Effect of histidine on myocardial mitochondria and platelet aggregation during thrombotic cerebral ischemia in rats

目的：研究组氨酸对脑血栓形成的影响及可能机制．方法：采用光化学诱导“脑—心卒中”模型并给组氨酸（ｉｖ５ｍｇ·ｋｇ－１）治疗．结果：脑血栓形成后４和２４ｈ全血血小板聚集的峰值为（５１±０５）Ω和（４３±０５）Ω．心肌线粒体体积（Ｖ）、体密度（Ｖｖ）、面密度（Ｎｍ）及外膜表面（Ｓｖ１）增加（８２±５５，０５９±０１６，０１１±００３和２２±００５，Ｐ＜００１），但数密度（Ｎｖ）、内膜比表面（δ２）和嵴膜比表面（δ３）减少（００７±００２，２８±０８和２４±０７，Ｐ＜００１），心肌病理学改变有别于缺血性坏死和缺血再灌所致的心脏损伤．组氨酸治疗后，全血血小板聚集降为（２９±１１）Ω（Ｐ＜００１），与内膜有关的体视学参数可逆改变．结论：组氨酸可抑制全血血小板聚集，并减轻由于脑缺血所致的心肌线粒体损伤．     

糖尿病大鼠血中内源性一氧化氮合酶抑制物增高

目的：测定糖尿病大鼠血中内源性ＮＯ合酶抑制物二甲基精氨酸（ＤＭＡ）的含量，方法：在链佐星诱发的糖尿病大鼠测定血清ＤＭＡ的含量和乙酰胆碱（ＡＣｈ）诱导血管内皮依赖性舒张，结果：与对照组相比，糖尿病大鼠ＤＭＡ血清浓度显增加（５．４±１．０ｖｓ０．７±０．３μｍｏｌ．Ｌ＾－１，Ｐ〈０．０１）；丙二醛含量也高于对照组（２．５±０．３ｖｓ２１．５±０．１μｍｏｌ．Ｌ＾－１，Ｐ〈０．０１）；糖尿病大鼠ＡＣｈ     

cGMP介导以注入L—精氨酸诱导的大鼠血管加压素释放效应

目的：探讨ｃＧＭＰ是否介导Ｌ－精氨酸（一氧化氮合酶物）引起的血管加压素（ＡＶＰ）释放增多效应。方法：用放射免疫法测定大鼠血浆中ＡＶＰ水平。结果：侧脑室分别注射Ｌ－精氨酸和８－溴－ｃＧＭＰ（一种可透过膜的ｃＧＭＰ衍生物）能刺激血浆ＡＶＰ水平增加［分别从（３．２±０．５）升至（５．８±１．４）ｎｇ·Ｌ＾－１，从（２．６±０．３）升至６６．６±０．４）ｎｇ·Ｌ＾－１，Ｐ〈０．０１］，同时注射Ｌ－精氨酸和     

低氧对下丘脑促肾上腺皮质素—释放激素和前垂体cAMP的作用

目的：探讨急、慢性低氧对下丘脑－前垂体－皮质轴的作用机制。 方法：大鼠及高原鼠兔暴露于不同海拔高度及时间，动物ｉｃｖ ＣＲＨ、Ａｒｇ和ＮＥ。 结果：低氧１小时，大鼠前垂体ｃＡＭＰ显上升ｃＡＭＰ分别由对照组的２．２３±０．１３增至５ｋｍ的７．７±０．７和８ｋｍ的１３．４±１．９ｎｍｏｌ／ｇ湿组织。ｉｃｖ２μＬ０．７５ｎｍｏｌ的ＸＲＨ使前垂体ｃＡＭＰ由对照线３．５±０．４升至２２．４±２．２ｎｍｏｌ     

聚肌胞治疗婴幼儿秋季腹泻

秋季腹泻７５例，其中３０例（男性１６例，女性１４例；年龄１２±４ｍｏ）采用纠正水、电解质及酸碱平衡用药为对照组。另４５例（男性２６例，女性１９例；年龄１２±４ｍｏ）在与对照组相同的一般疗法外加用聚肌胞１－２ｍｇ／次，ｉｍ，ｑｏｄ，共２－３次。结果：聚肌胞组明显优于对照组（退热时间为１．０±０．７６ｖｓ１．７±０．８ｄ；止泻时间为２．４±１．１ｄｖｓ４．１±１．２ｄ，Ｐ值均＜０．０１）。     

