Coronary blood flow reserve (CFR) was assessed by transesophageal Doppler echocardiography in normal subjects (group A. n=20),hypertensive non-left ventricular hypertrophy (non-LVH)Patients (group B,n=22). hypertensiv...Coronary blood flow reserve (CFR) was assessed by transesophageal Doppler echocardiography in normal subjects (group A. n=20),hypertensive non-left ventricular hypertrophy (non-LVH)Patients (group B,n=22). hypertensive patients with LVH(group C.n=32)and coronary heart disease patients (group D. n=33) with the volume sample placed at the bifurcation of the left main and left main and left descending coronary artery. Coronary blood flow velocity (CBFV)was evaluated at rest.2 minutes after dipyridamole (0. 56mg/kg. i. v.) . and 2 minutes after aminophylline i.v. The ratio of dipyridamole to rest maximal diastolic velocity (D/R PDV) was considered the index of coronary blood flow reserve.It was found that D/R PDV was significantly less in groups C and D compared with that in groups A and B (D PDC,1.84±0. 57. 1. 57±0. 41 versus 2.59±0.70 and 2.22+0.58,respectively),with no difference in D/R PDV between groups C and D.Twenty-four out of 32 patients in group C with D/R PDV were less than 2.0 compared to 29 out of 33 patients in group D (P>0.05).Significant negative correlation was found between D/R PDV. D/R PSV and interseptal thickness. left ventricular mass index in hypertensive patients.These data show that impaired CFR in hypertensive patients with LVH is comparable to that in patients with coronary heart disease.展开更多
Objective: To study the changes of a collagen-binding protein (Colligin) and myosin heavy chain isoform (α/β-MHC) gene and protein in left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats...Objective: To study the changes of a collagen-binding protein (Colligin) and myosin heavy chain isoform (α/β-MHC) gene and protein in left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats and the effects of three kinds of adrenergic receptor blockers: Carvedilol (CAR) , Metoprolol (MET) and Terazosin (TER) on these changes, and to elucidate the effects and new mechanism of CAR on left ventricular hypertrophy regression. Methods: A model of hypertrophy induced by coarctation of abdominal aorta(CAA)was used in this study. Thirty two male wistar rats were divided randomly into four groups 4 weeks after CAA operation: CAA, CAR, MET and TER. Hemodynamics, ventricular remodeling parameters, expressions of Colligin and α/β-MHC mRNA, protein expressions of Collagen Ⅰ / Ⅲ and Colligin were investigated in the four groups and sham operation group. Results: Left ventricle hypertrophy was observed clearly 16 weeks after operation. The ratio of α/β-MHC mRNA decreased, while expressions of Collagen Ⅰ /Ⅲ proteins and Colligin mRNA/protein increased( P < 0.05). CAR could ameliorate left ventricle hypertrophy prior to MET and TER. CAR could also change the expressions of α/β-MHC, Collagen Ⅰ /Ⅲ and Colligin in both gene and protein levels ( P < 0.05), while MET and TER have no effect on them ( P > 0.05). Conclusion: The effects of CAR on extracellular matrix proteins and MHC isoform shift regression of left ventricle may be due to antiproliferative or antioxidative mechanism, which was independent of beta-adrenergic receptor antagonist.展开更多
文摘Coronary blood flow reserve (CFR) was assessed by transesophageal Doppler echocardiography in normal subjects (group A. n=20),hypertensive non-left ventricular hypertrophy (non-LVH)Patients (group B,n=22). hypertensive patients with LVH(group C.n=32)and coronary heart disease patients (group D. n=33) with the volume sample placed at the bifurcation of the left main and left main and left descending coronary artery. Coronary blood flow velocity (CBFV)was evaluated at rest.2 minutes after dipyridamole (0. 56mg/kg. i. v.) . and 2 minutes after aminophylline i.v. The ratio of dipyridamole to rest maximal diastolic velocity (D/R PDV) was considered the index of coronary blood flow reserve.It was found that D/R PDV was significantly less in groups C and D compared with that in groups A and B (D PDC,1.84±0. 57. 1. 57±0. 41 versus 2.59±0.70 and 2.22+0.58,respectively),with no difference in D/R PDV between groups C and D.Twenty-four out of 32 patients in group C with D/R PDV were less than 2.0 compared to 29 out of 33 patients in group D (P>0.05).Significant negative correlation was found between D/R PDV. D/R PSV and interseptal thickness. left ventricular mass index in hypertensive patients.These data show that impaired CFR in hypertensive patients with LVH is comparable to that in patients with coronary heart disease.
文摘Objective: To study the changes of a collagen-binding protein (Colligin) and myosin heavy chain isoform (α/β-MHC) gene and protein in left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats and the effects of three kinds of adrenergic receptor blockers: Carvedilol (CAR) , Metoprolol (MET) and Terazosin (TER) on these changes, and to elucidate the effects and new mechanism of CAR on left ventricular hypertrophy regression. Methods: A model of hypertrophy induced by coarctation of abdominal aorta(CAA)was used in this study. Thirty two male wistar rats were divided randomly into four groups 4 weeks after CAA operation: CAA, CAR, MET and TER. Hemodynamics, ventricular remodeling parameters, expressions of Colligin and α/β-MHC mRNA, protein expressions of Collagen Ⅰ / Ⅲ and Colligin were investigated in the four groups and sham operation group. Results: Left ventricle hypertrophy was observed clearly 16 weeks after operation. The ratio of α/β-MHC mRNA decreased, while expressions of Collagen Ⅰ /Ⅲ proteins and Colligin mRNA/protein increased( P < 0.05). CAR could ameliorate left ventricle hypertrophy prior to MET and TER. CAR could also change the expressions of α/β-MHC, Collagen Ⅰ /Ⅲ and Colligin in both gene and protein levels ( P < 0.05), while MET and TER have no effect on them ( P > 0.05). Conclusion: The effects of CAR on extracellular matrix proteins and MHC isoform shift regression of left ventricle may be due to antiproliferative or antioxidative mechanism, which was independent of beta-adrenergic receptor antagonist.
