卡托普利对自发性高血压大鼠血管平滑肌细胞增殖及癌基因和抑癌基因的影响

目的：观察卡托普利（CaP）对自发性高血压大鼠（SHR）血管平滑肌细胞（VSMC）增殖的作用及对原癌基因及抑癌基因的影响。方法：氚-胸腺嘧啶核苷（3H－TdR）参入，电镜，原位来交及Northernblot杂交。结果：CaP在降低SHR血压同时，能减少VSMC的线粒体，粗面内质网及3H－TdR参入量（P<0.01），并能逆转c－fos，c－myc，c－sis原癌基因mRNA表达增强（P<0.05或0.01），p53抑癌基因mRNA表达减弱（P＜0．01）。结论：Cap能抑制SHR的VSMC增殖，与癌基因调控的分子生物学机制有关。     

THE INFLUENCE OF CAPTOPRIL AND NALOXONE ON THE VALSALVA MANOEUVRE AND SYSTOLIC TIME INTERVALS IN HEALTHY VOLUNTEERS

1. The aim of the study was to ascertain whether the inhibition of the sympathetic nervous system by angiotensin-converting enzyme (ACE) inhibitors is mediated by endogenous opioids. Naloxone was used to evaluate the effects of the latter on systolic time intervals (STI) and Valsalva manoeuvre-induced blood pressure and heart rate changes. 2. Baseline recordings were done in 12 healthy male volunteers and repeated 2h after oral administration of 75 mg of captopril and again after naloxone 0.4 mg/kg was administered intravenously over 10 min. 3. After captopril there was a significant reduction in systolic (P<0.02) and mean blood pressure (P<0.04) without any changes in heart rate. Furthermore, captopril increased the Valsalva ratio (P<0.06) but did not influence inotropism as indicated by STI. Naloxone did not influence any of these findings. 4. The changes in the Valsalva ratio after captopril were mediated by an increase in the maximum bradycardia in nine of the 12 subjects. 5. The results indicate that endogenous opioids do not play a role in the putative sympatholytic effect of ACE inhibition.     

小剂量肝素联用巯甲丙脯酸治疗慢性肺心病急性发作期66例疗效分析

目的探讨综合疗法并用小剂量肝素、巯甲丙脯酸治疗慢性肺心病急性发作期的疗效.方法慢性肺心病急性发作期患者随机分为治疗组(66例)、对照组(62例),两组均进行综合治疗,但治疗组加用了小剂量肝素和巯甲丙脯酸,然后观察并比较其症状、体征、血气指标和血液黏稠度.结果治疗组的血液流变学变化、症状与体征的改善及总好转率明显优于对照组P＜0.01.结论慢性肺心病急性发作期病人在综合治疗的基础上加用小剂量肝素和巯甲丙脯酸可显著提高疗效.     

Effect of Captopril on Antithrombus Function of Endothelium

ＥｆｆｅｃｔｏｆＣａｐｔｏｐｒｉｌｏｎＡｎｔｉｔｈｒｏｍｂｕｓＦｕｎｃｔｉｏｎｏｆＥｎｄｏｔｈｅｌｉｕｍＸＩＯＮＧＹｉ－ｌｉ（熊一力）；ＺＨＡＯＨｕａ－ｙｕｅ（赵华月）（ＤｅｐａｒｔｍｅｎｔｏｆＭｅｄｉｃｉｎｅ，ＴｏｎｇｊｉＨｏｓｐｉｔａｌ，Ｔｏｎｇ...     

Captopril and time dependent changes in post- to pre-glomerular resistance ratios in remnant kidneys of pre-hypertensive rats

Wilke , W. Lee & Person , A. E. G. 1992. Captopril and time dependent changes in post- to pre-glomerular resistance ratios in remnant kidneys of pre-hypertensive rats. Acta Physiol Scand 144 , 253–261. Received 26 June 1991, accepted 8 October 1991. ISSN 0001–6772. Department of Physiology, Colorado State University, Fort Collins, Colorado, USA and Department of Physiology and Biophysics, University of Lund, Sweden. Micropuncture experiments were performed on intact and remnant kidneys of male Sprague-Dawley rats before and after angiotensin converting enzyme inhibition with captopril (0.5 mg kg^-1 iv). Partially nephrectomized rats were studied at 2 and 8 weeks post-surgery before the development of systemic hypertension. At 2 weeks, nephrectomized rats had a numerically higher tubular stop-flow pressure than controls (43 ± 2 mmHg vs. 38 ± 2 mmHg; P = 0.08) and a higher post- to pre-glomerular resistance ratio (Re/Ra) (0.40 ± 0.03 vs. 0.31± 0.03; P = 0.08). At 8 weeks, stop-flow pressure and post- to pre-glomerular resistance ratios were similar in remnant and intact kidneys. Captopril had no effect on stop-flow pressure in 2 week post-surgery nephrectomized rats or either control group, but it increased stop-flow pressure in 8 week post-surgery nephrectomized rats (40 ± 2 to 44 ± 2 mmHg, P= 0.04). This increase in stop-flow pressure was associated with an increase in the post- to pre-glomerular resistance ratio (0.33 ± 0.02–0.42 ±0.02, P = 0.009). Stop-flow pressure was positively correlated with the post- to pre-glomerular resistance ratio in 2-week post-surgery nephrectomized rats and their respective controls when combined (r = 0.89, P= 0.0001) and 8-week post-surgery nephrectomized rats and their respective controls combined (r= 0.78, P = 0.0001). Stop-flow pressure was not significantly correlated with mean arterial pressures or welling-point pressures in these groups. We conclude that stop-flow pressure in remnant kidneys of pre-hypertensive rats is primarily determined by the post- to pre-glomerular resistance ratio, and increases in stop-flow pressure and post- to pre-glomerular resistance ratios in remnant kidneys are transient in the absence of systemic hypertension. The role of the renin-angiotensin system in determining the ratio and stop-flow pressure is dependent on time post-nephrectomy. Captopril-induced increases in stop-flow pressure and post- to pre-glomerular resistance ratio at 8 weeks, suggests that its primary effect at that time is not a preferential post-gIomerular vasodilation subsequent to reductions in intrarenal angiotensin II.     

