ABSTRACT
Objective To study the effect of berberine on arrhythmia caused by stretch of rats' myocardium,in vitro,after myocardial ischemia (MI) for 30 min.Methods The study was carried out in the laboratory of Heilongjiang traditional Chinese medicine university.A total of 40 Wistar rats were randomly (random number) divided into 4 groups,namely normal control group,berberine group、MI group and MI + berberine group.After perfusion of rat' s heart with Langendorff perfusion device,the model of MI was made with ligation of left anterior descending branch for 30 min.Berberine was dissolved in Tyrode' s solution to a concentration of 300 μmol/L.The hearts were stretched for 5 s by 0.2 ml.The effect of stretching was observed for 30 s to record 90％ monophasic action potential (MAPD90),premature ventricular beats (PVB) and ventricular tachycardia (VT).Quantitative data were compared with ANOVA.Qualitative data were compared with a x2 test.Differences with a value of P ＜ 0.05 were considered statistically significant.Results MAPD90 in normal control and MI group obviously prolonged after the hearts were stretched ( P ＜ 0.01 ).And MAPD90 in MI group was even longer than that of normal control group (P＜0.05).Berberine had no influence on MAPD90 before myocardiuml stretched (P ＞0.05),while it could reduce the degree of prolongation in MAPD90 after myocardium stretched (P ＜ 0.05 or P ＜0.01 ).The incidence rate of PVB and VT in normal control and MI group increased after stretched.The berberine in dose of 300 μmol/L could reduce the incidence of PVB and obviously inhibit the occurrence of VT ( P ＜ 0.01 ).Conclusions Berberine could obviously inhibit the occurrence of stretch-inducedarrhythmias after myocardial infarction.
ABSTRACT
ObjectiveTo investigate the effect of β-adrenoceptor (β-AR) blockers on G protein and heart function changes in rats with acute myocardial infarction (AMI) MethodsWistar rats with AMI induced by left anterior descending coronary branch ligation were randomly divided into compared with sham operation group. Eight weeks after therapy, hemodynamics was assessed by inserting catheters and the level of G protein was detected by Western blot analysis. ResultsCompared with the sham operation group, systolic blood pressure(SBP), diastolic blood pressure (DBP), left ventricular systolic pressure(LVSP) and left ventrieular pressure maximal rate of rise and fall(±dp/dtmax) in AMI group were significantly decreased, while left ventricular end diastolic pressure (LVEDP) and Gs and Gi protein levels were significantly increased (all P<0.05). Compared with AMI group, LVSP and ± dp/dtmax were increased, but LVEDP and Gi protein level were significantly decreased in metoprolol and carvedilol group. LVEDP and Gi protein level were decreased in carvedilol group compared with metoprolol group. ConclusionsCarvedilol can effectively suppress the change of G protein and improve the heart function after AMI, and the effect is better than that of metoprolol. This may be related with its β2-AR blocking effect.
ABSTRACT
AIM:To explore the effect of long-term (6 months) endogenous testosterone deprivation by orchidectomy on the function of voltage-dependent potassium channels of vascular smooth muscle cells in rats. METHODS:Wistar rats were raised for 6 months after castration. Isometric tension measurement of aortic rings,whole-cell patch-clamp technique and Western blotting analysis were employed to examine the functional and posttranscriptional alterations of voltage-dependent potassium channels. RESULTS:Voltage-dependent potassium channel blocker,4-aminopyridine,significantly decreased the constriction of aortic artery rings from male rats after 6-month castration. In castrated rats the amplitude of voltage-dependent potassium currents of aortic artery smooth muscle cells was significantly decreased compared with that in control rats. Meanwhile,the expression of Kv 1.5 channel protein,which plays an essential role in mediating vasomotor function,was also reduced. The functional and molecular alterations of voltage-dependent potassium channels were both restored when the rats were concomitant applied with physiological level of testosterone after castration. CONCLUSION:Long-term deprivation of endogenous testosterone in rats significantly attenuates the function of voltage-dependent potassium channels,and the decreases in expression of Kv1.5 channel protein accounts for this alteration. Long-term application of physiological concentration of testosterone,which recovered the impaired function of voltage-dependent channels,may be beneficial for male gender with hypotestosteronaemia.