高血压大鼠学习记忆障碍及降压药物疗效

目的：观察高血压大鼠学习记忆功能的损害并评价比较降压药物的治疗效果。方法：自发性高血压大鼠（ＳＨＲ，１６ｗｋ）分３组（ｎ＝６），其中两组分别使用尼群地平、卡托普利，另一组为对照组；肾血管性高血压Ｗｉｓｔａｒ－Ｋｙｏｔｏ（ＷＫＹ）大鼠（ＲＨＲ，１６ｗｋ）共６组（ｎ＝６），其中５组分别使用卡托普利、美多洛尔、普萘洛尔、硝苯地平、哌唑嗪，另一组不用药。再设一正常对照ＷＫＹ（１６ｗｋ，ｎ＝６）组。治疗８ｗｋ后，连续５ｄ进行跳台试验，每天１０次。结果：两种未经治疗的高血压大鼠ｄ５的主动回避反应计分均有不同程度的下降（ＳＨＲ：０．９±１．１，ＲＨＲ：４．２±１．２ｖｓ，ＷＫＹ：８．７±１．８，Ｐ均＜０．０１）；用药ＳＨＲ两组与对照ＳＨＲ组相比（３．６±１６，４．３±１．８ｖｓ０．９±１．１，Ｐ＜０．０５），记分明显改善；ＲＨＲ美多洛尔７．７±１．６，ＲＨＲ普萘洛尔８．３±１．９，ＲＨＲ卡托普利８．０±２．０，ＲＨＲ硝苯地平７．２±１．７，ＲＨＲ哌唑嗪７．３±１．７，与ＲＨＲ对照（４．２±１．２）比较，Ｐ均＜０．０１；主动回避反应计分有显著提高。进一步比较不同药物治疗组，当降压程度相似时，各组主动回避反应计分无明显差别。?     

山莨菪碱抗脂质过氧化的研究

以离体红细胞为对象，研究山莨菪碱（Ａｎｉ）对外加Ｈ２Ｏ２及氧自由基发生系统（ＦｅＣｌ２／抗坏血酸）的抗氧化作用，观察在红细胞中加入Ａｎｉ前后Ｈ２Ｏ２诱导的红细胞溶血试验变化，并分别用荧光偏振法、ＴＢＡ比色法测定了在红细胞中加入Ａｎｉ前后氧自由基发生系统作用下的红细胞膜微粘度、红细胞脂质过氧化物（ＬＰＯ）。结果表明：Ａｎｉ（１．５，２．０ｍｍｏｌ·Ｌ－１）可显著抑制Ｈ２Ｏ２（１００ｍｍｏｌ·Ｌ－１）诱导的红细胞氧化溶血（溶血度分别为：０．３４９±０．０２３、０．２９４±０．０２６，对照组为：０．４４８±０．０３４，Ｐ＜０．０１）；Ａｎｉ（１．０，１．５ｍｍｏｌ·Ｌ－１）可显著抑制ＦｅＣｌ２（０．１ｍｍｏｌ·Ｌ－１）／抗坏血酸（０．５ｍｍｏｌ·Ｌ－１）引起的红细胞ＬＰＯ增加（分别为：５．４６８±０．１７４、４．８９６±０．１９２，对照组为６．１８１±０．２１２μｍｏｌ·Ｌ－１，Ｐ＜０．０１），显著降低红细胞膜微粘度（分别为：０．３６３±０．０２３、０．２９９±０．０１５，对照组为０．４８１±０．０２６Ｐａ·ｓ，Ｐ＜０．０１）。提示Ａｎｉ对氧自由基引发的膜脂质过氧化有保护作用。     

硫酸镁对离体豚鼠心肌细胞钙通道的影响

目的：研究硫酸镁（ＭｇＳＯ）对心肌细胞膜钙离子通道的影响，探讨ＭｇＳＯ４抗心律失常机制。 方法：全细胞膜片箝技术。 结果：细胞外液低镁（０．３ｍｍｏｌ·Ｌ＾－１）使心肌细胞钙电流（ＩＣａ）从１．６±０．６ｎＡ增至１．９±０．４ｎＡ（Ｐ〈０．０５），冲洗后回复至１．７±０．５ｎＡ（Ｐ〈０．０５ｖｓ镁０．３ｍｍｏｌ·Ｌ＾－１，Ｐ〉０．０５ｖｓ台氏液）。ＩＣａ随浓度增高进行性递减；ＭｇＳＯ４４ｍｍｏｌ·     

