AIM: To observe the changes in mitogen-activated protein kinases (MAPKs) activity and gene expression of c-fos after coronary artery balloon injury in swine. METHODS: Six of the seventeen Chinese swine were as control group, and the others underwent coronary angioplasty to LAD or CLx. The animals were sacrificed at three and thirty days following the procedure. The cross-sections were stained hematoxylin-eosin, strichrome, and Verhoef-van Giesen after the target segments were dissected free from the hearts, and the morphologic characteristics were investigated by computer-assistant analysis system. The target segments were also processed to examine the gene expression of c-fos by reverse transcription-polymerase chain reaction (RT-PCR) and to measure the activity of MAPKs by biochemistry. RESULTS: MAPKs activity and gene expression of c-fos in the dilated segments were significantly higher than that of normal segments three days after coronary balloon injury (51.5%, P

AIM: To investigate the effect of endothelin (ET), angiotensin II (AngII) and homocysteine (Hcy) on C-type natriuretic peptide (CNP) synthesis and release. METHODS: Human endothelial cell was cultured; CNP was measured by radioimmunoassay method. RESULTS: ET and AngII could augment CNP synthesis in human endothelial cells. Compared with control group, 10-9,10-8,10-7 mol/L ET and Ang II increased CNP content of endothelial cells by 1%(P＞0.05), 49%(P＜0.05),117%(P＜0.01) and 137% (P＜0.01),165%(P＜0.01),201%(P＜0.01),respectively. A great dose of ET and Ang II also stimulated CNP release from cultured human endothelial cells. Hcy had no effect on CNP synthesis, but 10-9，10-8,10-7 mol/L Hcy enhanced CNP release from cultured human endothelial cells by 17%(P＞0.05),84%(P＜0.01) and 555%(P＜0.01), respectively. CONCLUSION: ET, AngII and Hcy might be involved in the synthesis and release of human endothelial cell CNP.

The breakdown voltage plays an important role in evaluating residual life of stator insulation in generator. In this paper, we discussed BP neural network that was used to predict the breakdown voltage of stator insulation in generator of 300 MW/18 kV. At first the neural network has been trained by the samples that include the varieties of dielectric loss factor tanδ, the partial discharge parameters and breakdown voltage. Then we tried to predict the breakdown voltage of samples and stator insulations subjected to multi-stress aging by the trained neural network. We found that it's feasible and accurate to predict the voltage. This method can be applied to predict breakdown voltage of other generators which have the same insulation structure and material.

AIM and METHODS: In a model of balloon injury of rat aorta, the dynamic changes of C-type natriuretic peptide (CNP) in plasma and aortic tissues and the effect of exogenous CNP on intima/media (I/M) ratios were studied. RESULTS:CNP levels in plasma were significantly increased by 80.7% (P

AIM: To study the role and regulation of calcineurin(CaN) in angiotensin II(AngⅡ)-stimulated cardiacmyocyte hypertrophy of rats. METHODS: Using AngⅡ to induce the cultured cardiac myocyte hypertrophy of rats, and investigating the effect of CaN inhibitor on [ 3H]-leucine incorporation of AngⅡ-stimulated cardiomyocytes and the regulation of various factors on CaN activity in cardiomyocytes.RESULTS: AngⅡ can stimulate the CaN activity in cultured neonatal rat cardiomyocytes in a dose- and time-dependent manner. In cardiac myocytes incubated with 10, 100, 1000 nmol?L -1 of AngⅡ for 12h, the CaN activities increased respectively by 13%,57%( P

Objective.The present study investigated the role of endogenous carbon monoxide(CO)in the pathogenesis of neointimal formation induced by balloon injury in rat.Method.Endothelial denudation of the left common carotid artery of rat was carried out by three passages of a Fogarty 2F balloon catheter.DNA,collagen and elastin contents of each intima-media were estimated;and heme oxygenase(HO)activity and CO production in vascular smooth muscle cell(VSMC)were measured after administration of HO inhibitor.Result.Our data showed that neointima occurred in the rat on day 7 and day 21 after balloon injury,and at the same time HO activity and CO production in VSMC were markedly increased.Administration of HO inhibitor,zinc deuteroporphyrin 2,4-bisglycol(ZnDPBG),could effectively inhibit HO activity and CO production,significantly enhance neointimal formation(aortic intima/media ratio were 21.4±1.8% vs 17.6±2.0%,P＜0.05 on day 7;and 30.5±2.4% vs 23.0±2.2%,P＜0.01 on day 21,respectively,compared with balloon alone group).Conclusion.We concluded that 1)inhibition of CO production may enhance neointimal formation induced by endothelial denudation,implying endogenous CO play an protective role in response to vascular injury,and 2)induction of HO activity may be applied clinically for preventing restenosis after angioplasty.

