抗心肌缺血药物的进展研究

心肌缺血指的是心脏的血液灌注降低,造成心脏的供氧量骤减,心肌能量代谢无法正常运行,无法供给心脏正常运作的一种病理状态。目前,治疗心肌缺血的药物有很多种,现对抗心肌缺血药物的进展进行综述。     

抗慢性心力衰竭药物研究进展

目的 :阐明慢性心力衰竭药物治疗进展。方法 :对洋地黄类、血管扩张剂、钙拮抗剂、血管紧张素转换酶抑制剂、β 受体阻断剂等进行论述。 结果 :给慢性心力衰竭的药物治疗提出新的方向。结论 :影响肾素 血管紧张素系统的药物有一定前景     

抗高血压药物临床应用进展

原发性高血压是冠心病、脑卒中、心、肾功能衰竭的最主要发病因素。临床上控制高血压愈来愈受到重视。15受体阻断剂1．1比索洛尔（bisoprolol）由德国默克药厂生产。该药为第二代p受体阻断剂,具有高度h受体选择性及较长半衰期,选择性高于阿替洛尔、美托洛尔等心脏选择性p受体阻断剂。因无内源性拟交感活性,在作为p受体阻断剂使用的治疗剂量范围内无膜稳定性作用／可用于治疗原发性高血压、冠心病、心绞痛、心力衰竭及心律失常等。该药既具有亲水性,又具有亲脂性,口服吸收良好。由于不具备血管扩张性,不能直接扩张血管平滑肌。常见不良…     

抗心肌缺血药2,6-二甲基-4-双取代苯基-1,4-二氢吡啶-3,5-二羧酸酯的合成

本文报道了9个新的2,6-二甲基-4-双取代苯基-1,4-二氢吡淀-3,5-二羧酸酯的合成。初步药理试验表明:化合物I_6具有较强的抑制KCl诱发兔主动脉条的收缩作用,增加冠脉血流量和心输出量,降低心肌耗氧量;增强小鼠抗缺氧能力;对大鼠心肌缺血有保护作用;能缩小兔缺血心肌再灌流引起的心肌梗塞范围。     

抗心绞痛药物构效关系的研究进展

抗心绞痛药物的发展始于19世纪50年代的亚硝酸异戊酯，该系列化合物治疗心绞痛已有100多年的历史。随着钙拮抗剂和β受体阻滞剂的发展，心绞痛的治疗有了更多的选择，硝苯地平和普萘洛尔分别是此两类药物的典型代表。近年来，雷诺嗪等新型药物的研发使抗心绞痛治疗药物更加丰富。本文综述了近年来各类抗心绞痛药物的构效关系研究进展。     

抗高血压药物对男性高血压患者性功能障碍的影响

男性性功能可能由于抗高血压药物治疗而恶化。较新型的抗高血压药(钙拮抗剂、ACEI、AT1受体拮抗剂)比起利尿剂和β受体阻断剂有较好的依从性和持续性,联合使用至少两种抗高血压药物可达到期望的血压值。     

抗心肌缺血药2,6-二甲基-4-双取代苯基-1,4-二氢吡啶-3,5-二羧酸酯的合成

本文报道了9个新的2,6-二甲基-4-双取代苯基-1,4-二氢吡淀-3,5-二羧酸酯的合成。初步药理试验表明:化合物I₆具有较强的抑制KCl诱发兔主动脉条的收缩作用,增加冠脉血流量和心输出量,降低心肌耗氧量;增强小鼠抗缺氧能力;对大鼠心肌缺血有保护作用;能缩小兔缺血心肌再灌流引起的心肌梗塞范围。     

VALUE研究为高血压药物治疗增添新价值

VALUE研究是迄今为止最大规模的考察血管紧张素受体阻断剂(ARB)对高血压长期预后影响的临床研究.其结果表明:以缬沙坦或氨氯地平为基础的药物治疗均能使大多数高血压患者获得有效的血压控制,并且同样有效地减少高血压患者心血管转归事件.严格控制血压,及早将收缩压降低至160mmHg以下,对高危高血压患者的临床转归至关重要.联合使用钙拮抗剂、ARB和利尿剂可能获益更大.     

论治疗溃疡性结肠炎中成药的剂型衍化

慢性非特异性溃疡性结肠炎(ulcerative colitis,UC)是以腹泻或腹泻与便秘交替出现、粘液或脓血便、左下腹或脐周或小腹痛、消瘦、全身疲乏无力等为主要症状,以结肠粘膜慢性炎症和溃疡形成为病理特点的一种消化道疾患.近年来,UC发病率呈逐年上升趋势.由于该病治愈难度大,愈后又常反复,并与结肠癌的发病存在一定关系, 因此被世界卫生组织列为现代难治病之一. 众所周知,中医中药早已形成了较为完整的理论体系,对UC的治疗也不乏精辟独到之处. 笔者从临床应用的中药剂型衍化方面论述如下.     

