[Effects of L-arginine and aminoguanidine on the endotoxin induced lung injury in rats].
Jianxin Zhang, Liping Li, Shuting Dong, Lanfang Li, Lijun Xie, Liang Liang
Abstract
Jianxin Zhang, Liping Li, Shuting Dong, Lanfang Li, Lijun Xie, Liang Liang
Abstract
AIM: To investigate the effects of L-arginine and nitric oxide synthase (NOS) inhibitor Aminoguanidine (AG) on endotoxin induced lung injury in rats. METHODS: Forty eight healthy male SD rats weighing (300 +/- 20) g were used. The animals were anesthetized with 20% urethane 1 g x kg(-1). Common carotid artery (CAA) and common carotid vein (CAV) were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into six groups: group 1: control: group 2: LPS (5 mg x kg(-1) intravenous injection, i.v.); group 3: AG (50 mg x kg(-1) intraperitoneal injection, IP); group 4: high dose L-arginine (500 mg x kg(-1), IP); group 5: low dose L-arginine (250 mg x kg(-1) IP). Group 6: L-arginine + AG (250 mg x kg(-1), 50 mg x kg(-1), IP). Group 1: The animals were killed 6 h after 0.9% saline solution was given. Group 2: 0.9% saline solution was given 3 h after LPS i.v. and the animals were killed 3 h after medication. Group 3, 4, 5 and 6: AG, L-arginine and L-arginine+ AG were given 3 h after LPS i.v. respectively and the animals were killed 3 h after medication respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-arginine, AG and L-arginine + AG significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated endotoxin induced lung injury. AG and L-arginine + AG significantly decreased NO content in plasma, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-arginine, AG and L-arginine + AG have beneficial effects on lung injury induced by LPS.
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AIM: To investigate the effects of L-arginine and nitric oxide synthase (NOS) inhibitor Aminoguanidine (AG) on endotoxin induced lung injury in rats. METHODS: Forty eight healthy male SD rats weighing (300 +/- 20) g were used. The animals were anesthetized with 20% urethane 1 g x kg(-1). Common carotid artery (CAA) and common carotid vein (CAV) were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into six groups: group 1: control: group 2: LPS (5 mg x kg(-1) intravenous injection, i.v.); group 3: AG (50 mg x kg(-1) intraperitoneal injection, IP); group 4: high dose L-arginine (500 mg x kg(-1), IP); group 5: low dose L-arginine (250 mg x kg(-1) IP). Group 6: L-arginine + AG (250 mg x kg(-1), 50 mg x kg(-1), IP). Group 1: The animals were killed 6 h after 0.9% saline solution was given. Group 2: 0.9% saline solution was given 3 h after LPS i.v. and the animals were killed 3 h after medication. Group 3, 4, 5 and 6: AG, L-arginine and L-arginine+ AG were given 3 h after LPS i.v. respectively and the animals were killed 3 h after medication respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-arginine, AG and L-arginine + AG significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated endotoxin induced lung injury. AG and L-arginine + AG significantly decreased NO content in plasma, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-arginine, AG and L-arginine + AG have beneficial effects on lung injury induced by LPS.
Key concepts: Saline, Arginine, Nitric oxide, Intraperitoneal injection, Nitric oxide synthase, Lung, Pulmonary artery, Chemistry