AIM: To investigate the expression of voltage-gated chloride channels (ClC)-3 protein and mRNA in human glioma specimen and its biological function. METHODS: The expression of C1C-3 was observed by immunohistochemical staining in 24 cases of human glioma, 4 cases of brain metastic cancer specimens and 5 cases of normal brain tissue as control; The C1C-3 mRNA expression were detected in the specimens with positive expression of ClC-3 protein by RT-PCR. RESULTS: ClC-3 protein was found negative in 4 cases of normal brain tissues and positive in 19 cases of human glioma and 4 cases of brain metastic cancer specimens. ClC-3 protein was mainly expressed in the membrane or cytoplasm of neoplastic cells and microvascular endothelial cells. The expression of ClC-3 mRNA was detected in 16 cases of human glioma and 4 cases of brain metastasis cancer specimens among the tissues with the positive expression of ClC-3 protein. The level of protein and RNA of ClC-3 in high malignant oligodendrogliomas was higher than that in low malignant ones. CONCLUSION: ClC-3 is generally expressed in human glioma and brain metastic cancer and is probably correlated with the classification of its pathological malignance.

Objective To evaluate the beneficial effects of early coronary reperfusion on left ventricular remodeling (LVRM) and systolic function in patients with acute myocardial infarction (AMI).Methods Eighty-one patients with first AMI in the convalescent stage and having undergone left ventriculography (LVG) and coronary arteriography (CAG) were divided into four groups: the anterolateral wall (ALW) myocardial infarction (MI) non-reperfusion (n=20) and reperfusion (n=21), and inferoposterial wall (IPW) MI non-reperfusion (n=20) and reperfusion (n=20), according to infarct location and early treatment with or without successful coronary reperfusion therapy within 6 hours after onset of symptoms. By LVG, the parameters of LVRM and systolic function in the four MI groups were analyzed and compared with those in normal group (n=25) and between the two reperfusion and non-reperfusion MI groups.Results In both ALW and IPW MI non-reperfusion groups, the left ventricular (LV) end-diastolic volume (EDV), circumference (EDC), short-axis dimension (EDD), short to long axis ratio (ED-D/L), sphericity index (ED-SI) and end-systolic volume (ESV) were all significantly increased (P<0.01-0.001), while LV ejection fractions (LVEF) were significantly decreased (both P<0.001) when compared with those of normal group; and the increase in ESV and decrease in LVEF were both significantly greater in ALW than in IPW MI groups (both P<0.01).In both ALW and IPW MI reperfusion groups, however, the EDV, EDD, ESV, as well as the extent and severity of regional wall motion abnormality (RWMA) were significantly smaller (P<0.05-0.001), while LVEF were significantly higher (P<0.01-0.001) when compared with those in the two non-reperfusion MI groups respectively. There were no longer significant differences in LVEF and ESV between ALW and IPW MI groups (both P>0.05). The EDC in IPW MI reperfusion group and the ED-D/L and ED-SI in ALW MI reperfusion group were also significantly reduced compared with those in the two non-reperfusion MI groups respectively (P<0.05-0.001). All the above parameters in the two reperfusion MI group were decreased to the normal in comparison with normal group except ESV and LVEF, and ED-D/L and ED-SI in IPW MI group.Conclusion It was indicated that in both ALW and IPW MI non-reperfusion groups, LVRM had occurred in convalescent stage of AMI with an increase in EDV and EDC, spherical change in LV shape, and accompanying reduction in LV systolic function; and early coronary reperfusion in AMI could reduce the extent and severity of RWMA, prevent from LV enlargement and remodeling, and preserve or improve LV systolic function with more prominence in ALW MI.

OBJECTIVESTo compare the effects of losartan, enalapril and their combination in the prevention of left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat.

METHODSAMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups : 1) AMI control group (n = 19), 2) losartan group (n = 22, 3 mg x kg(-1) x d(-1)), 3) enalapril group (n = 20, 1 mg x kg(-1) x d(-1)), 4) losartan-enalapril combinative group (n = 22, 3 and 1 mg x kg(-1) x d(-1) respectively). 5) Sham-operated group (n = 10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1) AMI controls (n = 11), 2) losartan group (n = 10), 3) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11), 5) sham-operated group (n = 6) and 6) normal controls (n = 8).

RESULTSThere were no significant differences among the 4 AMI groups in MI size (41.7% to approximately 43.4%, all P > 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW) in AMI group were all significantly increased (P < 0.05 to approximately 0.001); whereas the maximum left ventricular pressure rising and dropping rates (+/- dp/dt) and their corrected values by LV systolic pressure (+/- dp/dt/LVSP) were significantly reduced (all P < 0.001), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group, LVEDP, LVV, LVAW and LVRW were all significantly decreased (P < 0.05 to approximately 0.001); while +/- dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P < 0.05 to approximately 0.001) except -dp/dt/LVSP in losartan group (P > 0.05). There were no significant differences in the above indices among the 3 treatment groups (all P > 0.05).

CONCLUSIONBoth losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.

Animals ; Antihypertensive Agents ; pharmacology ; Drug Synergism ; Enalapril ; pharmacology ; Female ; Losartan ; pharmacology ; Myocardial Infarction ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Ventricular Function, Left ; drug effects ; Ventricular Remodeling ; drug effects

OBJECTIVETo compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats, especially evaluating the efficacy of low dose enalapril.

METHODSAMI was induced by ligating the left coronary artery in 149 female SD rats. 48 hours after the procedure, the 97 surviving rats were randomized to one of the following four groups: (1) AMI controls (n = 24), (2) high-dose (10 mg x kg(-1) x d(-1), n = 25), (3) middle-dose (1 mg x kg(-1) x d(-1), n = 23), and (4) low-dose (0.1 mg x kg(-1) x d(-1), n = 25) enalapril groups. In addition, sham-operated (n = 13) and normal rats (n = 10) were randomly selected to serve as non-infarction controls. Enalapril was delivered by direct gastric gavage. After 4 weeks of therapy, hemodynamic studies were performed, then the rat hearts were fixed with 10% formalin and pathology analysis was performed. Exclusive of the dead rats and those with MI size < 35% or > 55%, complete experimental data were obtained from 67 rats, which were comprised of (1) AMI controls (n = 13), (2) high-dose enalapril (n = 13), (3) middle-dose enalapril (n = 12), (4) low-dose enalapril (n = 12), (5) sham-operated (n = 8) and (6) normal (n = 9) groups.

RESULTSThere were no significant differences among the four AMI groups in infarction size (all P > 0.05). Compared with the sham-operated group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), absolute and relative weight (LVAW, LVRW) in AMI group were all significantly increased (all P < 0.001), while maximum LV pressure rising and dropping rates (+/- dp/dt) and their corrected values by LV systolic pressure (+/- dp/dt/LVSP) were all significantly reduced in the AMI control group (P < 0.01 - 0.001), indicating LVRM occurred and LV systolic and diastolic functions were impaired. Compared with the AMI group, LVEDP, LVV, LVAW and LVRW were all significantly decreased in the three enalapril groups (control P < 0.001), with the reduction of LVEDP, LVV and LVAW being more significant in high-dose than in low-dose enalapril groups (all P < 0.05), and the +/- dp/dt/LVSP were significantly increased only in the high and middle-dose enalapril groups (P < 0.01).

CONCLUSIONSHigh, middle and low doses of enalapril were all effective in preventing LVRM after AMI in the rat, with low dose enalapril being effective and high dose superior. As for LV functional improvement, only high and middle-dose enalapril were effective.

Angiotensin-Converting Enzyme Inhibitors ; administration & dosage ; pharmacology ; Animals ; Dose-Response Relationship, Drug ; Enalapril ; administration & dosage ; pharmacology ; Female ; Myocardial Infarction ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Ventricular Remodeling ; drug effects