Bcl-2在缺血性神经细胞损伤中的作用及药物的影响

Bcl-2基因是线虫c-elegans的抗凋亡基因Ced-9的人类同源基因,可参与调控细胞凋亡过程,包括抑制脑缺血半影区的神经细胞凋亡。该文就Bcl-2抗缺血性神经细胞损伤的作用和可能机制,以及抗脑缺血药物对Bcl-2的影响作一综述。     

抗癫痫药物鼻腔给药治疗癫痫发作研究进展

以全身疾病为治疗目的的鼻腔给药具有相对生物利用度高、吸收迅速、起效快、使用方便等特点,而且药物可以绕过血脑屏障、具有一定的脑靶向性,非常适合于癫痫发作的急救、自救治疗。笔者就抗癫痫药物鼻腔给药治疗癫痫发作的研究进展,从药物动力学、药效学、临床应用等方面进行综述。     

乙酰基蝙蝠葛苏林碱抗缺血性脑损伤作用

用细胞培养方法和大鼠脑缺血损伤模型,研究乙酰基蝙蝠葛苏林碱(O,O-acetyldaurisoline,Adau)对缺血性脑损伤的保护作用。结果表明,Adau对低钾、高钾、Bay K 8644及去甲肾上腺素所引起PC12细胞内游离钙浓度增加有抑制作用,其IC₅₀分别为4.63±0.72,0.15±0.02,93.7±17.6和10.0±1.4μmol·L^-1。Adau在整体大鼠双动脉结扎(2.5,5,10mg·kg^-1,iv)和四动脉结扎(5,10mg·kg^-1,iv)模型上,均能降低缺血脑组织脂质过氧化物含量,增加超氧物歧化酶(SOD)活性。提示Adau对脑缺血损伤有明显的保护作用。     

Pentosephosphate cycle metabolites as energy-supplying anti-ischemic agents]

A brief review of the experimental data on the energy-yielding effects of pentose-phosphate cycle metabolites is presented. The cardiotropic effects of NADP, fructose-1,6-diphosphate, fructose-6-phosphate, D-ribose and ribose-5-phosphate were analysed with relation to their influence on viability of the ischemic myocardium.     

Mechanism of the anti-ischemic protection of the kidneys by diuretics

Experiments on rats showed that single doses of diuretics furosemide, ethacrynic acid, mannitol, hypertonic solution of sodium chloride administered subcutaneously 30 and 60 min and intravenously 10 and 20 min before complete arrest of the blood flow in the single kidney for 2.5 hours decrease creatinine content in the blood and increase survival rate of the animals. The anti-ischemic protection occurs provided that the natriuretic effect of the drugs coincides with the ischemic factor action. Morphometry revealed the ability of furosemide to prevent the development of hyperhydration of the epithelial cells, to increase lumina of the proximal and distal tubules. The role of hydrodynamic factors in the mechanism of anti-ischemic protection of the kidneys with diuretics is discussed.     

The anti-ischemic effects of 3-hydroxypyridine derivatives in cerebrovascular pathology

The effect of the antioxidant mexidol and two new derivatives of 3-oxypyridine, namely LBK-10 and LBK-39 on the circulation of blood and metabolism of the brain in the postischemic period was studied in acute experiments on narcotized cats under conditions of autohemoperfusion of the cerebral vessels with a stable volume of blood. Therapeutic injection of mexidol and LBK in a dose of 20 mg/kg inhibited the development of the no-flow phenomenon and restored the ischemia damaged metabolism in the brain tissues. LBK-10 reduced the lactate content in the blood flowing from the brain and contributed to constriction of the cerebral vessels.     

Brain uptake of an anti-ischemic agent by nasal administration of microparticles

N(6)-cyclopentyladenosine (CPA) has neuronal anti-ischemic properties, but it is not absorbed into the brain from the bloodstream, where it shows poor stability and induces side effects. Microparticulate drug delivery systems designed for CPA nasal administration and constituted by mannitol or chitosan, were prepared by spray-drying and characterized. Mannitol-lecithin microparticles showed high CPA dissolution rate, whereas chitosan microparticles controlled its release rate. In vitro mucoadhesion studies indicated that CPA-loaded chitosan microparticles had higher mucoadhesive properties compared to mannitol particles. Ex vivo studies on sheep nasal mucosa showed that mannitol microparticles promoted CPA permeation across the mucosa, whereas chitosan microparticles controlled CPA permeation rate in comparison with CPA raw material. In vivo studies were carried out on rats. No CPA was detected in rat cerebrospinal fluid (CSF) and brain sections after intravenous administration. In contrast, after nasal administration of loaded microparticles CPA was found in the CSF at concentrations ranging from high nM to microM values and up to two order of magnitude higher than those obtained at systemic level. CPA was also found in the olfactory bulb at concentrations around 0.1 ng/mg of tissue. These results can open new perspectives for the employment of CPA against brain damages following stroke.