STUDY ON INTERCELLULAR ADHESIONMOLECULE-1 AND P-SELECTIN IN LIVER ISCHEMIA AND REPERFUSION INJURY

ResumeObjectifL'articleapourbutd'dtudierieroledeL'adhesionmolecule--iintercellulaire(ICAM--I)etP--sdlectindanslagendsedelesionhdpatiqueparischemie--reperlusion.MethodesLe/Oiedesratscumisdl'ischdmie--reper/usionpendant60minutesaservicommemodule.Lesanimauxscutdivisdsen3groupes.iegroupefantome;iegrooveischemiquedecontrblecUl'donneseulementduserumphysiologique,etiegroupetraitsoUondonnel'anticorpsmonoclonalanti--P--selectine(Mab)ddosedeZing/kg15minutesavantlareperfusion.RdsultatsCommeresulta…     

A PRELIMINARY BIOCHEMICAL STUDY ON THE PROTECTIVE EFFECTS OF QINGKAILING INJECTION ON LIVER INJURY

Angongniuhuang pill(安宫牛黄丸)iSone of the three famous drugs(?)of traditionalChinese medicine for severe cases of “febrilediseases”.Consisting mainly of CalculusBovis 牛黄,Moschus 麝香,Cornu Rhino~-ceri 犀角 and Margarita 珍珠,it serves as     

PROTECTIVE EFFECT OF RADIX SALVIAE MILTIORRHIZAE ON APOPTOSIS OF NEURONSDUREVG FOCAL CEREBRAL ISCHEMIA AND REPERFUSION INJURY

We have found that Radix Salviae Miltiorrhizae (RSM) plays a protective role in ischemic brain injury,which attracted us to investigate the effect of RSM on apoptosis of neurons during cerebral ischemia and reperfusion. The apoptotic cells in ischemic brains at different reperfusion intervals were tested with the method of TdT-mediated dUTP-DIG nick end labeling (TUNEL), and the effect of RSM on the apoptosis of neurons was studied in left middle cerebral artery (LMCA) occlusion in rat models (n=18). The results showed that few scattered apoptotic cells were observed in right cerebral hemisphere after LMCA occlusion and reperfusion, and that a lot of apoptotic cells were found in left ischemic cerebral cortex and caudoputamen at 12 h reperfusion, and they reached peak at 24-48h reperfusion. However, in rats pretreated with RSM, the number of apoptotic cells in left cortex and caudoputamen reduced significantly and the neuronal damage was much milder at 24h reperfusion as compared with those of saline-treated rats. From this study, we conclude that administration of RSM can reduce the apoptosis of neurons induced by cerebral ischemia and reperfusion and afford significant cerebroprotection in the model of focal cerebral ischemia and reperfusion.     

THE EXPERIMENTAL STUDY OF BREVESCAPIN INJECTION ON MYOCARDIAL ISCHEMIA

Experimental myocardial infarction models were established in 23 dogs through ligating left anterior descending coronary artery. The effects of Brevescapin (灯盏花)injection on hemodynamics and infarct size in dogs were studied by NBT staining, electronmicroscopic observation, serum CPK assessment and coronary artery tree casting to compare the differences between the treatment group and control group. The results indicate that Brevescapin injection has the effects of slowing heart rate, decreasing cardiac contractility, reducing cardiac oxygen consumption and cardiac work, decreasing blood pressure, decreasing total peripheral vascular resistance and reducing myocardial infarct size (treatment group 6.78±1.97%, control group 15.68±4.00%, P<0.001), The probable pharmacology of Brevescapin is discussed.     

