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1.
Chinese Journal of Emergency Medicine ; (12): 274-276, 2009.
Article in Chinese | WPRIM | ID: wpr-394815

ABSTRACT

Objective To investigate the effects of preconditioning with 3-nitropropionie acid on myocardial apoptosis induced by ischemia-reperfusion injury.Method Twenty-four rabbits were randomly divided into control group(group C,n=8),precondition group(group 3-NPA,n=8)and 5-HD group(group 5-HD,n=8).The group 5-HD was treated intravenously with 5 mg·kg-1 5-HD(ATP-sensitive potassium channels blocker),group C and group 3-NPA received normal saline instead of 5-HD.Ten minutes later,5-HD group and 3-NPA group were injected with 3-NPA(3 mg·kg-1)and the group C was injected with normal saline.Twenty-four hours later,the left anterior descending coronary artery was ligated for 30 min and then unclamped for 120 min to estabhsh ischemi-a-reperfitsion injury model.After reperfusion,the infarct sizes of ventricular myocardium,apoptotic myocardial cells and the expressions of Bcl-2 and Bax protein were measured.Results Infarct sizes and apoptotic myocardial cells in group 3-NPA were less than those in the others(P<0.01).The expressions of Bcl-2 in group 3-NPA.in-creased as compared with group C(P<0.05)and group 5-HD(P<0.05),whereas the expressions of Bax in group 3-NPA decreased as compared with group C(P<0.05)and group 5-HD(P<0.05).Conclusions Preconditioning with 3-nitmpropionie acid reduces myocardial apoptosis induced by isehemia-reporfusion injury which is attributed to the opening of mitochondrial KATP channels.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 257-259, 2005.
Article in Chinese | WPRIM | ID: wpr-322947

ABSTRACT

Summary: The effects of diazoxide treatments on electrophysiologyic properties in guinea pig papillary muscles undergoing ischemia/reperfusion was studied using intracellular microelectrode technique. Twenty-four guinea pigs were randomly divided into three groups (n=8 in each group). In control group, St.Thomas solution was given. In experimental group, St.Thomas solution with diazoxide (100 mol/L) was given. In pretreatment group, the muscle was treated with diazoxide 20 min before arrested with St.Thomas cardioplegia. The results showed that the APD50 and APD90 in experimental and pretreatment groups were significantly shorter after 5 and 10 min reperfusion (P<0.01, P<0.05), but longer after 30 min reperfusion (P<0.01, P<0.05) than in control group. In experimental and pretreatment groups, APA, OS, Vmax recovered more quickly than those in control group. The time to re-systole after reperfusion in control group was longer than that in experimental and pretreatment groups. There was no significant difference in RP among three groups. The time of arrest in pretreatment group was longer than that in experimental and pretreatment group (P<0.05). This study indicates that protective effects of St.Thomas solution with diazoxide is better than that of pretreatment with diazoxide or St.Thomas solution alone.

3.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 558-560, 2005.
Article in Chinese | WPRIM | ID: wpr-234580

ABSTRACT

The effects of cyclosporine A (CsA) on Angiontensin Ⅱ (Ang Ⅱ )-induced protein contents, c-fos protein levels and cytosolic Ca2+ level ([Ca2+ ]i) in cultured cardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. [Ca2+ ]i labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confocal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang Ⅱ (10-7 mol/L), which could be inhibited by CsA in a dose-dependent manner. It was found that Ang Ⅱ could increase the c-fos protein expression, which could be inhibited by CsA in a dose-dependent manner.Ang Ⅱ induced the [Ca2+ ]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca2+ , but inhibited significantly the Ang Ⅱ-induced [Ca2+ ]i elevation. It was concluded that CsA can suppress the Ang Ⅱ-induced c-fos protein expression and [Ca2+ ]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang Ⅱ -induced cardiomyocyte hypertrophy by CsA.

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