2005Chinese Journal of Current Advances in General SurgeryRequires access

The interventional effect of nitric oxide synethase inhibitors on traumatic shock

Yin Jin-ling

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Abstract

Objective: To evaluate the effects of a selective inhibitor of inducible nitric oxide synthase(iNOS)-aninoguanidine(AG) and a non-selective inhibitor of nitric oxide synthase-(NOS)L-NAME on traumatic shock in rats.Methods: Animal models of traumatic shock were established in 40 Wistar rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45mmHg(4.67~6.00kPa).Hypotension was maintained for 30min before the collected blood was infused back into the rats supplemented with Ringer’s solution of the same volume,the rat models were then randomly divided into 3 groups: traumatic shock group (n=10);AG group(which was subdivided into AGⅠ,AGⅡ groups ,each consisting of 10 rats and receiving 10 and 50mg/kg AG ininfusion respectively during resuscitaiton),and L-NAME group(with 10mg/kg L-NAME infusion during resuscitation,n=10).Plasma NO level was determined before and after shock,immediately after resuscitaion and 0.5,2,4h after resuscitation ,and the survival rate within 24h were recorded with tissue samples of the lung,liver,kidney and intestine obtained 24h after shock for microscopic examination.Results:Plasma NO level was increased markedly after traumatic shock in the rat models.In the AG Ⅱ group,the elevated NO level following the shock was obviously reduced after resuscitaiton with less tissue damages and higher survival rate,as compared with the other groups.The best protective effect against traumatic shock was observed in AGⅡ group,In spite of obvious decrease of plasma NO level after resuscitation,L-NAME exhibited little efficacy in alleviating the tissue damages in the organs and hence failed to improve the survial rate of rats.Conclusions:NO plays an important role in the pathological process of traumatic shock,and the application of AG may improve the condition,L-NAME can decrease plasma NO level after resuscitation,but fail to improve the outcome of traumatic shock in rats. [

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Objective: To evaluate the effects of a selective inhibitor of inducible nitric oxide synthase(iNOS)-aninoguanidine(AG) and a non-selective inhibitor of nitric oxide synthase-(NOS)L-NAME on traumatic shock in rats.Methods: Animal models of traumatic shock were established in 40 Wistar rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45mmHg(4.67~6.00kPa).Hypotension was maintained for 30min before the collected blood was infused back into the rats supplemented with Ringer’s solution of the same volume,the rat models were then randomly divided into 3 groups: traumatic shock group (n=10);AG group(which was subdivided into AGⅠ,AGⅡ groups ,each consisting of 10 rats and receiving 10 and 50mg/kg AG ininfusion respectively during resuscitaiton),and L-NAME group(with 10mg/kg L-NAME infusion during resuscitation,n=10).Plasma NO level was determined before and after shock,immediately after resuscitaion and 0.5,2,4h after resuscitation ,and the survival rate within 24h were recorded with tissue samples of the lung,liver,kidney and intestine obtained 24h after shock for microscopic examination.Results:Plasma NO level was increased markedly after traumatic shock in the rat models.In the AG Ⅱ group,the elevated NO level following the shock was obviously reduced after resuscitaiton with less tissue damages and higher survival rate,as compared with the other groups.The best protective effect against traumatic shock was observed in AGⅡ group,In spite of obvious decrease of plasma NO level after resuscitation,L-NAME exhibited little efficacy in alleviating the tissue damages in the organs and hence failed to improve the survial rate of rats.Conclusions:NO plays an important role in the pathological process of traumatic shock,and the application of AG may improve the condition,L-NAME can decrease plasma NO level after resuscitation,but fail to improve the outcome of traumatic shock in rats. [

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Available abstract

Objective: To evaluate the effects of a selective inhibitor of inducible nitric oxide synthase(iNOS)-aninoguanidine(AG) and a non-selective inhibitor of nitric oxide synthase-(NOS)L-NAME on traumatic shock in rats.Methods: Animal models of traumatic shock were established in 40 Wistar rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45mmHg(4.67~6.00kPa).Hypotension was maintained for 30min before the collected blood was infused back into the rats supplemented with Ringer’s solution of the same volume,the rat models were then randomly divided into 3 groups: traumatic shock group (n=10);AG group(which was subdivided into AGⅠ,AGⅡ groups ,each consisting of 10 rats and receiving 10 and 50mg/kg AG ininfusion respectively during resuscitaiton),and L-NAME group(with 10mg/kg L-NAME infusion during resuscitation,n=10).Plasma NO level was determined before and after shock,immediately after resuscitaion and 0.5,2,4h after resuscitation ,and the survival rate within 24h were recorded with tissue samples of the lung,liver,kidney and intestine obtained 24h after shock for microscopic examination.Results:Plasma NO level was increased markedly after traumatic shock in the rat models.In the AG Ⅱ group,the elevated NO level following the shock was obviously reduced after resuscitaiton with less tissue damages and higher survival rate,as compared with the other groups.The best protective effect against traumatic shock was observed in AGⅡ group,In spite of obvious decrease of plasma NO level after resuscitation,L-NAME exhibited little efficacy in alleviating the tissue damages in the organs and hence failed to improve the survial rate of rats.Conclusions:NO plays an important role in the pathological process of traumatic shock,and the application of AG may improve the condition,L-NAME can decrease plasma NO level after resuscitation,but fail to improve the outcome of traumatic shock in rats. [

Key concepts: Traumatic Shock, Shock (circulatory), Nitric oxide synthase, Medicine, Resuscitation, Nitric oxide, Blood pressure, Anesthesia

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