芸香甙的药代动力学研究

目的研究芸香甙在兔体内的药代动力学。方法家兔一次静注芸香甙５ｍｇ·ｋｇ－１后，利用荧光分光光度法测定不同时间的血药浓度。应用３Ｐ８７药动学软件程序对数据进行计算机处理。结果芸香甙的药时（Ｃ－Ｔ）方程为：Ｃ＝８５．９７８９ｅ－０．９０４４Ｔ＋３４．５１０５ｅ－０．０５８７Ｔ＋４．３８３８ｅ－０．００４６Ｔ。芸香甙的主要药代动力学参数如下：Ｔ１／２ａ：（０．７６０９±０．１０６６）ｍｉｎ，Ｔ１／２ｂ：（１２．５６６７±３．７１３９）ｍｉｎ，Ｔ１／２ｃ：（１６２．５６５１±５０．６０３５）ｍｉｎ，Ｋ１２：（０．５１２３±０．１３１６）ｍｉｎ－１，Ｋ２１：（０．３２９８±０．０７３７）ｍｉｎ－１，Ｋ１３：（０．０７３９±０．０１８２）ｍｉｎ－１，Ｋ３１：（０．０１００±０．００３７）ｍｉｎ－１，Ｋ１０：（０．０７７４±０．０１６０）ｍｉｎ－１，Ｖｃ：（０．０４０４±０．００４４）Ｌ·ｋｇ－１，ＡＵＣ：（１６７９．７５８３±４８０．６０４５）ｍｇ·Ｌ－１·ｍｉｎ－１，ＣＬ（ｓ）：（０．００３１±０．０００８）Ｌ·ｋｇ－１·ｍｉｎ－１。结论芸香甙在兔体内的Ｃ－Ｔ变化符合三室开放模型；芸香甙在体内的分布、消除迅速。     

4,5—二氢—6—[（苯乙酰基—哌嗪基）苯基]—5—甲基—3（2H）—哒…

４，５－二氢－６－［（苯乙酰基－哌嗪基）苯基］－５－甲基－３（２Ｈ）－达嗪酮（ＳＭⅡ４）０．１－２．５μｍｏｌ．Ｌ＾－＾１能使血小板激活因子（ＰＡＦ）及血栓素Ａ２类似物Ｕ４６６１９诱导的兔血小板聚集剂量一效应曲线左移且最大反应降低。其ｐＤ２分别为６．０±ｓ０．４及６．１±ｓ０．３．ＳＭⅡ４还能抑制ＡＤＰ，花生四烯酸（ＡＡ）及Ｕ４６６１９诱导的人血小板聚集，其ＩＣ５０分别是１．２，１．３及１．６．．     

Therapeutic effects of hydroxysafflor yellow A on focal cerebral ischemic injury in rats and its primary mechanisms

The therapeutic effects of hydroxysafflor yellow A (HSYA), extracted from Carthamus tinctorius. L, on focal cerebral ischemic injury in rats and its related mechanisms have been investigated. Focal cerebral ischemia in rats were made by inserting a monofilament suture into internal carotid artery to block the origin of the middle cerebral artery and administrated by HSYA via sublingular vein injection in doses of 1.5, 3.0, 6.0 mg kg(-1) at 30 min after the onset of ischemia, in comparison with the potency of nimodipine at a dose of 0.2 mg kg(-1). Then, 24 h later, the evaluation for neurological deficit scores of the rats were recorded and postmortem infarct areas determined by quantitative image analysis. At the end of the experiment, blood samples were taken to determine plasma 6-Keto-PGF1alpha/TXB2 by radioimmunoassays and blood rheological parameters. The effects exerted by HSYA on thrombosis formation by artery vein by-pass method and ADP-induced platelet aggregation in vivo and in vitro were investigated, respectively. The results indicated that more than 30% of the area of ischemic cerebrum was observed in the ischemic model group. HSYA dose-dependently improved the neurological deficit scores and reduced the cerebral infarct area, and HSYA bore a similarity in potency of the therapeutic effects on focal cerebral ischemia to nimodipine. The inhibition rates of thrombosis formation by HSYA at the designated doses were 20.3%, 43.6% and 54.2%, respectively, compared with saline-treated group. Inhibitory activities of HSYA were observed on ADP-induced platelets aggregation in a dose-dependent manner, and the maximum inhibitory aggregation rate of HSYA was 41.8%. HSYA provided a suppressive effect on production of TXA2 without significant effect on plasma PGI2 concentrations. Blood rheological parameters were markedly improved by HSYA, such as whole blood viscosity (from 21.71 +/- 4.77 to 11.61 +/- 0.90 mPa.s), plasma viscosity (from 2.73 +/- 0.53 to 1.42 +/- 0.07 mPa.s), deformability (from 0.66 +/- 0.26 to 0.77 +/- 0.33) and aggregation of erythrocyte (from 3.24 +/- 0.41 to 2.57 +/- 0.30), but no significant effect of HSYA on homatocrit was found (from 51.38 +/- 4.68% to 49.91 +/- 2.32%). HSYA appears to be a good potential agent to treat focal cerebral ischemia, and the underlying mechanisms exerted by HSYA might be involved in its inhibitory effects on thrombosis formation and platelet aggregation as well as its beneficial action on regulation of PGI2/TXA2 and blood rheological changes in rats.     

