ABSTRACT
Objective To evaluate the effect of isoflurane preconditioning on myocardial ischemiareperfusion (I/R) injury induced by antioxidative remodeling in aged rats.Methods Fifty-six SPF aged male Sprague-Dawley rats,aged 22-24 months,weighing 420-480 g,were divided into 5 groups by a random number table method:sham operation group (S group,n=16),oxygen free radical scavenger tempol group (T group,n=16),myocardial I/R group (I/R group,n=8),tempol plus myocardial I/R group (TI group,n =8),and tempol plus isoflurane preconditioning plus myocardial I/R group (TII group,n=8).Tempol 125 mg · kg-1 · day-1 was intraperitoneally injected for 4 weeks in group T.Myocardial I/R was induced by ligation of anterior descending branch of left coronary artery for 30 min followed by 2-h reperfusion to establish myocardial I/R injury model in group I/R.The model was established after antioxidant treatment in group TI.In group TII,1.5％ isoflurane was inhaled for 30 min followed by 15-min washout,and then the model was established.Animals were sacrificed at the end of reperfusion,and the left ventricle was obtained for determination of the percentage of myocardial infarct size (by TTC staining),glutathione (GSH) and oxidized glutathione (GSSG) concentrations and superoxide dismutase (SOD) activity in S and T groups (by enzyme-linked immunosorbent assay),and expression of Cu/ZnSOD,MnSOD and nitrotyrosine in S and T groups (by Western blot).Results Compared with S and T groups,the percentage of myocardial infarct size was significantly increased in I/R,TI and TII groups (P＜ 0.05).Compared with I/R and TI groups,the percentage of myocardial infarct size was significantly decreased in group TII (P＜0.05).Compared with group S,no significant change was found in the expression of GSH or Cu/ZnSOD (P＞0.05),the expression of GSSG and nitrotyrosine was down-regulated,the GSH/GSSG ratio was increased,the activities of total SOD and MnSOD were increased,and the expression of MnSOD was up-regulated in group T (P＜0.05).Conclusion Isoflurane preconditioning can reduce myocardial I/R injury induced by antioxidative remodeling in aged rats.
ABSTRACT
Objective To evaluate the role of serine-threonine kinase (Akt)/glycogen synthase kinase-3 beta (GSK-3β) signaling pathway in isoflurane preconditioning-induced inhibition of mitochondrial permeability transition pore protein (mPTP) opening during myocardial ischemia-reperfusion (I/R) in rats.Methods Ninety-six male Sprague-Dawley rats,aged 3-4 months,weighing 200-250 g,were randomly divided into 4 groups (n =24 each) using a random number table:control group (group C);I/R group;isoflurane preconditioning group (group IPC);Akt inhibitor MK-2206 group (group MK).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by 2 h of reperfusion.In group IPC,1.5％ isoflurane was inhaled for 30 min followed by 45 min washout,and then the model of myocardial I/R injury was established.In group MK,MK-2206 300 μg/kg (in dimethyl sulfoxide) was injected intraperitoneally at 30 min before isoflurane inhalation.At 2 h of reperfusion,8 rats were selected and sacrificed,and the hearts were removed for determination of myocardial infarct size.At 2 h of reperfusion,8 rats were selected,and blood samples were collected from the right internal jugular vein for determination of serum cardiac troponin Ⅰ (cTnI) concentrations.The rats were then sacrificed,and myocardial specimens were obtained for determination of the expression of phosphorylated GSK-3β (p-GSK-3β) in cytoplasm and mitochondria (by Western blot) and co-expression of p-GSK-3β with adenine nucleotide translocator (ANT),voltage-dependent anion channel or cyclophilin D in myocardial tissues (using co-immunoprecipitation).At 2 h of reperfusion,8 rats were selected and sacrificed,myocardial cells were obtained,and the opening time of mPTP was determined with a laser scanning confocal microscope.Results Compared with group C,the myocardial infarct size and serum cTnI concentrations were significantly increased,and the expression of p-GSK-3β in cytoplasm and mitochondria was up-regulated in I/R and IPC groups,the co-expression of p-GSK-3β with ANT was significantly down-regulated,and the opening time of mPTP was shortened in group I/R,and the co-expression of p-GSK-3β with ANT was significantly up-regulated,and the opening time of mPTP was prolonged in group IPC (P＜0.05).Compared with group I/R,the myocardial infarct size and serum cTnI concentrations were significantly decreased,the expression of p-GSK-3β in cytoplasm and mitochondria was up-regulated,the co-expression of p-GSK-3β with ANT was significantly up-regulated,and the opening time of mPTP was prolonged in group IPC,and the opening time of mPTP was significantly prolonged (P＜0.05),and no significant change was found in the other parameters in group MK (P＞0.05).Compared with group IPC,the myocardial infarct size and serum cTnI concentrations were significantly increased,the expression of p-GSK-3β in cytoplasm and mitochondria was up-regulated,the co-expression of p-GSK-3β with ANT was significantly down-regulated,and the opening time of mPTP was shortened in group MK (P＜0.05).No co-expression of p-GSK-3β with voltage-dependent anion channel or cyclophilin D was found in myocardial tissues.Conclusion The mechanism by which isoflurane preconditioning inhibits mPTP opening during myocardial ischemia-reperfusion is partially related to activation of Akt/GSK-3β signaling pathway in rats.
ABSTRACT
Objective To scrutinize the CT features of pulmonary actinomycosis and analysize the causes of misdiagnosis.Methods CT images of eleven patients with pulmonary actinomycosis proved by pathology were retrospectively reviewed.Among them,6 were scanned with additional enhanced CT scan.Results Among the 11 patients,the lesions located in the inferior lobe in 7 patients,and in the superior lobe in 4 patients.The lesions affected two or more pulmonary segments in 9 patients,6 of them involving two lobes.Irregular mass or nodules with necrotic low-attenuation areas were the main signs in all patients,and segmental consolidations were found in 6 patients.Peripherally progressive enhancement was found in all patients with contrast enhanced CT scan.Vicinity pleural thickening was found in 11 patients,while extrapleural fat deposition was found in 6 patients.One case showed erosion of the chest wall and rib.Conclusion Pulmonary actinomycosis is a chronic suppurative granulomatous inflammation,which is often misdiagnosed with neoplasm or other lung disease because of its mass-like performance.The peripherally progressive enhancement on CT has a certain diagnostic value for P\pulmonary actinomycosis.