Yapay Zeka Hızlı Bakış & Çıkarımlar
AI InsightLung injury was aggravated by the administration of the NO inhibitor L-NAME.
📌 3 Maddede Bu Makale
Özet
The aim of this study was to investigate the role of NO in the pathogenesis of lung injury associated with pancreatitis, and the relation between malondialdehyde (MDA) and myeloperoxidase (MPO). Forty Wistar male rats were divided into control or pancreatitis groups, and treated with saline, L-arginine (100 mg/kg i.v.), NO donor, or N-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg i.v.), an inhibitor of NO synthase. Pancreatitis was induced in rats intravenously via the administration of cerulein (10 µg/kg/h) for 4 h). Eight hours after the induction of acute pancreatitis (AP), amylase and lipase in plasma significantly increased in all animals in which mild pancreatitis was induced in comparison with the control group. Cerulein induced gross pancreatic and lung edema as reflected by an increase in the wet/dry ratio. L-arginine significantly decreased pancreatic and lung edema. L-arginine treatment prevented the increase of MDA levels in the pancreas (760 ± 252 nM/g tissue) and lung (520 ± 188 nM/g tissue). In contrast, L-NAME increased MDA levels in the pancreas (3280 ± 474 nM/g tissue) and lung (2650 ± 411 nM/g tissue). Compared with the AP group, MPO activity was reduced by L-arginine (17.2 ± 3.7 U/g pancreas versus 6.2 ± 2.2 U/g pancreas; 28.4 ± 3.3 U/g lung versus 11.1 ± 3.0 U/g lung). In contrast, L-NAME treatment significantly increased MPO levels in the pancreas (32.8 ± 4.7 U/g pancreas) and lung (43.7 ± 7.1 U/g lung). In conclusion, L-arginine treatment improved the course of mild pancreatitis and prevented lung injury. Lung injury was aggravated by the administration of the NO inhibitor L-NAME.
Abstract
The aim of this study was to investigate the role of NO in the pathogenesis of lung injury associated with pancreatitis, and the relation between malondialdehyde (MDA) and myeloperoxidase (MPO). Forty Wistar male rats were divided into control or pancreatitis groups, and treated with saline, L-arginine (100 mg/kg i.v.), NO donor, or N-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg i.v.), an inhibitor of NO synthase. Pancreatitis was induced in rats intravenously via the administration of cerulein (10 µg/kg/h) for 4 h). Eight hours after the induction of acute pancreatitis (AP), amylase and lipase in plasma significantly increased in all animals in which mild pancreatitis was induced in comparison with the control group. Cerulein induced gross pancreatic and lung edema as reflected by an increase in the wet/dry ratio. L-arginine significantly decreased pancreatic and lung edema. L-arginine treatment prevented the increase of MDA levels in the pancreas (760 ± 252 nM/g tissue) and lung (520 ± 188 nM/g tissue). In contrast, L-NAME increased MDA levels in the pancreas (3280 ± 474 nM/g tissue) and lung (2650 ± 411 nM/g tissue). Compared with the AP group, MPO activity was reduced by L-arginine (17.2 ± 3.7 U/g pancreas versus 6.2 ± 2.2 U/g pancreas; 28.4 ± 3.3 U/g lung versus 11.1 ± 3.0 U/g lung). In contrast, L-NAME treatment significantly increased MPO levels in the pancreas (32.8 ± 4.7 U/g pancreas) and lung (43.7 ± 7.1 U/g lung). In conclusion, L-arginine treatment improved the course of mild pancreatitis and prevented lung injury. Lung injury was aggravated by the administration of the NO inhibitor L-NAME.