Effects of lodoxamide on ischemic reperfused myocardium

The beneficial effects of lodoxamide tromethamine (U42585E) have been examined in a canine model of myocardial ischemic injury. Lodoxamide was infused 20 mg/kg/h i.v. starting 30 min before occlusion of the proximal left circumflex coronary artery (LCX) and continuing through 90 min of ischemia. Lodoxamide produced a significant reduction in ultimate infarct size measured at 24 h by postmortem tetrazolium perfusion staining. Infarct size expressed as a percent of the anatomical area at risk was 21.7 +/- 2.7 in the treated group vs. 47.0 +/- 3.1 in the control group (mean +/- SEM). No significant difference in area at risk was observed between treated and control groups. Salvage occurred primarily in subepicardial and midmyocardial tissue without apparent lateral protection. Histological examination confirmed gross results of postmortem staining. The protection appeared to be unrelated to myocardial oxygen demand since no hemodynamic differences between groups were observed at the time of occlusion of throughout the 24-h experimental course. Concurrent studies of ex vivo platelet aggregation showed no effect of lodoxamide on adenosine diphosphate (ADP), collagen, and arachidonic acid-induced aggregation. In vivo antithrombotic effects were evaluated in four conscious dogs by inducing LCX thrombosis with low-amperage stimulation (50 microA for 24 h) of the intimal surface. Occlusive thrombi occurred in all four dogs and were similar to controls. These results suggest that lodoxamide reduces myocardial ischemic injury by a mechanism unrelated to oxygen demand or antiplatelet effects.     

Valsartan improves mitochondrial function in hearts submitted to acute ischemia

The effect of valsartan, an angiotensin II-type I receptor blocker, on the mitochondrial function, was studied using an ex vivo animal model (hearts from Wistar rats), perfused in a Langendorff system and then submitted to global acute ischemia. Parameters evaluated were: membrane electrical potential (DeltaPsi, using a tetraphenylphosphonium-TPP+-electrode), oxygen consumption by the respiratory chain (Clark-type O2 electrode), phosphorylation lag phase (time necessary to phosphorylate a fixed amount of ADP) and ATP/ADP ratio (adenine nucleotides quantified by high-pressure liquid chromatography-HPLC). Valsartan acts preferentially in the phosphorylation, increasing ATP/ADP ratios (succinate: 1.6+/-0.4 versus 0.5+/-0.1--P<0.05; ascorbate/N,N,N',N'-tetramethyl-P-phenylenodiamine-TMPD: 1.1+/-0.2 versus 0.4+/-0.1--p<0.05 versus ischemia in the absence of valsartan) and decreasing lag phase (glutamate/malate: 50.0+/-9.6 s versus 127.2+/-19.03 s-84.6+/-16.2% versus 215.3+/-32.2%; P=0.01; succinate: 111.8+/-33.1 s versus 275.73+/-45.99 s-168.2+/-49.8% versus 414.9+/-69.2%; P=0.02 or ascorbate/TMPD: 11.0+/-3.9 s versus 62.4+/-11.63 s-34.9+/-12.4% versus 198.1+/-36.9%; P=0.001 versus ischemia in the absence of valsartan). This enables a higher energy production in hearts submitted to acute ischemia, for which having energy becomes critical to preserve mitochondrial function. These mechanisms allow us to better understand valsartan cytoprotection in ischemic cardiomyopathy.     

