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-

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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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.

Structural changes in the myocardium under conditions of increased left and right ventricular afterload were studied using polarization microscopy and histological, histochemical, and stereological methods. Increased afterload not complicated by heart failure was characterized by low number of damaged cardiomyocytes (3.3-6.5%) and moderate structural changes in the ventricular myocardium (contractures of different severity). Increased afterload complicated by heart failure was characterized by high ratio of damaged cardiomyocytes (5.6-19.2%) and severe reversible (grade I and II contractures) and irreversible (grade III contractures and lump degradation of myofibrils) structural changes. Irreversible damage to most cardiomyocytes included plasmatic impregnation, which was most pronounced in the subendocardial layer of ventricles operating under conditions of increased afterload. Comparative study showed that increased left and right ventricular afterload induces similar pathomorphological changes in the contractile myocardium. Our results indicate that increased afterload to the right or left ventricle is accompanied by the development of stereotypical structural changes in the myocardium. Profound and severe disturbances can cause heart failure.

The period immediately following massive pulmonary embolism largely determines its further course, that is, whether compensation will occur or whether heart failure will ensue. Prognostically favorable or unfavorable histochemical characteristics of myocardial metabolism during this period are revealed in this study.Key Words: experimental massive pulmonary embolism; heart; histoenzymology Our previous study looked at the histoenzymological changes taking place in the ventricular myocardium during two variants of acute massive embolism of the pulmonary arteries (PAME): uncomplicated or complicated by the development of cardiac insufficiency [14]. In the former case the material for investigation was collected 6 h after the induction of PAME, in the latter after the animal's death, which ensued suddenly and, as a rule, early. Hence, further studies were carried out with due consideration for the time differences in order to compare the time course of metabolic changes in the ventricular myocardium during different variants of experimental PAME. MATERIALS AND METHODSForty mongrel dogs weighing 15 to 20 kg were used in the study, with closed chest and spontaneous respiration. Premedication consisted of intramuscular promedole in a dose of 10 mg/kg, and narcosis during the experiment was provided by fractionated intravenous infusion of sodium thiopental in a dose of 20 mg/kg. Catheterization of the heart and blood vessels, recording of hemodynamic parameters, and simulation of acute PAME were carried out as deRussian State Medical University, Moscow (Presented by V. S. Savel'ev, Member of the Russian Academy of Medical Sciences) scribed previously [3]. The protocol of the experimental and control studies is presented in Fig. 1. The experimental animals were divided into 3 groups, one group consisting of animals ( Fig. 1, /) which developed heart failure eventuating in death during the first 30 min after PAME was induced (decompensated PAME) and the other two groups (Fig. 1, I1, II1) of animals without signs of circulatory insufficiency (compensated PAME).Specimens for morphological study were taken from the right and left ventricles, fLxed in 10% neutral formalin buffered after Lillie, and embedded in paraffin. Slices 5-7 g thick were stained with hematoxylin-eosin and Schiff's reagent with amylase control. The glycogen content in the myocardium was assessed using a five-point scale. Histoenzymological study was carried out on 10-g cryostat slices. The activities of succinate dehydrogenase (SDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH), glyceraldehyde phosphate dehydrogenase (GAPDH), lactate dehydrogenase (LDH), gluceraldehyde phosphate dehydrogenase NADPH diaphorases were detected routinely [2,11] and assessed on a five-point scale. The activities of SDH, LDH, NADH and NADPH diaphorases were measured using a Microvideomat television device (Opton) and a Wang-720 computer [4,5]. The data were processed by mathematical statistics using Student's t test.

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