| Acute lung injury is a pathological process during which different degrees of injury of alveolar epithelial cells and lung vascular endothelial cells result in in-crease of alveolar permeability, characterized by infiltration of polymorphonucle-ar neutrophil (PMN) in the lung, bactericidal activity of free oxygen radicals produced via " respiratory burst" , tissue injury mediated by the production of free oxygen radicals, enzymes and cytokines. Tissue injury is more aggravated by activated PMN and adhesion of endothelial cells. ICAM - 1 plays a crucial role in the inflammatory response as an important inflammatory mediator, whose level of expression is closely related to the degree of lung injury. Activation of lung endothelial cells, migration of leukocytes, degranulation of granulocytes and capillary leakage induced by TNF - a results in diffuse lung microvascular endothelial cells injury and increase in microvascular permeability. TNF -α can also induce the release of IL - 1 from endothelial cells and macrophage, which stimulate the synthesis of other cytokine in turn. Accompanied surfactant chan-ges also occur in the acute lung injury. Inflammatory response can be influenced by anesthetics and method of anesthesia, but there are rare studies on the influ-ence of sevoflurane and desflurane on the injured lung.In this experiment, the influence and mechanism of sevoflurane and desflu-rane on acute lung injury in rats were studied in the model of LPS - induced a-cute lung injury in rats. The experiment was divided in 4 parts, part 1: influ-ence of sevoflurane and desflurane on the permeability of alveoli and capillary inacute lung injury; part 2; influence of sevoflurane and desflurane on metabolism of oxygen free radicals and NO in acute lung injury; part 3 : influence of sevoflu-rane and desflurane on ICAM - 1 and TNF -α; part 4: influence of sevoflurane and desflurane on the contents of SP ?A and phosphatidylcholine ( PC) in pul-monary alveolar lavage fluid (PALF) of normal and acute injured lungs.- MaterialsExperimental animals: 116 Wistar rats, regardless of sex, provided by Chi-na Medical University Laboratory Animal Center, weight 200 ~ 290g.Experimental instruments: Ohmeda 7000 Aneshesia machine, animal venti-lator (Havard 55 -3438) , Datex anesthetic gas monitor, Olympus light micro-scope, RM -6000 multi -lead physiology monitor (Kohden, Japan) , PTC -100 PCR amplification device,KODAKID gel imaging analytical system, Dupont ST -21 low temperature and high speed centrifuger( U. S. A) , Olympus AX70 microphotograph system (Japan) , MetaMorph/Olympus DP10/BX51 microimage analytical system( Japan) , Metamorph image system( UIC Company, U. S. A) , KADAKID gel image analyzing system (USA) , GIS -700D digitized gel scan-ning analyzing system (Shanghai). Hitachi transmission electron microscope.Chemical and reagents: pentobarbital sodium (ShangHai) , Lipopolysac-charide(Escheruchia coli 055: B5, Sigma ) , TNF - α ICAM - 1 immunohisto-chemicology were supplied by WuHan BoShiDe company and iNOS immunohis-tochenicology supplied by Beijing Zhongshan company. SP - A antibody was sup-plied by Santa Cruze company.Methods1. Influence of sevoflurane and desflurane on the permeability of alveoli and capillary in acute lung injury of rats caused by LPS. After anesthesia, 36 Wistar rats were randomly assigned to one of 6 groups after injection Evans blue50mg/kg. Group C: mechanically ventilated for 4 hours after injection of 1.2 ml normal saline; Group L: mechanically ventilated for 4 hours after injection of LPS 5 mg/kg; Group S1L and S2L: mechanically ventilated for 4 hours after in-jection of LPS 5 mg/kg, inhaled 1.0 MAC and 1. 5 MAC of sevoflurane at the same time; Group D1L and D2L: mechanically ventilated for 4 hours after injec-tion of LPS 5 mg/kg, inhaled 1.0 MAC and 1.5 MAC of desflurane at the same time. Lung permeability index ( LPI) , Evans blue leakeage, lung wet/dry weight ratio ( W/D) and lung water content, and inflammatory cells percentage in pulmonary... |
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