Effect of komplamin and nikoshpan on brain circulation and metabolism in the postischemic period

Intravenous administration of komplamin to anesthetized cats before the brain ischemia or in the early period following ischemia prevents the development of the postischemic phenomenon of the cerebral blood flow nonrecovery and beneficially influences the cerebral metabolism: restores oxygen and glucose consumption by the brain, decreases pyruvic acid level in the arterial and venous blood, attenuates the phenomenon of acidosis. Nikoshpan improves the blood supply to the brain, restores oxygen and glucose consumption by the brain in the postischemic period only if administered before the brain ischemia.     

三七总皂甙对实验性脑缺血脑血流及血脑屏障的影响作用

目的 观察三七总皂甙对脑缺血后再灌流期间血脑屏障及脑血流的影响。方法 利用大鼠局灶性脑缺血再灌流和全脑缺血再灌流损伤两种实验模型。结果 与相应对照组比较，不论是全脑缺血还是局灶性脑缺血1h后再灌注3d，应用三七总皂甙的各组动物及水肿明显减轻，血脑屏障通透性改善，大脑局部血流量显著增加。结论 三七总皂甙对脑缺血后脑水肿、血脑屏障、大脑局部血流量具有保护作用。     

脑缺血动物模型及其实验治疗学应用

脑缺血是指由于大脑特定部位的血流供应受阻所导致的血氧不足或脑缺氧,以致不能满足供能的需要,造成脑组织死亡或脑梗塞/缺血性中风。脑缺血的病理生理机制以及缺血性脑损伤后的神经修复是当今神经科学研究的热点之一。动物模型的成功复制为脑缺血的实验治疗学研究起了巨大的推动作用。本文就国内外已经建立的弥漫性脑缺血、局灶性脑缺血动物模型的方法学文献作系统综述,同时列举这些模型的优缺点及其在实验治疗学中的应用,为实验性神经保护药物的药效学筛选提供科学指导。     

Dopamine enhancement of the cerebral microcirculation in a local ischemic lesion

The effect of dopamine on the local cerebral blood flow in parietal brain cortex region of rats was studied in conditions of local ischemia induced by middle cerebral artery occlusion. Registration of the local cerebral blood flow was performed on a ALF-21 laser doppler flowmeter ("Transonic System Inc.", USA). Dopamine produces a pronounced effect on cerebral circulation in conditions of local brain ischemia thus causing a significant increase in blood flow both in ischemic and intact hemispheres. The effect is observed both in the acute stage of ischemic brain injury and in the remote period of brain ischemia.     

Effect of mexidol on combined vascular pathology of brain and heart

The effect of mexidol on cerebral blood flow under conditions of experimental myocardial infarction and combined disturbances of cerebral and coronary perfusion in comparison with intact and false-operated rats and rats after global transient ischemia of brain was studied. It is established that mexidol (200 mg/kg) more prominently enhances the blood flow in the parietal region of brain cortex of rats with combined ischemia of brain and heart as compared to intact rats and rats after experimental myocardial infarction. Under conditions of combined pathology, mexidol produces the same cerebrovascular effect as that in animals with cerebral ischemia.     

Effect of dopamine on the blood circulation and metabolism in the brain during ischemia

In acute experiments on anesthetized cats under blood autoperfusion of cerebral and peripheral vessels with a stable volume of blood during cerebral ischemia there was revealed the vascular and metabolic effects of dopamine on cerebral circulation. Administration of dopamine by perfusion in a dose of 100 micrograms/kg/min for 35 min after ischemia inhibited the development of postischemic hypoperfusion of the brain and also eliminated postischemic hypotension. A significant effect of dopamine on oxidative metabolism of the brain was observed.     

缓激肽预处理对大鼠局灶性脑缺血的影响

目的研究缓激肽预处理对大鼠局灶性脑缺血/再灌注损伤的影响。方法线栓法制备大鼠大脑中动脉缺血/再灌注模型,在缺血前由颈外动脉泵入缓激肽,对照组给予等量生理盐水,缺血2 h再灌注24 h后,观察脑梗死体积、脑含水量、血脑屏障通透性及组织病理学的变化。结果缺血前15 m in给予缓激肽组与对照组相比,梗死体积减小、水肿程度减轻、血脑屏障通透性降低、相关脑区神经元损伤程度减轻。结论预先给予缓激肽可对脑缺血损伤起保护作用,这可能是通过保护脑血管、减少梗死体积来起作用的。     

Cerebrovascular and antiserotoninergic activity of the combination of tropoxin and mexidol

The results of experiments on narcotized rats showed that tropoxin substantially reduces the constrictor reactions of cerebral blood vessels to meta-chlorophenylpiperazine, while not increasing the blood flow in the carotid system of either intact rats or animals with model ischemic damage of brain. In contrast, mexidol increases the cerebral blood flow in rats under conditions of global transient ischemia of brain. A combination of tropoxin and mexidol retains both the anti-serotoninergic activity of tropoxin and the vasodilating effect of mexidol.     