CLINICAL AND EXPERIMENTAL STUDY OF THE EFFECTS OF RADIX OPHIOPOGONIS(RO)ON CARDIAC HEMODYNAMICS DURING MYOCARDIAL ISCHEMIA

RO significantly increased the myocardial con-tractility in patients with coronary heart disease ofdeficiency of both vital energy and Yin and protectedthe heart-pumping function during myocardial ische-mia.These effects were shown by improvement inhemodynamic parameters.Clinically,RO obviouslyraised not only stroke-volume index(SVI),stroke-work index(SWI)and cardiac index(CI)but also theratio of preejection period/left ventricular ejectiontime(PEP/LVET)(all P<0.01).All these changesoccurred soon after the first administration,becoming     

PREVENTION OF MYOCARDIAL REPERFUSION INJURY WITH FREE RADICAL SCAVENNGERS AN EXPERIMENTAL STUDY

The changes in endogenous superoxide dismutase (ESOD) during myocardial ischemia and reperfusion and the efficacy of oxygen free radical scavengers in myocardial protection were investigated in an isolated heart model connected with the recirculating nonpulsatile perfusion circuit. Subjected to a 2-hour period of global ischemia (27 C), the heart was reperfused with 37 C oxygen diluted auto-blood for 60 minutes. Superoxide dismutase plus catalase was added into the cardioplegic solution and reperfusates. ESOD activity was measured by pyrogallol method. The results of the experiment showed that ESOD activity after ischemia and reperfusion was decreased and the addition of oxygen free radical scavengers (SOD and CAT) to the cardioplegic solution and the reperfusates greatly reduced the leakage of myocardial enzymes, coronary vascular resistance, and the ultrastructural damages of the myocardium. These results suggest that the use of SOD and CAT may inhibit myocardial reperfusion injury by scavenging oxygen-derived free radicals.     

ISCHEMIC PRECONDITIONING RELIEVES ISCHEMIA/REPERFUSION INJURY OF HIPPOCAMPUS NEURONS IN RAT BY INHIBITING p53 AND BAX EXPRESSIONS

Objective To examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats, and explore the role of p53 and bax in this process. Methods We examined the effect of IPC on delayed neuron death, neuron apoptosis, expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining, flow cytometry, RT-PCR, and immunohistochemistry technique. Results IPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216±9 cells/0.72 mm2 vs. 30±5 cells/0.72 mm2, P<0.01), decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06%±0.21% vs. 4.27%±0.08%, P<0.01), and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC. Conclusion IPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ische- mia/reperfusion, and this process may be related to the reduced expressions of p53 and bax.     

STUDY ON THE MECHANISM AND EFFECTS OF GLY-TYR-NH2 AND GLY-TYR-LYS ON RAT LUTEAL CELLS IN VITRO

The action of Gly-Tyr-NH2,(GY-NH2) and Gly-Tyr-LYS(GYK) on ^125I-LH binding,cAMP accumulation and progesterone production was investigated.Incubation of rat luteal cells for 2.5h with GH-NH2 and GYK at dosage of 0.2mmol/L caused a significant inhibition of basal and gonadotropin-stimulated steroidogenesis.GYNH2 and GYK were also foumnd to reduce cAMP formation in response to hCG.The activity of adenylate cyclase of luteal cells was inhibitd by 0.2mmol/LGY-NH2 and GYK.GY-NH2 and GYK at a concentration of 0.2mmol/L were not found to have an inhibitory effect on 8Br-cAMP-stimulated progesterone production.GY-NH2 and GYK did not affect ^125I-LH binding to LH receptors on the luteal cellsurface.These results suggest that GY-NH2 and GYK inhibit steroidogenesis at the step of gonadotropin-stimulated c AMP for mation in luteal cells.Adenylate cyclase in luteal cells was also inhibited.     

