Effect of exogenous pulmonary surfactant on isolated lung injury induced by ischemia-reperfusion in rats.
- Author:
Ying MENG
1
;
Ju ZHAO
;
Ying-mao RUAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; In Vitro Techniques; Lung; blood supply; pathology; Male; Nitric Oxide Synthase; metabolism; Nitric Oxide Synthase Type III; Pulmonary Surfactant-Associated Protein A; metabolism; Pulmonary Surfactants; pharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; pathology
- From: Acta Academiae Medicinae Sinicae 2004;26(3):302-305
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of exogenous pulmonary surfactant (PS) on the acute lung injury to ischemia-reperfusion injury.
METHODSThe model of ischemia-reperfusion was established. Thirty male Sprague-Dawley rats were randomly divided into control (n = 10), I/R (n = 10), and PS (n = 10) groups.
CONTROL GROUPthe isolated rat lungs were reperfused for 4 hours. I/R group: the isolated rat lungs were reperfused for 2 hours after 2 hours ischemia. PS group: exogenous pulmonary surfactant (10 mg/100 g BW) were given to the ischemic lungs through bronchus 2 hours before reperfusion. Wet to dry lung weight ratio (W/D) and pulmonary artery pressure (PAP) were checked. Immunohistochemical technique was used to determine the immune reactivity of lung tissues to endothelia nitric oxide synthase (eNOS) and surfactant protein A (SP-A). The pulmonary changes were also observed by light and electronic microscopes.
RESULTSW/D and PAP in I/R group were significantly higher than in PS group (P < 0.01). The expression of eNOS and SP-A in I/R group were significantly lower than those in PS group (P < 0.05).
CONCLUSIONSPS can significantly protect lung injury induced by ischemia-reperfusion in the isolated rat lungs. This protective effect is associated with the mechanism that the exogenous PS may reduce SP-A loss in the ischemia-reperfusion and activate the up-regulation of eNOS.
