ABSTRACT
Objective To evaluate the immediate and short term therapeutic efficacy of percutaneous transluminal septal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy (HOCM) and to investigate the prevention of the related complications. Methods PTSMA was conducted in 3 patients with HOCM refractory to medication. The immediate effect was evaluated by pressure monitor, but the follow up effect by observation of the clinical symptoms and ultrasonic cardiogram. Results The left ventricular outflow tract gradients triggered by ventricular premature beats decreased from 143 mmHg (ranging from 70 to 180 mmHg) to 53 mmHg (ranging from 30 to 80 mmHg). Complete atrioventricular block (Ⅲ?AVB) with atrioventricular node rhythm was found in 1 case, and complete right branch bundle block (CRBBB) in another one. Follow up of the 3 cases at 6 months after operation revealed remarkable improvement of the patients' cardiac function (NYHA), disappearance of angina pectoris, and obvious attenuation of ventricular septal hypertrophy and SAM (systolic anterior motion of mitral) phenomenon. Conclusion PTSMA is an effective method with satisfactory short term effect for the patients with HOCM refractory to medication.
ABSTRACT
Objective To constructed the cell model transferred angiotensin Ⅱ (AngⅡ ) type 2 receptor (AT2R) in vascular smooth muscle cells(VSMC) Method The VSMCs, isolated from the aorta of rat, were cultured by routine method. Recombinant adenoviral vector, AdCMV-AT2R, containing rat AT2 receptor gene was constructed by homologous recombination, and then it was used to transfer AT2 receptor gene to VSMC in vitro. The rate of AT2R expression in VSMC was analysed by flow cytometry. The expression of mRNA, protein were detected by RT-PCR, Western blot and immunohistochemistry respectively. The angiotensin Ⅱ (AngⅡ) type 1 receptor (A T1R) was determined as well. Result The expression rate of AT2R in VSMC was increased signific antly after transferred by AdCMV-AT2R with time, and the peak value detected by flow cytometry was about 89.51% at 48 hours. RT-PCR, Western blot and immunohistochemistry showed that the expression of AT2R mRNA and protein were increased obviously in transferred VSMC. There were no significantly change of AT1R expression during AT2R expression. Conclusion Our study indicates that AdCMV-AT2R did generate high level expression of AT2 receptor and its expression did not affect AT1R exp ression in cultured VSMC. The VSMCs transferred AT2R gene may be used as a good model to study the effect of AT2R on their biological action such as proliferation, migration and apoptosis.
ABSTRACT
Objective To study the proliferation and migration of vascular smooth muscle cell (VSMC) after transferred angiotensin Ⅱ (AngⅡ) type 2 receptor (AT2R) gene. Methods The recombinant adenoviral vector, AdCMV-AT2R, containing rat AT2 receptor gene was constructed by homologous recombination, and transfered to rat VSMC in vitro. The expression of AT2R mR NA was detected by RT-PCR. The rate of expression and the change of cell cycle in VSMC were analysed by flow cytometry. These assays including cell devision index. Incorporation of bromodeoxyuridine(BrdU) and 3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenyltetrazolium bromide( MTT) were used to determine the proliferation of VSMC. The modified Boyden's chamber method was used to test the migration of VSMC. The r e-organization of F-actin in VSMC was analysed by confocal microscopy. Results RT-PCR showed that the expression of AT2R mRNA increased substantially in transferred VSMC, and the peak value of expression rate is about 89.51% at 48 hours. When the expression of AT2R is at peak value, the ratio of S, G2 and M periods was reduced from 31.7% to 13.9%(P<0.05). The OD values of MTT and BrdU incorporation were reduced by 61.4% and 51.6% respectively(P<0.0(1). the number of VSMC migration was reduced by 62.2%(P<0.05) and the expression of F-actin was also decreased signific antly. Conclusion AdCMV-AT2R induced high level expression of AT2 receptor in cultured rat VSMC and its expression can significantly inhibit the proliferation and migration of rats VSMC in vitro.