Effect of ketamine on cerebral circulation of intact and ischemic animals

The influence of ketamine on the local cerebral circulation was studied in intact rats and under the conditions of global brain ischemia. The drug increased the local blood flow in intact rats. Despite pronounced hypotension accompanying the global brain ischemia, ketamine helped maintenance of the cerebral circulation.     

他汀类药物对脑梗死病人血清中TNF-α及IL-6的影响

随着对脑梗死病人发病机制不断深入的研究,脑缺血后的炎症反应越来越引起人们的重视,而阻断脑缺血后炎症级联反应是改善脑缺血-再灌注损伤的理想策略。他汀类药物临床试验表明,它具有抗氧化、抗炎症、抗兴奋毒性以及抑制血小板聚集和血栓形成等降脂以外的抗缺血性脑损害作用,可大大降低脑梗死的发生率。本文拟从脑梗死病人血清中2个重要的炎性因子肿瘤坏死因子(TNF-α)和白细胞介素6(IL-6)进行论述,以阐明他汀类药物对脑梗死病人炎性因子的影响。     

银杏叶提取物联合依达拉奉对气虚血瘀型脑缺血/再灌注大鼠血液学的影响

目的观察银杏叶提取物(EGb)与依达拉奉(ED)联合应用对大鼠气虚血瘀型脑缺血/再灌注损伤的保护作用。方法采用饥饿、疲劳、高脂饮食等复制大鼠气虚血瘀模型,再用线栓法阻断大脑中动脉2h,再灌注治疗72h后,观察EGb、ED及EGb+ED对气虚血瘀型脑缺血/再灌注损伤大鼠神经功能障碍、缺血侧脑组织病理学改变、血液学、血沉等的影响。结果与模型组比较,EGb、ED和EGb+ED均能改善气虚血瘀型脑缺血/再灌注损伤大鼠神经功能障碍(P<0.01),减轻神经细胞损伤,降低血液中WBC、GR、PLT、PCT、RBC、HGB和HCT,加快ESR,其中EGb+ED在降低RBC、PLT、PCT,加快ESR方面比单药应用更为明显(P<0.05)。结论银杏叶提取物联合依达拉奉能改善气虚血瘀型脑缺血/再灌注损伤大鼠气虚血瘀症状和神经功能障碍,改善脑组织病理形态,降低血液中WBC、GR、PLT、PCT、RBC、HGB和HCT,加快ESR,共同发挥减轻脑缺血/再灌注损伤的炎症反应、防止血栓形成等脑保护作用。     

盐酸埃他卡林对大鼠局灶性脑缺血后脑组织损伤和血液流变学的作用

目的研究盐酸埃他卡林(Ipt)对局灶性脑缺血后脑组织损伤保护作用及对血液流变学变化的影响。方法线栓法阻断SD大鼠大脑中动脉造成大鼠局灶性脑缺血。神经功能行为学评分参考Longa法,脑水肿形成检测采用Ellis公式,TTC染色法测定脑梗死范围。以DPH为荧光探针,采用荧光偏振法测定脑缺血6h后红细胞膜脂流动性,微粘度。结果脑缺血6h后,脑梗死范围达对侧脑半球的(24.75±6.66)%,预防性给予Ipt(1.0～4.0mg·kg-1,ip)可使脑梗死范围分别减少0.95%,6.6%(P<0.05),14.34%(P<0.01)。Ipt2.0和4.0mg·kg-1还可降低大鼠的神经功能行为评分及脑组织含水量。尼莫地平(Nim)0.3mg·kg-1也可减少脑梗死范围,降低脑组织含水量,降低神经功能行为评分。脑缺血6h后,红细胞变形能力下降,红细胞膜脂流动性降低,红细胞聚集程度及膜微粘度皆明显提高。预防性给予Ipt(2.0～4.0mg·kg-1,ip)及Nim0.3mg·kg-1可显著改善上述血液流变学指标。Ipt4.0mg·kg-1治疗作用的时间窗为3h,超过4h则治疗作用不显著。Nim0.3mg·kg-1治疗作用不明显。结论盐酸埃他卡林对局灶性脑缺血引起的脑损伤有一定的保护作用。     

