EC-SOD overexpression to the lung ameliorated MCT-induced PH in rats. We suggest that EC-SOD may act as an antioxidant in PH and that increased oxidative stress may be important in the pathogenesis of MCT-induced PH.

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AimsThe aim of this study was to determine differences in the acute and chronic impact of adaptive servo-ventilation (ASV) on left chamber geometry and function in patients with chronic heart failure (CHF). Methods and resultsAn acute ASV study was performed to measure echocardiographic parameters before and 30 min after the initiation of ASV therapy in 30 CHF patients (mean age: 69 years, 23 male). The chronic effects of ASV therapy were also evaluated in 26 of these 30 patients over a mean follow-up period of 24 weeks. Patients were divided into two groups according to the status of ASV therapy [ASV group (n ¼ 15) and withdrawal group (n ¼ 11)]. In the acute study, heart rate and blood pressure were significantly decreased 30 min after the ASV therapy compared with baseline. Stroke volume and cardiac output were significantly increased in conjunction with a reduction in systemic vascular resistance. Multivariate regression analysis revealed baseline E/e ′ to be an independent predictor for absolute increase in cardiac output. In the chronic study, a significant reduction of left ventricular (LV)/left atrial (LA) volumes and the severity of mitral regurgitation (MR), and improved LV diastolic function parameters were noted in the ASV group. These beneficial effects were not observed in the withdrawal group. ConclusionThe acute beneficial impact of ASV is mainly associated with the reduction of afterload resulting in an increase in stroke volume and cardiac output. In contrast, chronic ASV therapy produces LV and LA reverse remodelling resulting in an improvement in LV function and the severity of MR in patients with CHF.--

Angiotensin II (ANG II) induces vascular smooth muscle contraction and functions as a growth factor stimulating vascular smooth muscle cell (VSMC) hypertrophy. We wondered whether ANG II might induce expression of alpha 1-adrenergic receptors (ARs) in cultured VSMCs, which would then potentially accentuate the effects of catecholamines in the cells. Rat VSMCs were preincubated with phenoxybenzamine to inactivate alpha 1-ARs; the cells were then treated with ANG II for 24 h. ANG II-treated cells expressed an increased number of alpha 1-ARs compared with controls, suggesting that ANG II increased the rate of alpha 1-AR synthesis. ANG II markedly induced accumulation of alpha 1A/D- and alpha 1B-AR mRNAs in a concentration- and time-dependent manner. This effect of ANG II was blocked by the specific ANG II-receptor agonist [Sar1-Ile8]ANG II. ANG II-induced accumulation of alpha 1A/D-AR mRNAs was completely abolished by transcriptional inhibitor actinomycin D. ANG II markedly increased the transcriptional rate of the alpha 1A/D-AR gene without changing stability of alpha 1A/D-AR mRNAs. Protein kinase C (PKC) activator 4 beta-phorbol 12-myristate 13-acetate also induced accumulation of alpha 1A/D-AR mRNAs, and PKC inhibitor H-7 completely blocked ANG II-induced accumulation of the alpha 1A/D-AR mRNAs. Neither the biologically inactive ANG II analogue des-Phe8-ANG II nor the calcium ionophores A-23187 and BAY K-8466 induced alpha 1A/D-AR mRNAs. Finally, ANG II preincubation increased alpha 1-AR agonist phenylephrine-stimulated expression of the c-fos gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Aim: High-sensitivity C-reactive protein (hsCRP) is a predictor of cardiovascular events. Although oxidative stress may also be related to cardiovascular disease, there are few studies comparing the two. We therefore examined the association of hsCRP, serum lipids, and derivatives of reactive oxygen metabolites (D-ROMs) in coronary artery disease. Methods: We measured the levels of serum lipids, hsCRP, plasma brain natriuretic peptides (BNP) and D-ROMs in 131 consecutive patients undergoing cardiac catheterization. We divided these subjects into three groups according to their levels of hsCRP.