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BACKGROUND: Craniocerebral injury can cause a series of visceral complications, among which cardiovascular complication is paid special attention.OBJECTIVE: To investigate the effects of craniocerebral injury on changes of circulatory and local angiotensin Ⅱ (Ang Ⅱ ) and local angiotensin Ⅱ receptor 1 (AT1) in the heart.DESIGN: Randomized controlled experiment taking animals as subjects.SETTING: Beijing Tiantan Hospital, and the College of Basic Medicine,Capital University of Medical Sciences.MATERIALS: The experiment was conducted at the Central Laboratory of Capital University of Medical Sciences and the Central Laboratory of Beijing Tiantan Hospital from 2003 to 2004. Totally 40 healthy male Wistar rats were divided randomly into craniocerebral injury group and control group with 20 in each group.METHODS: Rats in craniocerebral injury group were treated with weightdrop method to establish the model of craniocerebral injury, while rats in control group received no impact. Twenty-four hours after hitting, 10 rats in each group were selected to assay their Ang Ⅱ and AT1; the other 10 in each group were selected to observe their myocardial forms.myocardium of rats assayed with light microscope after hematoxylin-eosin staining and transmission electron microscope.It was significantly higher in craniocerebral injury group than in control ity: It was obviously higher in craniocerebral injury group than in control Ⅱ and AT1: The area of positive reactant and gray value in craniocerebral toxylin-eosin staining: Strong acidophil staining was found on myocardial cellular plasma in craniocerebral injury group. The results showed that cytoplasm shrank obviously; muscle fiber broke, decreased or disappeared.Focal hydropic degeneration, lysis or necrosis was observed in myocardium.Ultrastructural pathological observation revealed pathological damage of myocardium.CONCLUSION: Craniocerebral injury in rats can cause myocardial damage, and changes of angiotensin system may be one of the factors.
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AIM: To observe the expression of TGF ?1 in hepatocytes during acute hemorrhagic and necrotic pancreatitis (AHNP) and to study the relationship between TGF ?1 and apoptosis in hepatocytes. METHODS: AHNP was induced in 40 rats weighting 260-280 g by intraductal administration of 5% sodium taurocholate. The pathologic morphologic changes of liver and pancreas were observed under light microscope. The hepatocyte apoptosis was examined through TdT (terminal deoxynucleotidyl transferase) mediated dUTP nick end labeling (TUNEL) and the expression of TGF ?1 in hepatocytes was analyzed through immunohistochemistry. RESULTS: The liver injuries were found at 3 h after the inducement. These changes were aggravated with the development of the disease. The apoptotic hepatocytes were found after 3 h (P
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Aim To investigate the effects of Panax Notoginseng Saponins(PNS) on expressions of Caspase-1,Caspase-3 and Caspase-8 after transient focal cerebral ischemia-reperfusion(CIR).Methods CIR injury was induced by middle cerebral artery occlusion(MCAO) in rats.The rats were treated with PNS(25 mg?kg~(-1)) and Nimodipine(1 mg?kg~(-1)).The drugs were administered 5 min before cerebral ischemia,and 12,24 and 36 h after cerebral ischemia.Sham operation group and model group were givenequal volume normal saline.The expressions of Caspase were observed by using immunochemistry after cerebral ischemia for 2 h followed by reperfusion for 46 hours.Results The expressions of Caspase-1 and Caspase-3 protein increased after cerebral ischemia.PNS decreased the expressions of Caspase-1(P