The effect of captopril on cerebral blood flow in hypertensive rats before and after cerebral ischemia

Acute experiments were conducted on narcotized hypertensive rats (vasorenal hypertension) to study the effect of captopril (5 mg/kg, intraperitoneal injection) on arterial pressure and cerebral blood flow and its autoregulation before and after transitory (10-12 min) ischemia of the brain (bilateral occlusion of the carotid arteries). Captopril normalized the arterial pressure, but changes in the cerebral blood flow proved to be insufficiently stable, particularly in the postischemic period. Normalization of autoregulation of the cerebral blood flow was noted. In captopril treatment the survival rate among rats with ischemia of the brain increased.     

首乌神颗粒改善学习记忆的部分机制研究

本研究了SWS对小鼠的凝血时间的影响，结果发现SWS能明显延长正常小鼠尾出血时间；缺血再灌注模型组小鼠的尾出血时间明显比正常组小鼠短，而SWS大剂量组可明显延长缺血再灌注小鼠尾出血时间；SWS可明显降低大鼠血小板的聚集性及凝聚性。提示SWS可改善微循环，进而保护脑神经细胞。本进一步对SWS改善学习记忆障碍的部分机制展开了研究，结果SWS可使大鼠脑组织中乙酰胆碱和γ—氨基丁酸含量明显增高，并均能显对抗大鼠脑缺血再灌引起的脑组织钙含量的升高，井呈剂量依赖性。提示SWS能明显对脑细胞起保护作用。     

Angiogenesis and stroke

Stroke results from focal cerebral ischemia due to occlusion of a cerebral blood vessel, usually an artery. Where ischemia is chronic or intermittent, collateral circulation may develop by enlargement of preexisting anastomotic channels or sprouting of new capillaries from existing vessels (angiogenesis). Angiogenesis has three attributes of particular interest in relation to cerebral vascular disease: 1) it is the principal mechanism by which the brain is vascularized; 2) unlike vasculogenesis, it continues in adulthood; and 3) as in other tissues, it can be induced in the CNS by hypoxia or ischemia. Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis. The angiopoietins, Ang-1 and Ang-2, and their common receptor, Tie-2 or Tek, constitute another signaling system that regulates angiogenesis, and which interacts with VEGF. Four recent studies provide evidence for the induction of angiogenesis, VEGF and VEGF receptor expression in experimental models of cerebral ischemia. Further understanding of the role of VEGF, VEGF receptors and angiogenesis in the brain's response to ischemia may have implications for prognosis and treatment in stroke.     

Experimental and clinical research on the effect of senzit on the cerebral blood flow and hemostatic function in cerebral ischemia

Senzit increased volume velocity of the cerebral blood flow and oxygen delivery to the brain tissues under normal conditions at the expense of a decrease of the cerebral vessels tone. In transient cerebral ischemia the drug prevents disorders of cerebral circulation and a lowering of oxygen tension in the brain tissue. A prophylactic administration of senzit in carotid arterial occlusion prevents the development of edema and death of animals. Oral senzit produced an increase of blood supply to the brain and hypocoagulation changes in hemostasis system in patients with chronic insufficiency of cerebral circulation.     

Neuroprotective Effects of Kangen-karyu on Spatial Memory Impairment in an 8-Arm Radial Maze and Neuronal Death in the Hippocampal CA1 Region Induced by Repeated Cerebral Ischemia in Rats

In the present study, we investigated the neuroprotective effects of Kangen-karyu (KGK) in a repeated cerebral ischemia model (2 × 10 min, 1-h interval). A 21-day pre- and postischemic treatment with KGK (10 – 300 mg/kg) and aspirin (5 mg/kg) improved the spatial memory impairment and neuronal death in the hippocampal CA1 region induced by repeated cerebral ischemia. However, a 7-day post-ischemic treatment with KGK did not attenuate the spatial memory impairment and neuronal death in this model. To determine the mechanism of action of KGK, we investigated the effects of a 14-day pre-ischemic treatment with KGK on cerebral blood flow in the hippocampal area of the repeated cerebral ischemia model using laser Doppler flowmetry. The 14-day pre-ischemic treatment with KGK increased the cerebral blood flow during reperfusion. These results suggest that a 21-day pre- and post-ischemic treatment with KGK can protect against brain damage caused by cerebral ischemia by increasing the cerebral blood flow in the hippocampal area.     

