卡维地洛预防老年冠心病患者PCI术后再狭窄的临床观察

目的观察卡维地洛预防老年冠心病患者经皮冠状动脉介入(PCI)术后再狭窄的临床效果。方法200例患者随机分为卡维地洛组(100例)和对照组(100例)。观察PCI前、后及随访6个月冠状动脉造影、血清氧化指标oxLDL、MDA和内皮功能指标NO、ET和SOD变化情况。结果卡维地洛组最小管腔直径和管腔净获得较对照组明显增加(2.0mm±0.5mmvs1.2mm±0.3mm,P<0.05和1.6mm±0.4mmvs0.6mm±0.3mm,P<0.01),再狭窄率明显下降(21.8%vs43.3%,P<0.05);血清oxLDL和MDA较对照组明显减少分别为(0.56±0.12)mg/Lvs(0.86±0.15)mg/L,P<0.01和(7.48±1.08)nmol/mlvs(16.86±4.80)nmol/ml,P<0.01。结论卡维地洛可以降低老年冠心病患者PCI术后6个月冠状动脉再狭窄的发生率。

Use of Solid SMEDDS in Delivery of Carvedilol

Aim A new solid SMEDDS (self-microemulsifying drug delivery system) capsule has been developed to increase the solubility and dissolution rate. Methods The solubilities of carvedilol in various bases were investigated. Ternary phase diagrams were used to evaluate the self-emulsification and self-microemulsfication domains. The particle size distribution and ζ-potential were determined. The mean diameter of the three formulae decreased with an increase of Lutrol F68. Results The in vitro dissolution rate of ...

Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development

Objective: To explore the molecular regulation mechanism of carvedilol in attenuating the reversion back towards fetal energy metabolism during the development of cardiac hypertrophy induced by coarctation of abdominal aorta (CAA) in male Wistar rats. Methods: Hemodynamic and ventricular remodeling parameters, free fatty acid content in the serum were measured in the experimental animals at 16 weeks after the surgical CAA, the rats receiving carvedilol intervention (CAR) after CAA, and those with sham operation (SH). The expressions of muscle carnitine palmitoyltransferaseⅠ (M-CPTⅠ) and medium chain acyl-CoA dehydrogenase (MCAD) mRNA in the cardiac myocytes from every group were studied with RT-PCR. Results: Significant left ventricular hypertrophy were observed in the rats 16 weeks after coarctation operation (P<0.05), together with significant free fatty acids accumulation and downregulation of M-CPTⅠ and MCAD mRNA (P<0.05) in CAA group. Carvedilol at a dose of 30 mg/kg/d for 12 weeks inhibited the left ventricular hypertrophy induced by pressure overload and enhanced the gene expressions of rate-limiting enzyme (M-CPTⅠ) and key enzyme of fatty acid (MCAD) in the CAR group compared with CAA group (P<0.05). Conclusion: Pressure overload-induced hypertrophy in CAA rats causes the reversion back towards fetal enery metabolism, that is, downregulates the expressions of rate-limiting enzyme and key enzyme of fatty acid oxidation. The intervention therapy with carvedilol, a vasodilating alpha- and beta-adrenoreceptor antagonist, attenuates the reversion of the metabolic gene expression to fetal type through upregulating M-CPTⅠ and MCAD mRNA expressions. Thus, carvedilol may exert cardioprotective effects on heart failure by the mechanism of preserving the adult metabolic gene regulation.

