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  • Author or Editor: M Boros x
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Oxido-reductive stress is a crucial factor of the tissue response during ischemia-reoxygenation injuries. Reperfusion affects primarily the microvasculature in a manner consistent with an acute inflammatory reaction. In this respect, the salient data suggest an important connection between endothelial cell-derived humoral mediators and the perivascular mast cell system. Increased endothelin-1 and decreased nitric oxide formation, mast cell degranulation and leukocyte accumulation coexist in gastrointestinal ischemia-reperfusion syndromes too. Constitutively produced nitric oxide inhibits, while increasingly formed endothelin-1 significantly enhances the degranulation of the intestinal mast cells. The endothelin-A receptor-dependent mast cell degranulation per se plays a secondary role in reperfusion-induced structural injury, but contributes significantly to leukocyte recruitment into the reperfused intestinal mucosa. It is conceivable therefore, that the nitric oxide - endothelin-1 - mast cell cycle is involved in the mechanism of ischemia-reperfusion-induced endothelial cell-leukocyte interactions, where mast cells act to amplify the process of leukocyte sequestration. The alteration in the balance between endothelial cell-derived proadhesive vasoconstrictor and antiadhesive vasodilator factors exerts a significant influence on the mucosal integrity, and the antagonism of endothelin-A receptor activation in this setting tips the equilibrium toward tissue salvage.

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During intestinal ischaemia-reperfusion, endotoxin can be translocated. Pretreatment with sublethal doses of endotoxin develops tolerance to ischaemia-reperfusion in different organs; however, the tolerance to intestinal ischaemia-reperfusion in the lung has rarely been investigated. Our aim was to study the role of endotoxin pretreatment in the mechanical responses and inflammatory activation induced by intestinal ischaemia-reperfusion in the lung. Wistar rats were preconditioned with a sublethal dose of endotoxin on day −3 or −1. On day 0, anesthetized, paralyzed and mechanically ventilated rats were subjected to a 60-min occlusion of the superior mesenteric artery and a subsequent 240-min reperfusion. The low-frequency forced oscillation technique was employed to characterize the separate mechanical responses of the airways and respiratory tissues. Intestinal ischaemia-reperfusion caused a significant decrease in airway resistance and increases in tissue resistance and elastance, nitric oxide synthase and myeloperoxidase activities. Pretreatment with endotoxin modified both the pulmonary mechanical responses and the inflammatory markers in the lung during intestinal ischaemia-reperfusion. We conclude that endotoxin or the endotoxin-induced processes (and humoral mediators) have significant roles in the pathomechanism of the remote pulmonary effect of intestinal ischaemia-reperfusion.

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Because of similar pathophysiologic changes, oleic acid (OA)-induced pulmonary edema has been well established as an experimental model of certain types of ARDS. Data in the literature indicate changes mostly in global pulmonary mechanical parameters (lung resistance and compliance) during permeability-type edema. Therefore, we designed this study (1) to separate the OA-induced mechanical responses into airway and parenchymal components, and (2) to examine the relationship between the mechanical parameters and the degree of edema. Anaesthetized, paralyzed, mechanically ventilated rats were given iv. OA in doses of 0 (C n=9), 0.05 (OA0.05 n=8), 0.1 (OA0.1 n=10) and 0.3 (OA0.3 n=5) ml/kg. Respiratory system impedance was measured with a wave-tube low-frequency forced oscillation technique, and a model fitting was used to estimate airway (Raw) and lung tissue parameters (G, parenchymal damping; H, elastance). Pulmonary edema was quantified by gravimetric analysis (WW/DW, wet-to-dry weight ratio). In the OAL0.05 group, transient, but significant increase in Raw, only slight increase in H, and no response in G was observed. Different responses were obtained in OA0.1: significant Raw, G, and H values in survivors; rapid and significantly higher responses in all three parameters in non-survivors. Extremely large parameter values were measured in OA0.3. We found that OA caused dose-related increases in WW, DW and WW/DW. Highly significant correlations were found between the degree of edema and G or H, but not Raw. This study demonstrates that low dose of OA had only transient lung mechanical effects; however, it resulted in mild edema. The higher dose elicited significant airway and tissue changes (smaller responses in survivors than in non-survivors), and severe edema. The strong correlation between lung tissue parameters and the degree of edema suggests that the OA-induced acute lung injury is manifested primarily in the alterations in parenchymal mechanics.

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The aim of this study was to outline the consequences of a hypertonic saline-dextran-40 (HSD) infusion-induced peripheral flow stimulus on the ventricular function in closed-chest, pentobarbital-anesthetized dogs. We hypothesized that HSD-induced elevation in endothelin-1 (ET-1) and nitric oxide (NO) release can have a role in myocardial contractile responses; and that cardiac mast cells (MC) degranulation may be involved in this process. The consequences of disodium cromoglycate (a MC stabilizer) or ETR-p1/fl peptide (an endothelin-A receptor antagonist) treatment were evaluated. A 4 ml/kg iv HSD40 infusion significantly increased cardiac index and myocardial contractility, and resulted in a decreased peripheral resistance. The postinfusion period was characterized by significant plasma NO and ET-1 elevations, these hemodynamic and biochemical changes being accompanied by a decreased myocardial ET-1 content, NO synthase activity and enhanced myocardial MC degranulation. Disodium cromoglycate treatment inhibited the HSD40-induced elevations in myocardial contractility and MC degranulation, and similar hemodynamic changes were noted after treatment with ETR-p1/fl peptide, together with a normalized myocardial myocardial ET-1 content, NO synthesis and a significant reduction in MC degranulation. These results indicate that peripheral NO and ET-1 release modulates the cardiac contractility through myocardial ET-A receptor activation and MC degranulation.

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Interventional Medicine and Applied Science
Authors: K. Szakszon, Z. L. Veres, M. Boros, S. Sz. Kiss, B. Nagy, E. Bálega, á. Papp, E. Németh, I. Pataki and T. Szabó


We report a case of an infant with spontaneous chylothorax due to the congenital malformation of a small lymph vessel of the chest wall. Conservative therapy with omitting long-chain fatty acids from the diet, fat-free nutrition, total parenteral nutrition and intravenous somatostatin did not result in the decrease of pleural effusion. Thoracic surgical intervention performing thoracic duct ligation and using fibrin sealants was applied after 10 days of unsuccessful conservative therapy, and resulted in the complete recovery of the patient. Our experience support the already existing observations, that in cases where the daily loss of chyle exceeds 100 ml per age years and/or lasts longer than 2 weeks, early surgical intervention is recommended.

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