Progress in preventive effects of cordyceps sinensis on ischemic brain

Cerebral ischemia is due to cerebral blood supply disorders caused by ischemia and hypoxia resulting in localized ischemic brain necrosis or brain softening of the disease,leading to irreversible brain damage and subsequent loss of neuronal function is a serious threat to human health One of several diseases.For patients with cerebral ischemia,often the lack of effective and extensive treatment.In addition,cerebral ischemia with morbidity,morbidity and mortality are characterized by high,so by the medical profession at home and abroad attention.As a traditional Chinese medicine,cordyceps sinensis(CS)is a complex of ergot fungus,which is parasitized on the larvae of the bat-moth family.The compound is composed of cordycepin,cordyceps polysaccharide,cordyceps sinensis peptides,ergosterol,mannitol,fatty acids and trace elements such as a variety of ingredients,with a wide range of pharmacological effects.Over the years,domestic and foreign scholars on the pharmacological effects of cordyceps sinensis were more comprehensive study of its prevention and treatment of cerebral ischemia is also deepening,found that cordyceps sinensis on cerebral ischemia with anti-inflammatory,reduce oxidative damage and neuronal ischemia damage,reduce neuronal apoptosis,improve memory cognition,reduce thrombosis,inhibit NO production,enhance mitochondrial energy supply,scavenging free radicals and other prevention and treatment.But no relevant review.In this paper,the domestic and foreign literatures on the prevention and treatment of cerebral ischemia by cordyceps sinensis were summarized,analyzed and summarized in order to provide useful information for the research and further development of cordyceps sinensis.     

缺血性脑血管病与血脑屏障的关系及其临床用药研究进展

存在于脑组织和血液之间的一个复杂的组织结构即血脑屏障,通过对血脑两侧物质转运的控制,以达到维持中枢神经的组织内环境相对稳定为目的。缺血性脑血管病发病过程即脑缺血再灌注过程,容易破坏血脑屏障,出现脑出血与脑水肿等。脑缺血再灌注后,多种因素均能引起血脑屏障功能和结构的改变。本文对影响血脑屏障改变的因素及脑缺血再灌注损伤与血脑屏障之间的关系进行阐述,并对近年来缺血性脑血管病的临床用药进行归纳总结,为探讨脑缺血再灌注损伤的有效防治提供理论依据。     

Effect of thromboxane synthetase inhibitor on cerebral circulation and metabolism during experimental cerebral ischemia in spontaneously hypertensive rats

The protective effect of thromboxane synthetase inhibitor, OKY-046, on brain ischemia was studied in spontaneously hypertensive rats. Cerebral ischemia was developed by bilateral carotid artery ligation (BCL) for 1 or 3 h and thereafter, circulation was restored for 15 min. OKY-046, 5 or 30 mg/kg, or saline as control was administered i.v. before BCL. Neither blood pressure nor blood gases were altered by OKY-046 or saline injection. During BCL, cerebral cortical blood flow was reduced to 25 and 15% of the resting value at 30 and 60 min, respectively, and these changes were not different among the groups. In rats with ischemia longer than 1 h, the blood flow was well preserved by OKY-046, 30 mg/kg, to 10-17% of the resting level, thus significantly higher than that (less than 5%) in non-treated rats. After 15 min recirculation, the supratentorial lactate level was lower and adenosine triphosphate (ATP) was higher in OKY-046-treated rats than in the saline-treated ischemic rats. Plasma thromboxane B2 was increased markedly in 1 h ischemic-reperfused rats without treatment and the increase was almost completely inhibited by OKY-046. In contrast, 6-keto-prostaglandin F1 alpha was increased 8.5-fold after ischemia and the increase was not affected by the treatment. OKY-046 seems to have an antiischemic effect on acutely induced cerebral ischemia. Selective inhibition of thromboxane A2 production and an inversely high level of prostaglandin I2 may be an important contribution to protection of the microcirculation during ischemia and preservation of ischemic cerebral metabolism.