Objective To explore the correlation between expression of nuclear factor kappa B (NF-kappa B) in peripheral blood monouclear cells(PBMC) and the severity of coronary artery lesion in patients with acute coronary syndrome(ACS). Methods The 81 patients were diagnosed with coronary heart disease, and all of them underwent immediate or selective coronary angiography(CAG) The nuclear protein level of activated NF-B was detected by Western blot and semi-quantity image analysis was done. Coronary angiograms were scored according to Gensini integration. The relationship between NF-κB and Gensini score was analyzed. Results The protein expression of NF-κB in PBMC in ACS group was significantly higher than that in stable angina group and control group (0.85±0.18 vs. O.75±0.21 and 0.71±0.23, F=3.72, P<0.05). The protein expression of NF-κB was not correlated with Gensini score(r=0.07, P>0.05). Conclusions The ACS patients have the activation of NF-κB in PBMC. The protein expression of NF-κB is not correlated with Gensini score, which does not suggest an implication of the severity of coronary artery.

To observe the feasibility of ultrasonography as guide of ultrasound thrombolysis for treating lower limb arteriosclerosis obliterans.Methods: Fifteen cases of lower limb arteriosclerosis obliterans were treated with intravascular ultrasound thrombolysis.The whole processes were guided by ultrasonography.Results: Ultrasonography clearly showed the walls of the arteries,thrombus,artheromatous plaques and blood flow dynamics.It also showed on real time the structures,positions and work states of the catheter,guide wire and thromboltic probe during manipulation.It provided reliable surveillance and guide of ultrasound thrombolysis.All the obliterated arteries of the patients were successfully recanalized.Conclusion: Ultrasonography is a feasible means for surveillance and guide of intravascular ultraound theombolysis.

AIM: To investigate the changes of Gq-phosphoinositide pathway in left ventricular tissue of rats with chronic heart failure in order to assess the role of this signal pathway in the formation of heart failure. METHODS: Male Sprague-Dawle rats were divided into three groups: control, chronic heart failure and benazepril therapy group. Chronic heart failure was induced with adriamycin. Rats in benazepril group received benazepril 10 mg?kg-1?d-1 and adriamycin at the same time. Hemodynamic measurement was carried out after 4 weeks. The expression of G? q/11 protein in left ventricle was detected by Western blotting analysis and activity of phospholipase C was measured by the method of hydrolysis of nuclear substrate. RESULTS: Compared with control group, the ?dp/dtmax in chronic heart failure group significantly decreased, and protein G? q/11 expression, basic and stimulated phospholipase C activity significantly increased (P

Aim To evalute the effects of losartan on the cardiac function and secretion of nitric oxide(NO) and endothelin(ET) in patients with congestive heart failure(CHF) .Methods Sixty patients with class Ⅱ～Ⅳ CHF were randomised to receive a 12 weeks of routine therapy either with losartan(n ＝ 30)to be added from 25 mg to 50 mg daily or with enalapril(n ＝ 30) to be added from 2.5 mg to 5 mg daily. The cardiac systolic and diastolic funtion and the levels of NO and ET were observed before and after therapy respectively, with 30 normal control subjects seving as control. Results The abnormal cardiac systolic and diastolic function parameter were present in patients with CHF. The ET and NO levels in CHF patients were significantly higher than those in the control group(P＜0.05) . NYHA function class was improved in 85% of losartan-treated patients and in 84% of enalapril-treated patients after 12 weeks, as compared with cardiac function at baseline. ET and NO levels were significantly reduced(P＜0.01), NO/ ET ratio was increased (P＜0.05) after 12 weeks of therapy in two active groups. Conclusion The systolic and diastolic functions of patients with CHF are greatly improved by losartan treatment, which reverses the imbalance of NO/ET and it is suspected that this action may be another important mechanism of its treating heart failure.