The Relationships Of β-AR And GRK2 In PMVEC And Lung Injury In Rats With Severe Acute Pancreatitis

Objective To investigate pathological changes,variation ofβ-AR in pulmonary microvascular endothelial cells and variation of GRK2 in lung and to explore the therapeutic effect of methyprednisolone in severe acute pancreatitis-associated lung injury model in rats.Methods Male SD rats were divided into three groups randomly:the control group,the experimental group and the intervention group.In the control group, laparotomy were performed,duodenum and pancreas were flipped only.In the experimental group,acute necrotizing pancreatitis model was induced in rats by retrograde injection of 5%sodium taurocholate into biliopancreatic duct.In the intervention group,methylprednisolone(30mg/kg)was injected into rump musle of rats after models were developed.At 6 and 12 hours after model were developed, the maximum binding capacity(Bmax)and the Kd value of PMVECβ-AR was detected in lung by means of radioactive ligand binding assay.GRK2 expression was detected in lung by means of immunofluorescence.Serum IL-6 were quantitated using ELISA kits.The severity of pancreatitis and lung injury was determined by local pathological lesion(gross and histopathologie scoring).The lung tissure water content were detected,too.The effect of methylprednisolone were observed at the same time.Results1.The lung tissure water content increased at 6 hours after SAP model induction, and more at 12 hours(P＜0.05);higher than the control group(P＜0.01).2.The Bmax of PMVECβ-AR decreased at 6 hours after SAP model induction, and more at 12 hours(P＜0.05);lower than the control group(P＜0.01).3.The Kd value of PMVECβ-AR increased at 6 hours after SAP model induction, and more at 12 hours(P＜0.05);higher than the control group(P＜0.01).4.The expression of GRK2 in lung increased at 6 hours after SAP model induction, and more at 12 hours(P＜0.05);higher than the control group(P＜0.01).5.Intervention of methylprednisolone decreased water content,GRK2 expression, IL-6 in serum,Kd value of PMVECβ-AR and increased the Bmax of PMVECβ-AR(P＜0.05);and more at 12 hours(P＜0.05).Conclusions1.Lung injury occurs at 6 hours after SAP model induction in rats,and is more severe at 12 hours.2.β-AR in pulmonary microvascular endothelial cells was lower down in severe acute pancreatitis-associated lung injury model in rats.3.GRK2 expression in lung was higher up in severe acute pancreatitis-associated lung injury model in rats,and it maybe the mechanism of the decreasion ofβ-AR in pulmonary microvascular endothelial cells.4.The intervention of methylprednisolone may attenuate the severity of acute pancreatitis-associated lung injury.