THE EFFECTS OF ELECTROACUPUNCTURE ON THE REGIONAL CHANGES OF MONOAMINE NEUROTRANSMITTERS IN BRAIN OF RAT WITH CARBON TETRACHLORIDEINDUCED LIVER INJURY

Rats were randomly divided into threegroups:control,carbon tetrachloride(CCl_(/4)),andcarbon tetrachloride plus electroacupuncture(EA).The concentrations of 5-hydroxytrypta-mine(5-HT),5-hydroxyindoleacetic acid(5-HIAA),noradrenaline(NA)and dopamine(DA)were determined by spectrophoto-fluoremetry insix different brain regions(medulla oblongataplus pons,striatum,midbrain,hypothalamus,hippoeampus and cortex).Forty-eight hours after CCI_(/4),injection therewere large increases of 5-HIAA in all six re-gions and increases of 5-HT in the medullaobiongata plus pons and hypothalamus.The NAconcentrations were reduced in the midbrain andhippocampus along with a decrease of DA in themidbrain.However,after EA treatment the incrementof 5-HIAA in the medulla oblongata plus ponsand hippocampus was reduced,but DA in themidbrain was increased significantly.The re-sults suggest that electroacupuncture definitelyassists normalization of the pathological increaseof 5-HT metabolism and decrease of DAcontent in rat brain caused by CCl_(/4),injection.A brief discussion is presented on the possi-ble mechanisms of acupuncture therapy in he-patic encephalopathy and other hepatic diseases.     

雌激素对大鼠部分肝缺血再灌注损伤的影响

目的:观察雌激素在大鼠部分肝缺血再灌注损伤中的作用.方法:60只SD大鼠随机分为雌性组(F组)、雄性组(M组)、雌性卵巢切除组(O组)、雄性雌二醇组(E2组),每组15只,分别研究雌激素在大鼠部分肝缺血再灌注损伤中的作用,以血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)水平作为评定肝损伤的指标.结果:F组的ALT、AST、AKP水平明显低于M组及O组(P＜0.05);E2组的ALT、AST、AKP水平明显低于M组及O组(P＜0.05).结论:雌激素对大鼠部分肝缺血再灌注损伤具有明显的保护作用.     

芯芭的抗氧化作用及对肾缺血再灌注损伤的保护作用

目的：观察芯芭抗氧化自由基及对怠性肾缺血再灌注损伤的保护作用。方法：以小鼠肝组织匀浆，观察芯芭抗氧化自由基的作用。通过建立大鼠怠性肾脏缺血再灌注损伤模型，测定了芯芭对肾缺血存灌注后MDA、SOD以及肾组织Na^ ，K^ 一ATP酶和Ca^ —ATP酶活性的变化。结果：使用芯芭后，与对照组比较，MDA明显下降，SOD，Na^ ，K^ 一ATP酶和Ca^ —ATP酶活性显著上升。结论：芯芭有较强的抗氮化作用，对急性肾缺血再灌注损伤肾脏有显著的保护作用。     

复方丹参对肝硬变大鼠肝脏缺血再灌注损伤的影响

采用肝硬变大鼠模型，观察了复方丹参驿肝缺血再灌注损伤的防护作用，结果显示：复方丹参可显著减少损伤后的血清ＡＩＴ、ＬＤＨ水平，减少肝组织过氧化脂质的产生，减轻肝细胞的病理性损伤。表明复方丹参可增强肝硬变肝细胞的抗氧化能力，对其缺血再灌注损伤起到保护作用。     

吲哒帕胺,维拉帕米对心肌再灌注损伤保护作用的实验研究

目的：应用离体兔心Ｌａｎｇｅｎｄｏｒｆｆ灌注模型,比较吲哒帕胺和维拉帕米对心肌再灌注损伤的保护作用,为临床应用提供实验依据。方法：２１只雄性家兔随机分为对照组、维拉帕米组和吲哒帕胺组;全心缺血４０ｍｉｎ后再灌注,分别取再灌注１５、３０、６０和３６０ｍｉｎ左室壁心肌标本,做超微结构和肌动蛋白（ａｃｔｉｎ）免疫组化观察。结果：对照组超微结构和ａｃｔｉｎ改变明显,而维拉帕米组和吲哒帕胺组改变轻微。结论：     

