Changes of the sympatheticoadrenal system during experimental massive pulmonary embolism

Tverskaya, M. S.; Karpova, V. V.; Makarova, L D; Virganskii, A. O.; Chumakova, M. A.; Melchenko, Dmitry

doi:10.1007/bf00850899

Cited by 7 publications

(2 citation statements)

References 3 publications

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“…4). These findings support our earlier conclusion that the rate of such changes is an-important factor in determining the outcome of the pathological process, i.e., whether a state of compensation or decompensation will ensue [6]. The only substantial differences between the compensated and decompensated states lie in the magnitude of hyperchromatosis and pyknomorphic shrinkage (Fig.…”

Section: Resultssupporting

confidence: 85%

“…As a result, still less NE was synthesized than after one hour and its levels in the adrenergic neurons and their term_i-nals were also lower. Taken as a whole, the resuits of this control experiment support our hypothesis that the SNS is not activated by the 1st or 6th hour in control dogs and that the lowered content of NE in myocardial adrenergic plexuses is due to its diminished synthesis [6]. This led us to the important conclusion that the results of histological examination of material taken from an animal immediately after its anesthetization and immobilization should not be used for characterizing the so-called "normal state" or for making comparisons with the results obtained for other groups of animals.…”

Section: Resultssupporting

confidence: 73%

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Status of adrenergic nerve supply to the ventricular myocardia in experimentally produced massive pulmonary embolism

Tverskaya

Chumakova

et al. 1994

Bull Exp Biol Med

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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-

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Section: Resultssupporting

confidence: 85%

Section: Resultssupporting

confidence: 73%

Status of adrenergic nerve supply to the ventricular myocardia in experimentally produced massive pulmonary embolism

Tverskaya

Chumakova

et al. 1994

Bull Exp Biol Med

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Neurohormonal changes in acute pulmonary embolism (an experimental and clinical study)

Tverskaya¹,

Makarova²,

Сергеева³

et al. 1993

Bull Exp Biol Med

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Measurement of dehydrogenase activity in hepatocytes in massive pulmonary embolism

Щеголев

Yavolov

et al. 1999

Bull Exp Biol Med

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Experimental massive pulmonary embolism in dogs induces structural and metabolic changes in the liver. The severity of these changes depends on the duration of the postembolization period and the development of heart failure. Key Words: hepatocyte; dehydrogenases," pulmonaJT embolismMassive pulmonary embolism (MPE) poses a real threat for patient's life due to the development of acute cardiovascular insufficiency. In light of this, changes in the heart and pulmonary vessels are extensively studied [2,7,9]. However, other organs are also altered in MPE, in particular, liver dysfunction plays an important role in the pathogenesis of postembolization syndrome.The aim of the present study was to evaluate structural and metabolic changes in dog liver in MPE accompanied and not accompanied by heart failure. MATERIALS AND METHODSExperiments were carried out on 37 mature mongrel dogs weighing 18-20 kg. The animals were fed standard vivarium chow and received no chow 12 h before study. The experiments were carried on closed chest and under conditions of natural respiration. The animals were narcotized with sodium thiopental (20 mg/kg, intravenously) after promedol premedication (10 mg/ kg). Longitudinal fragments of canine sartorial muscle were used for embolization. MPE modeling and catheterization of the heart and vessels were described previously [1]. Heart rate (HR), ECG, respiration rate, and blood pressure in the aorta were recorded. The animals were divided into 4 groups: compensated MPE for 1 and 6 h (MPE without heart failure, euthanasia) and uncompensated MPE for 1 and 6 h (death from cardiovascular insufficiency within 1 and 6 h after MPE modeling). In two control groups the animals were immobilized and narcotized after premedication, the heart and vessels were catheterized, and the animals were euthanized after 1 and 6 h by sodium thiopental overdose.Liver samples were frozen and stored in liquid nitrogen. On parallel cryostat sections, activities of succinate dehydrogenase (SDH), 3-hydroxybutyrate dehydrogenase (BDH), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), and NADH and NADPH diaphorases were histochemically assayed [4]. Enzyme activities were evaluated using a Microvideomat TV image analysis system (Opton). Paraffin sections were stained with hematoxylin and eosin. The data were processed statistically.

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Changes of the sympatheticoadrenal system during experimental massive pulmonary embolism

Cited by 7 publications

References 3 publications

Status of adrenergic nerve supply to the ventricular myocardia in experimentally produced massive pulmonary embolism

Status of adrenergic nerve supply to the ventricular myocardia in experimentally produced massive pulmonary embolism

Neurohormonal changes in acute pulmonary embolism (an experimental and clinical study)

Measurement of dehydrogenase activity in hepatocytes in massive pulmonary embolism

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