BD针在重症急性胰腺炎急性肺损伤大鼠模型制备中的应用

Objective To investigate the improvement of BD intravenous catheters used in inducing the model of acute lung injury with severe acute pancreatitis in rats.Methods Total 40 healthy adult male SD rats were randomly assigned to 2 groups,SO group(n=10),SAP group(n=30),4% tauroeholate(0.1ml/kg)was injected via retrograde biliopancreatic ducts by using BD intravenous catheters via duodenal papilla.The serum amylase,blood gas analysis,ascites volume,lung water content and the pathological score of pancreas and lung structure under light microscope were recorded when the SAP model were induced in 3 h,6 h and 12 h.The relative data mentioned as above also detected in SO group after 12 h.Results The score of the SAP group was significantly higher than the SO group in blood amylase,ascites volume,lung water content,PaCO2,pancreas and lung histology(P＜0.05).Meanwhile,PaO2,oxygenation index were decreased significantly(P＜0.05).Conclusion It is efficient to establish simple,reproducible and stabile rat model of acute lung injury with severe acute pancreatitis by using BD intravenous catheters.     

七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

Objective To investigate the effects of sevoflurane pretreatment on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Methods Seventy -two Sprague -Dawley rats were randomly divided into 6 groups: NS group, LPS group and sevoflurane pretreatment (S-l h group, S-6 h group, S-12 h group and S-24 h group). The rat model of ALI was established by intratracheal instillation of LPS. Animals were sacrificed at 6 h after LPS or NS administration. Leukocyte count, concentration of TNF-α and IL-β in bronchoalveolar lavage fluid (BALF); pulmonary capillary permeability, myeloperoxidase (MPO) activity of lung tissue; lung histological changes were compared in rats with or without sevoflurane pretreatment (2.4% inspired for 30 min) at different times before LPS instillation. Results Compared with the NS group,severe injury of lung tissues and increase in leukocyte count in BALF, Production of TNF-α and IL-1β in BALF, pulmonary capillary permeability and MPO activity in the lung were significantly increased in rats treated with LPS (P<0.01). MPO activity, leukocyte count and production of IL-1βin BALF were reduced when sevoflurane was given 1 or 24 h before but not at 6 or 12 h before LPS instillation(P<0.01). Sevoflurane pretreatment also attenuated pulmonary capillary permeability and production of TNF-α in BALF (P<0.01). Pulmonary capillary permeability and concentration of TNF-α in S-l h and S-24 h group was lower than S-6 h and S-12 h group (P<0.01). Sevoflurane pretreatment was effective at 1 h and 24 h suggesting sevoflurane has early and late protection against LPS-induced lung injury. Conclusion Sevoflurane pretreatment has protective effects against acute lung injury when given 1 or 12 h before LPS instillation.     

七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

Objective To investigate the effects of sevoflurane pretreatment on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Methods Seventy -two Sprague -Dawley rats were randomly divided into 6 groups: NS group, LPS group and sevoflurane pretreatment (S-l h group, S-6 h group, S-12 h group and S-24 h group). The rat model of ALI was established by intratracheal instillation of LPS. Animals were sacrificed at 6 h after LPS or NS administration. Leukocyte count, concentration of TNF-α and IL-β in bronchoalveolar lavage fluid (BALF); pulmonary capillary permeability, myeloperoxidase (MPO) activity of lung tissue; lung histological changes were compared in rats with or without sevoflurane pretreatment (2.4% inspired for 30 min) at different times before LPS instillation. Results Compared with the NS group,severe injury of lung tissues and increase in leukocyte count in BALF, Production of TNF-α and IL-1β in BALF, pulmonary capillary permeability and MPO activity in the lung were significantly increased in rats treated with LPS (P<0.01). MPO activity, leukocyte count and production of IL-1βin BALF were reduced when sevoflurane was given 1 or 24 h before but not at 6 or 12 h before LPS instillation(P<0.01). Sevoflurane pretreatment also attenuated pulmonary capillary permeability and production of TNF-α in BALF (P<0.01). Pulmonary capillary permeability and concentration of TNF-α in S-l h and S-24 h group was lower than S-6 h and S-12 h group (P<0.01). Sevoflurane pretreatment was effective at 1 h and 24 h suggesting sevoflurane has early and late protection against LPS-induced lung injury. Conclusion Sevoflurane pretreatment has protective effects against acute lung injury when given 1 or 12 h before LPS instillation.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.