血红素氧合酶-1抗大鼠肾缺血再灌注损伤细胞凋亡实验研究

目的 探讨血红素氧合酶-1（HO-1）对肾缺血再灌注（IR）损伤中细胞凋亡的影响及其可能的作用机制.方法 24只雄性Wistar大鼠随机均分为单纯IR组、HO-1诱导组及HO-1抑制组,分别给予生理盐水、血晶素、锌原卟啉Ⅸ（ZnPPⅨ）腹腔内注射预处理.8h后行右肾切除用于检测HO-1蛋白表达及活性,左肾动脉夹闭缺血50min再灌注18h,检测血Cr、BUN及肾组织中丙二醛（MDA）浓度、髓过氧化物酶（MPO）活性及bcl-2蛋白表达与细胞凋亡指数（AI）.结果 血晶素与ZnPPⅨ预处理分别显著诱导与抑制了肾内HO-1蛋白表达及活性.与单纯IR组比较,HO-1诱导组Cr、BUN、MDA浓度及MPO活性显著降低,bcl-2蛋白表达升高伴AI明显下降,而HO-1抑制组Cr、BUN、MDA、MPO升高,HO-1表达降低伴AI显著升高.结论 HO-1可能通过抗炎、抗氧化、上调bcl-2蛋白表达等作用抑制肾IR损伤中的细胞凋亡.     

萘甲异喹对大鼠心肌缺血再灌注损伤的保护作用

目的：观察萘甲异喹（NI）对氧自由基损伤心肌的影响。方法：采用大鼠离体互作心脏，观察NI对心肌缺血再灌注损伤的保护作用。结果：NI显著保护心肌超氧化物歧化酶（SOD）活力的降低；减少心肌丙二醛（MDA）生成；减少心肌肌酸磷酸激酶（CPK）释放；降低心肌细胞内钙聚集；降低再灌注诱发的室颤（VF）和室速（VT）发生率；并减轻心肌超微结构的损伤。结论：NT对缺血再灌注损伤心肌的保护与其抗氧自由基作用有关。     

热休克对大鼠缺血-再灌心肌的保护作用探讨

目的：从离体和在体两方面探讨热休克反应对缺血再灌心肌的保护作用。方法：实验采用ＳＤ大鼠，随机分为热休克组和对照组。动物经热休克处理恢复２４ｈ后，离体部分取心进行Ｌａｎｇｅｎｄｏｒｆ灌流，复制缺血３０ｍｉｎ／再灌３０ｍｉｎ的模型，实验中全程记录心电图（ＥＣＧ）及心肌收缩幅度，并测定冠脉流出液的流量变化、肌酸激酶（ＣＫ）活性及丙二醛（ＭＤＡ）含量；在体部分行冠脉左前降支结扎／松绑术复制缺血３０ｍｉｎ／再灌３０ｍｉｎ的模型，实验全程记录ＥＣＧ并测定ＭＤＡ的含量。结果：离体部分热休克组再灌注２、５、１０、１５、２０、３０ｍｉｎ，６个时点心肌收缩幅度及冠脉流量的恢复率显著高于对照组，再灌最初５ｍｉｎ内心律失常的发生率显著低于对照组，再灌３０ｍｉｎ时心肌内ＭＤＡ的含量也显著低于对照组；在体部分热休克组再灌最初５ｍｉｎ内心律失常的发生率及再灌３０ｍｉｎ时心肌内ＭＤＡ的含量均显著低于对照组。结论：热休克反应对大鼠离体与在体的缺血再灌心肌均有一定的保护作用。     

阿司匹林和维拉帕米对兔心肌缺血/再灌注损伤保护作用的超微结构研究

目的：应用离体兔心Ｌａｎｇｅｎｄｏｒｆ灌注动物模型，研究阿司匹林和维拉帕米对心肌缺血／再灌注损伤的保护作用。方法：１４只兔随机分为对照组和实验组。离体兔心缺血４０ｍｉｎ后再灌注，分别取再灌注１５、３０、６０、３６０ｍｉｎ左室游离壁心肌，做超微结构观察。结果：实验组心肌超微结构改变轻，而对照组改变明显。结论：阿司匹林和维拉帕米对心肌缺血／再灌注损伤具有明显的保护作用。