Inhibition of platelet aggregation by verapamil: quantification by in vivo and in vitro techniques

Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 +/- 0.04 x 10(6)/mm3, vs. control, 1.2 +/- 0.09 x 10(6)/mm3, (p greater than 0.05). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 microM), was reduced by verapamil (verapamil, 15.3 +/- 1.2 x 10(3) micron3 vs. control 24.4 +/- 2.7 x 10(3) micron; p less than 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 +/- 1.1 x 10(3)micron3, vs control, 17.3 +/- 0.9 x 10(3) micron3 p less than 0.001). We conclude that verapamil exerts and inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.     

心肌缺血及再灌注大鼠血浆蛋白C活性变化的实验研究

目的：探讨心肌缺血及再灌时大鼠血浆蛋白C（PC）活性及血小板聚集率的变化和意义。方法：SD雄性大鼠40只,随机分为对照组（C,n=8）、缺血组（I,n=24）和缺血再灌组（IR,n=8）,缺血组按照造模后缺血时间的不同又分别分为缺血10 min（I10）、30 min（I30）及60 min（I60）组,每组8只。采用可逆性阻断大鼠左冠状动脉前降支的方法制备心肌缺血及再灌注模型,实验结束后即刻颈总动脉取血,以发色底物法检测血浆蛋白C活性,比浊法测定血小板聚集率。结果：心肌缺血模型组大鼠血浆PC活性均明显低于对照组（P〈0.01）,且随心肌缺血时间延长降低;缺血再灌组PC活性略有恢复,但仍低于对照组（P〈0.01）。血小板聚集率缺血10 min、缺血30 min组及IR组较对照组均明显升高（P〈0.01）,而缺血60 min组血小板聚集率与对照组比较无统计学意义。结论：心肌缺血及再灌注损伤可引起PC活性下降,PC活性的变化参与了心肌缺血及损伤的过程,较血小板聚集率敏感。因此,PC活性的变化有可能成为对评价缺血性心血管疾病有预报价值的指标。     

Anti-ischemic effects of fasudil, a specific Rho-kinase inhibitor, in patients with stable effort angina

Epicardial coronary stenosis causes myocardial ischemia; however, the role of coronary microvessels is poorly understood in the pathogenesis of effort angina. We have previously demonstrated that Rho-kinase pathway is substantially involved in coronary arterial hyperconstriction in patients with vasospastic angina and those with microvascular angina. In the present study, we tested our hypothesis that Rho-kinase is involved in coronary microvascular constriction in patients with effort angina. Intracoronary administration of fasudil (300 microg/min for 15 min), a specific Rho-kinase inhibitor, significantly increased oxygen saturation in coronary sinus vein from 37 +/- 3% to 41 +/- 3% (P < 0.05) but not in six age-matched controls (from 42 +/- 3% to 43 +/- 3%, P = NS). Furthermore, the fasudil treatment significantly ameliorated pacing-induced myocardial ischemia in patients with effort angina (magnitudes of symptom: 1.5 +/- 0.6 to 0.6 +/- 0.4, P < 0.01; ischemic ST-segment depression, 1.8 +/- 0.3 to 1.0 +/- 0.2 mm, P < 0.01; percent lactate production, 50 +/- 17% to 0.4 +/- 7%, P < 0.01) without significant hemodynamic changes. These results provide the first evidence that Rho-kinase is substantially involved in coronary microvascular dysfunction associated with myocardial ischemia in patients with effort angina, suggesting that Rho-kinase can be a novel therapeutic target in ischemic heart disease.     

重组葡激酶对中国实验小型猪冠脉血栓作用的研究

目的:观察重组葡激酶(r-SaK)对中国实验小型猪冠状动脉血栓、心肌缺血、心肌梗塞的影响.方法:直接电刺激中国实验小型猪冠状动脉造成动脉内膜损伤,逐渐形成冠脉内血栓.运用冠状动脉病理切片、显微成像、多媒体图象分析、心外膜电图、心肌组织化学染色、血清生化酶学检查、血液流变学等多种试验手段,研究了r-SaK静脉给药对冠脉血栓的溶栓作用.结果:r-SaK对冠脉血栓有显著的溶栓作用,与对照组比较,r-SaK两个剂量组均能明 显缩小冠脉血栓横切面积(P<0.01),减轻心肌缺血程度和范围(P<0.01),缩小梗塞区(P<0.01),降低CPK活性和血液粘度(P<0.05),抑制血小板粘附、血小板聚集及纤维蛋白原的形成(P<0.05).结论:r-SaK对冠状动脉血栓具有明显的溶栓作用,并可对抗心肌缺血、心肌梗塞等病理反应.     

