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

Tverskaya, M. S.; Makarova, L D; Сергеева, Н. А.; Virganskii, A. O.; Savvina, S. Yu.

doi:10.1007/bf00786153

Cited by 3 publications

(3 citation statements)

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“…However, we observed such a reaction in both ventricles, even though their loading changes in different directions in PAME [3]. This suggests that the observed activation of glycolysis is largely caused by the effects of systemic factors, primarily neurohumoral [3,16,17]. During the same period the level of NADPH diaphorase increases in the right ventricle, reportedly [9] due to its hyperfunction.…”

Section: Resultsmentioning

confidence: 62%

Histochemical study of myocardial metabolism in experimental massive pulmonary embolism

et al. 1995

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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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Section: Resultsmentioning

confidence: 62%

Histochemical study of myocardial metabolism in experimental massive pulmonary embolism

et al. 1995

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“…The processes of clot formation are associated with the production of numerous bioactive substances stimulating NPMNL [1]. On the other hand, hydrocortisone levels are appreciably increased in the blood of patients with acute massive pulmonary thromboembolism, which is never observed in experimental MEPA [9]. The data presented permit us to expect more intensive activation of NPMNL circulating in the blood in patients with massive pulmonary artery thromboembolism than in experi-mental MEPA.…”

Section: Resultsmentioning

confidence: 88%

Oxidative metabolism of neutrophilic polymorphonuclear leukocytes in experimental massive pulmonary embolism

et al. 1994

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“…Cardiac output is reduced and hypoxia occurs with ventilation perfusion mismatch. In total, these changes invoke sympathetic nervous system activation [23,24]. A 'catecholamine rain' begins in the body with sympathetic activity.…”

Section: Discussionmentioning

confidence: 99%

Plasma catestatin level predicts sPESI score and mortality in acute pulmonary embolism

İzcı

Acar

İnanır

2020

Arch Med Sci Atheroscler Dis

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Introduction: Acute pulmonary embolism (APE) is an emergent cardiothoracic disorder. The PESI score is used to estimate 30-day mortality in patients diagnosed with non-high-risk APE. Also, there are biomarkers for predicting prognosis and mortality in APE. Catestatin (CST) is accepted as a marker ofsympathetic nervous system activity which has been shown that the sympathetic nervous system activation can contribute pathogenesis in APE. So, we attempt herein to investigate the correlation of PE diagnosis and prognostic determination with plasma CST levels in PE patients. Material and methods: Blood samples were drawn at admission for laboratory assays and CST measurements. Plasma levels of CST were measured by ELISA according to the manufacturer's instruction. Transthoracic echocardiography was performed for the assessment of RV dysfunction using a Toshiba Applio 500 echocardiographic system within 24 h of the admission. Results: Plasma CST levels were higher in patients with APE than in the control group (17.5 ±6.1 ng/ml vs. 27.3 ±5.7 ng/ml, p < 0.001). Plasma CST levels were higher in the sPESI ≥ 1 (n = 72) than in the patients with sPESI < 1 (37.3 ±6.1 vs. 24.2 ±5.3 ng/ml, p < 0.001). There was a positive correlation between CST level and sPESI score (±0.581, p < 0.001). Mortality occurred in 20 patients with sPESI ≥ 1 (27.7%) and in 9 patients with sPESI < 1 (10.2%) (p = 0.010). Receiver operating characteristic (ROC) curve analysis using a cutoff level of 31.2 ng/ml, and the CST level predicted mortality with a sensitivity of 100% and specificity of 52.6% (AUC = 0.883, 95% CI: 0.689-0.921). Furthermore, the CST level was correlated with right ventricular dysfunction. Conclusions: CST can predict sPESI score and mortality in patients with APE.

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

Cited by 3 publications

References 2 publications

Histochemical study of myocardial metabolism in experimental massive pulmonary embolism

Histochemical study of myocardial metabolism in experimental massive pulmonary embolism

Oxidative metabolism of neutrophilic polymorphonuclear leukocytes in experimental massive pulmonary embolism

Plasma catestatin level predicts sPESI score and mortality in acute pulmonary embolism

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