right ventricle afterload.