复方卡托普利片中氢氯噻嗪的含量及均匀度测定

用紫外分光度法直接溯定复方卡托普利片中氢氯噻嗪的含量及均匀度。测定波长为272±1nm,平均回收率100.2%,变异系数0.3%,吸收度与氢氯噻嗪的浓度在1～10μg/ml 范围内具有线性关系。     

开博通治疗急性心肌梗塞临床观察

目的观察早期服用开博通治疗急性心肌梗塞的近期效果。资料与方法２０１例急性心肌梗塞症状后２４小时内入院且无明显低血压患者，自入院开始后在接受常规治疗基础上，１２８例加服开博通（治疗组），６０例加服安慰剂（对照组），均治疗４周。结果治疗组中前壁梗塞患者的室性心律失常、心力衰竭、梗塞延展发生率、４周病死率以及１年院外猝死率均低于对照组前壁梗塞患者，而下壁梗塞患者无此差异；治疗组中下壁梗塞患者并发房室传导阻滞者高于对照组下壁梗塞患者，而前壁梗塞患者无此差异。结论开博通能降低前壁梗塞患者的住院期重要并发症及早期病死率，且能降低１年院外猝死率。     

Deleterious effect of exogenous angiotensin-I on the extent of regional ischaemia and its inhibition by captopril

The endogenous activity of the local renin-angiotensin system(RAS) and the anti-ischaemic properties of captopril were investigatedin electrically driven rabbit Langendorff hearts (constant pressure:70 cmH₂O, Tyrode solution, Ca²⁺ 1.8 mmol.l^–1). Cumulativeconcentration-response curves showed no significant difference(P>0.05) between the reduction of the global coronary flow(CF) by exogenous angiotensin-I or angiotensin-II (EC₅₀ = 10^–10mol.l^–1). It is concluded that the local RAS in isolatedrabbit hearts is highly sensitive, whereas its endogenous activityis very low due to very low endogenous angiotensin-I content.Myocardial ischaemia (MI) was induced by the occlusion of aleft coronary artery branch and MI was quantified from NADHsurface fluorescence photography. MI was significantly enlarged(+35%) (P <0.05) by exogenous angiotensin-I (6x10^–9mol.l^–1). The reduction in CF and the increment in MIby angiotensin-I could be completely prevented by adding captoprilat a low concentration (10^–6 mol.l^–1) to the perfusionbuffer. In the absence of exogenous angiotensin-I, captoprilalone (10^–6 mol.l^–1) neither significantly enhancedCF (P >0.05), nor diminished MI (P >0.05), supportingthe finding of very low endogenous activity of tile local RASin this model. We, moreover, conclude that at a low concentration(10^–6 mol.l^–1) captopril does not possess directcardioprotective properties independent of its ACE inhibitingaction.     

Influence of a single dose of captopril on pulmonary haemodynamics and right ventricular function in mitral stenosis with pulmonary hypertension

Summary The response of the pulmonary circulation to captopril 75 mg has been examined in 21 patients with pulmonary hypertension secondary to mitral stenosis. The effects of captopril were measured every 15 min up to 2 h by recording pressures in the pulmonary and systemic circulations and by measuring cardiac output.Pulmonary artery systolic pressure fell significantly by 21.6% (from to 42.8 mm Hg), pulmonary artery diastolic pressure by 23.3% (from 26.2 to 20.1 mm Hg), and the pulmonary artery mean pressure by 23.2% (from 36.9 to 28.3 mm Hg). Right ventricular end-diastolic pressure also fell significantly by 7% (8.1 to 7.5 mm Hg). Heart rate decreased by 6.5% (from 76.3 to 71.3 beats·min^–1). Cardiac index and stroke volume index did not change. The total and vascular pulmonary resistance dropped significantly by 23.2% (from 721 to 553.7 dyn·s·cm^–5) and 40% (from 287.2 to 172 dyn·s·cm^–5), respectively. The right ventricular stroke work index fell by 33% (from 15.1 to 10.1 g/beat/m²). Systemic systolic pressure decreased by 10.5% (from 124.5 to 111.4 mm Hg). Thus, captopril lowered pulmonary pressures and resistances and no deterioration in right ventricular function was observed.