Carvedilol suppresses ventricular arrhythmia in a pressure over-load rabbit model through relieving transmural dispersion of repolarization with long-term administration

Objective： To investigate the effects of carvedilol （CVD） on transmural dispersion of repolarization（TDR） and arrhythmia in pressure over-load rabbits. Methods： Left ventricular hypertrophied（LVH） rabbit models were established by pressure over-load; All animal models were assigned into CVD group or LVH group randomly. The action potentials of endocardium, cpicardium and transmural ECG of arterially perfused left ventricular preparations were recorded concurrently. Action potential duration （APD）, TDR, ventricular arrhythmia and ultrasonic parameters, ratio of LVM to body weight （LVMI） were compared correspondingly. The stable plasma concentration of carvedilol in CVD group was detected by HPLC. APD, TDR and arrhythmia of LVH models were compared just preor post-perfusion with stable concentration of CVD. Results： In Contrast with values in LVH group, LVEFof CVD group were significantly elevated while the LVMI was remarkably reduced, TDRs were significantly shortened, and ratio of ventricular arrhythmia was lowered remarkably. No significant difference of APD, TDR and ratio of arrhythmia was found preor post-perfusion at stable plasma concentration of CVD. Conclusion： CVD can ameliorate the structure and function of pressure over-load ventricles; CVD contributes to the improvement of ventricular arrhythmia associated with its long-term effect on APD,TDR shortening ,whereas has nothing to do with its transient function on ionic channel blockade

Effect of carvedilol on cardiac function and left ventricular remodeling in rats after acute myocardial infarction

Objective: To observe the effect of carvedilol injection on left ventricular function and collagen remodeling in rat with myocardial infarction. Methods: Sixty rats with a model of myocardial infarction were randomly divided into nine groups. The rats of therapeutical group were treated with carvedilol injection (2 mg/d intraperitoneal injection) and/or captopil (2 g/L drinking water) . Acute myocardial infarction ( AMI) group did not receive drug treatment. The animals were sacrificed at 4 weeks and 8 weeks after coronary artery ligation. The levels of plasma angiotensin II and plasma aldosterone and left ventricle function were determined at different time. The collagen content and the ratio of type I and III collagen of noninfarcted area were also assessed. Results: Compared with AMI group, the levels of plasma and myocardium angiotensin II and plasma aldosterone in both carvedilol and captopil group decreased at the eighth week (P<0.05). In addition, carvedilol improved systolic and diastolic function (P<0. 05). Compared with sham group, both collagen content and the ratio of type I / III collagen of noninfarcted area increased in AMI4 and AMI8 group (P<0. 05). The hydroxyproline levels and the ratio of type I/III collagen significantly decreased after carvedilol and/or captopil treatment , compared with AMI group at 4 or 8 week (P <0. 05). Conclusion: Carvedilol can improve cardiac function after myocardial infarction and has beneficial effect on left ventricular remodeling.

Possibilities of GPS Kinematic Measurements for Geological Survey in East Slovakia

This paper deals with transformation procedures for observed GPS data from the world geodetic system WGS84 into the national geodetic grid datum SUTCN （system of united trigonometric cadaster network） and Baa（the Baltic Sea after adjustment）.Transformation from WGS84 into SUTCN is performed most frequently by means of the 7element Helmert transformation with three identical points.Geodetic network was adjusted by two ways.

Local drug interaction of metformin with carvedilol increases drug accumulation in the liver and kidney of rats

Drug transporters determine plasma and tissue exposure of a broad variety of drugs and play a critical role in drug-drug interaction （DDI）. In the present study, we aimed to investigate the effects of carvedilol on pharmacokinetics of metformin as well as the mechanism of their interaction. Results showed that plasma concentration of metformin was not significantly altered after single or 7-day co-administration of carvedilol, and the urinary excretion of metformin was also not influenced by carvedilol. However, the concentration of metformJn in the liver and kidney was markedly elevated. Similarly, carvedilol did not affect the renal elimination of metformin, but increased renal concentration in isolated kidney perfusion. On the other hand, carvedilol treatment did not affect the expressions of rOCTs and rMATE 1 in the liver and kidney of rats. After long-term co-administration, there were no differences in lactic acid （LCA）, uric acid （URIC） and creatinine （CREA） levels between two groups. These results indicated that carvedilol increased hepatic and renal distribution of metformin, resulting in local drug interaction.