Objective.In a model o f balloon injury of rat aortic endotheli um, the effects of C-type natriuretic pe ptide(CNP) on α1-adrenoreceptor and ino sitol 1,4,5-triphosphate (IP3) receptor were studied Methods. Aortic injuri es were produced by vascular endothelium -denudation.α1- adrenoreceptor in smoot h muscle sarcolemma and IP3 receptor in smooth muscle sarcoplasmic reticulum in the rat aorta were assayed by radioactiv e analysis method.Results. It was found that neointima was formed and the conten ts of DNA, collagen and elastin of each int ima-media were significantly increased i n 7 days and 21 days after balloon injury of rat aorta. α1-adrenoreceptor in smo oth muscle sarcolemma and IP3 receptor in sarcoplasmic reticulum were also upre gul ated. Results also showed that the admin i stration of CNP i.p significantly decrea sed the contents of DNA, collagen and el as tin of each intima-media, and inhibited the up-regulation of α1-adrenoreceptor and IP3 receptor.Conclusion. The inhibition of the up-regulation of α 1-adrenoreceptor and IP3 receptor by C NP might be one of the mechanisms of its suppressive action on intimal proliferation.

Objective　To study the role of hypertension-related gene (HRG-1) in cardiovascular disease. Methods　The expression of HRG-1 was analyzed with RT-PCR and Northern blotting. Vascular smooth muscle cell (VSMC) proliferation was measured with 3 H-TdR incorporation and was confirmed with histological analysis. Results　Northern blot analysis showed that HRG-1 mRNA was expressed not only in VSMC, but also in various rat tissues (heart, brain, lung, kidney, and liver). In addition, the expression of HRG-1 mRNA in heart, brain, kidney and liver of spontaneously hypertensive rat (SHR) was lower than that in the same tissues of Wistar-Kyotorat (WKY). Semi-quantitative RT-PCR and histological analysis showed that the expression of HRG-1 mRNA in ApoE-knockout mice and in animal models of restenosis was decreased and neointimal formation was observed in both models. ET, AII, and IL-1 stimulating VSMC proliferation reduced the expression of HRG-1 mRNA of VSMC. Atrial natriuretic factor (ANF), calcitonin gene-related peptide and adrenomedullin, inhibited VSMC proliferation and elevated the expression of HRG-1 mRNA. These effects could be blocked or attenuated by their corresponding antagonists or antibodies. Conclusion　HRG-1 is a gene related to VSMC proliferation. It may play an important role in several occlusive cardiovascular diseases including atherosclerosis, restenosis and hypertension.

Objective. The present study investigated the role of calcineurin in angiotensin II(AngII) induced cardiac myocyte hypertrophy of rats. Method. The primary cardiac myocytes were cultured under the standard conditions. The calcineurin activity in AngII treated cardiomyocytes was tested by using PNPP;protein synethsis rate was assessed by 3H leucine incorporation; atrial natriuretic factor(ANF) Mrna level was determined by Northern blot analysis. Cell viability was estimated by lactate dehydrogenase(LDH) levels in cultured medium and by dyed cell numbers. Result. After stimulation of 10,100 and 1 000nmol/L of AngII, calcineurin activities in the cardiomyocytes were increased by 13％ ,57％ (P< 0.05) and 228％ (P< 0.01) respectively, compared with control group. Cyclosporin A(CsA), a specific inhibitor of calcineurin, markedly inhibited the calcineurin activity and decreased the 3H leucine incorporation in AngII treated cardiomyocytes in a dose dependent manner. It was also found that CsA slightly reduced the Mrna level of ANF gene in AngII stimulated cardiomyocytes. Conclusion. During AngII induced cardiac myocyte hypertrophy, calcineurin signal pathway is activated, and inhibition of the pathway can attenuate AngII induced cardiac myocyte hypertrophy, which suggests that the calcineurin signal pathway may play an important role in AngII induced myocardial hypertrophy of rats.

Objective. To study the redistribution of endothelin-1 (ET-1) receptors in two subcellular organelles , the sarcolemmal membrane and the light vesicle, of rat heart during the progression of sepsis. Methods. Sepsis was induced by cecal ligation and puncture (CLP). ET1 receptor was assayed by using [125I]-ET1 binding. Marker enzyme activities, protein yield, and dry-to-wet weight ratio of cardiac membranes were measured. Results. Septic rat heart exhibited two distinct phases: an initial hyperdynamic phase( 9h after CLP; early stage of sepsis) followed by a hypodynamic (18h after CLP, late stage of sepsis) phase. [125I]-ET1 binding study showed that during early stage of sepsis, the Bmax of ET1 receptors was increased by 30％ in sarcolemma but decreased by 19％ in light vesicles, while during late stage of sepsis, the Bmax was decreased by 24％ in sarcolemma but increased by 38％ in light vesicles.The total binding of sarcolemma and light vesicles was increased by 25％ during early stage of sepsis but decreased by 17％ during late stage of sepsis. Conclusions. These data indicated that ET1 receptors in the rat heart were externalized from light vesicles to sarcolemmal membranes during early hyperdynamic phase while internalized from surface membranes to intracellular compartment during late hypodynamic phase of sepsis.