Prevalence of platelet nonresponsiveness to aspirin in patients treated for secondary stroke prophylaxis and in patients with recurrent ischemic events

To determine the prevalence of platelet nonresponsiveness to aspirin treatment for secondary stroke prophylaxis, the authors studied consecutive patients during a 29-month period. Information regarding their ischemic events, risk factors, and medications was collected. Platelet aggregation in response to collagen and arachidonic acid was used to determine platelet responsiveness to aspirin. A total of 653 patients were evaluated. Of these, 129 patients (20%) were determined to be nonresponsive to aspirin based on continued platelet aggregation in response to collagen, arachidonic acid, or both. A total of 87 (13%) of the 653 patients were clinical aspirin failures (ie, presented with new focal cerebral ischemic symptoms while taking aspirin). Of the patients with new cerebral ischemic symptoms, 57 (66%) were determined to be platelet nonresponsive to aspirin. The odds ratio for platelet nonresponsiveness to aspirin in patients who suffered a recurrent ischemic event while taking aspirin was 14.25 (95% confidence interval: 8.5-23.7; P < .5). Continued platelet aggregation despite aspirin treatment occurred in 20% of ambulatory patients treated for secondary stroke prophylaxis. The prevalence of nonresponsiveness to aspirin was statistically higher in those patients who suffered recurrent cerebral ischemia while taking aspirin (P < .5) compared with patients who remained without new ischemic symptoms.     

维生素C对缺氧大鼠心肌线粒体功能和ATP含量的影响

AIM: To observe the effects of large dose of vitamin C (Vc) on myocardial mitochondrial function, ATP content, and myocardial structure in acute and chronic hypoxic rats. METHODS: Rats were exposed to a simulated altitude 4000 m (barometric pressure = 43 kPa) for 3 and 30 d. Vc (0.75 g.kg-1.d-1) was injected i.p. The heart mitochondrial respiratory function were determined by Clark-type O2 electrode; mitochondrial membrane fluidity (MMF) were assayed through fluorescence polarizative method; the contents of ATP, ADP, and AMP in myocardial tissue were measured with HPLC. RESULTS: After administration of Vc, the ATP content was increased from 35 +/- 3 mg.g-1 to 53 +/- 3 mg.g-1 in acute hypoxic rats (P < 0.01), from 42 +/- 4 mg.g-1 to 48 +/- 3 mg.g-1 in chronic hypoxic rats (P < 0.01); Pa, O2 was increased from 7.2 +/- 1.4 kPa to 9.5 +/- 1.2 kPa in acute hypoxic rats (P < 0.01); mitochondrial respiratory control rate (RCR) was increased from 2.1 +/- 0.6 to 4.7 +/- 0.5 in acute hypoxic rats (P < 0.01), and from 3.3 +/- 0.7 to 4.5 +/- 0.6 in chronic hypoxic rats (P < 0.01); MMF was increased in acute and chronic hypoxic rats (P < 0.05); the degree of myocardial necrosis in vitamin C preventive rats was attenuated as compared with those of acute hypoxic rats. CONCLUSION: Vc is effective on improving myocardial energy metabolism and protecting against myocardial structural injury in hypoxic rats.     

缺血性脑血管病不同溶栓方法对血小板表面及血浆内GMP-140和IL-6的影响

目的 :测定缺血性脑血管病患者溶栓前后血小板表面 GMP- 140分子数、血浆 GMP- 140、白介素 - 6 ( IL - 6 )含量的变化 ,进而比较不同药物溶栓的效果。方法 :用放射免疫法测定 80例缺血性脑血管病患者和 30例健康志愿者对照组血小板表面GMP- 140分子数、血浆 GMP- 140和 IL - 6含量 ,并按缺血性质 ,临床脑神经功能缺损程度和不同药物 (尿激酶和东菱克栓酶 )治疗前后分组。结果 :脑血栓形成组和短暂性脑缺血发作组血小板表面、血浆 GMP- 140和 IL - 6含量均明显高于其对照组 ;溶栓后均明显低于溶栓前并随时间呈下降趋势 ;溶栓前与溶栓后 d3血小板表面及血浆 GMP- 140含量之间呈正相关 ( r=0 .5 5 ,r= 0 .6 5 ,P值均 <0 .0 5 ) ;两种方法溶栓临床评价比较差异无显著性意义 ( P>0 .0 5 )。结论 :缺血性脑血管病患者早期应用上述两种方法溶栓效果相同