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.
