Contribution of circulating platelet and leukocyte activation to primary pulmonary hypertension in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To evaluate the contribution of platelet and leukocyte activation in pathogenesis primary pulmonary hypertension (PPH).</p><p><b>METHODS</b>Pulmonary hypertension was induced by subcutaneous injection of 2% monocrotaline (MCT) in male Prague-Dawley (SD) rats. Blood samples were collected at the third week after MCT injection, and flow cytometry was used to determine the fibrinogen-binding platelet, CD11b expression on leukocyte and platelet-leukocyte aggregation.</p><p><b>RESULT</b>Three weeks after MCT injection, rats exhibited higher right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure(mPAP), as compared with controls. MCT induced vascular remodeling characterized by vascular medial wall thickening in pulmonary muscular arteries. The ratio of platelets fibrinogen binding was increased in rats 3 weeks after MCT injection than that of control group[(4.08 +/-1.59)% compared with (1.45 +/- 0.61)%, P<0.01]. CD11b expression in monocytes and neutrophils, but not in lymphocytes was increased significantly 3 weeks after MCT injection (P <0.01). Platelet-neutrophil aggregations increased in MCT injected rats as compared with controls (P <0.01).</p><p><b>CONCLUSION</b>Rats of PPH model demonstrate enhanced circulating platelet and leukocyte activation, which may contribute to the pathogenesis of PPH.</p>

Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.</p><p><b>METHODS</b>Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.</p><p><b>RESULTS</b>The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.</p><p><b>CONCLUSIONS</b>The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.</p>

Efficacy and safety of azosemide in patients with edema and ascites / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To assess the efficacy and safety of azosemide in patients with edema and ascites.</p><p><b>METHODS</b>A multicentral, randomized, double-blind, controlled clinical trial was applied. All 223 patients (cardiac edema 92, hepatogenic edema 63, renal edema 68) were randomized to azoesmide and furosemide group, and all patients were treated for 2 weeks. Patients with cardiac or renal edema took azosemide (30 mg/d) or furosemide (20 mg/d); patients with hepatogenic edema took azosemide (60 mg/d) or furosemide (40 mg/d). The dosage were adjusted to azosemide 60 mg/d (cardiac, renal edema), 90 mg (hepatogeic edema); or furosemide 40 mg/d (cardiac, renal edema), 60 mg (hepatogeic edema), if diuretic effects were not obtained at the end of third day.</p><p><b>RESULTS</b>At the end of the study, the weight changes were (2.87+/-3.10) kg and (2.81 +/-2.84) kg; the total effective rate of edema lessen was 89.19% and 89.81%; the total effective rate of heart function improvement was 64.44% and 66.66%; the 24 h urine output increased (321.85 +/-669.52) ml and (273.80 +/-645.72) ml for azosemide and furosemide, respectively. The total effective rate of ascites lessen (tested by B-ultrasound) was 89.28% and 86.66%; abdominal girth decreased (5.20 +/-3.58) cm and (5.03 +/-3.74) cm for azosemide and furosemide, respectively. The adverse event rate was 23.01% in azosemide group and 21.01% in furosemide group; the main adverse effects were hypokalemia, hyperuricemia, hypertriglyceridemia and thirsty.</p><p><b>CONCLUSION</b>Azosemide could effectively lessen edema, improve heart function and decrease ascitesûit is well tolerated and is particularly useful for the diuretic treatment.</p>