Morphine Preconditions Purkinje Cells against Cell Death under In Vitro Simulated Ischemia-Reperfusion Conditions

Background: Morphine pretreatment via activation of [delta]1-opioid receptors induces cardioprotection. In this study, the authors determined whether morphine preconditioning induces ischemic tolerance in neurons.

Methods: Cerebellar brain slices from adult Sprague-Dawley rats were incubated with morphine at 0.1-10 [mu]m in the presence or absence of various antagonists for 30 min. They were then kept in morphine- and antagonist-free buffer for 30 min before they were subjected to simulated ischemia (oxygen-glucose deprivation) for 20 min. After being recovered in oxygenated artificial cerebrospinal fluid for 5 h, they were fixed for morphologic examination to determine the percentage of undamaged Purkinje cells.

Results: The survival rate of Purkinje cells was significantly higher in slices preconditioned with morphine (>= 0.3 [mu]m) before the oxygen-glucose deprivation (57 +/- 4% at 0.3 [mu]m morphine) than that of the oxygen-glucose deprivation alone (39 +/- 3%, P < 0.05). This morphine preconditioning-induced neuroprotection was abolished by naloxone, a non-type-selective opioid receptor antagonist, by naltrindole, a selective [delta]-opioid receptor antagonist, or by 7-benzylidenenaltrexone, a selective [delta]1-opioid receptor antagonist. However, the effects were not blocked by the [mu]-, [kappa]-, or [delta]2-opioid receptor antagonists, [beta]-funaltrexamine, nor-binaltorphimine, or naltriben, respectively. Morphine preconditioning-induced neuroprotection was partially blocked by the selective mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate, or the mitochondrial electron transport inhibitor, myxothiazol. None of the inhibitors used in this study alone affected the simulated ischemia-induced neuronal death.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.     

放大胃镜在胃病中的应用

放大内镜由于具有变焦放大的功能，可以在消化道检查中清晰显示胃肠黏膜的腺管开口、微细血管等微细结构的变化，结合黏膜色素染色，可以比较准确地反映病变组织的病理学背景，更容易地在镜下区分不同性质的病变，提高了早期癌的镜下检出率。使得镜下诊断出现了新的标准，使内镜诊断提高到了一个新的水平，是医学发展的又一次革命性进步。     

《中国血栓研究会》(筹)第三次常务理事会会议纪要

会议于1994年5月2日～5月4日在杭州华北饭店召开,会上听取了1993年主要工作汇报并讨论了1994年工作计划。一致同意:需继续发展会员和进一步完善组织,因血栓性疾病涉及临床各科,要发展相关学科从事血栓防治和研究(如     

中国颚口线虫(Gnathostoma)的研究 1.乌鳢(Ophicephalus argus)体内颚口线虫幼虫的调查研究

笔者于1989年10月25日～11月1日在上海市就九江、南昌、上海青浦、上海淀山湖、上海南汇、上海昆山、镇江和南京八个地区乌鳢共80.35公斤(120条)。进行颚口线虫幼虫的     

Synthesis of a new hydroxyethylene dipeptide isostere Phe ψ[CH2CH(OH)]Phe as HIV-1 protease inhibitor

A new type of pseudodipeptide isostere exampled by Phe ψ[CH2CH(OH)]Phe was synthesized from phenylalanine. The H]V protease inhibitory activity (IC50) of Noa-His-Pheψ[CH2CH(OH)]Phe-Ile-Amp was 0. 8 pmol·L-1.     

愈肾汤治疗小儿急性肾炎

笔者自1985～1990年以来,应用愈肾汤治疗小儿急性肾炎100例,结果:痊愈(症状消失,小便化验正常,随访1年无复发)64例,好转(症状改善,小便化验有少量红、白细胞)28例,无效8例。总有效率92%。     

Effects of Volatile Anesthetics on Glutamate Transporter, Excitatory Amino Acid Transporter Type 3: The Role of Protein Kinase C

Background: Glutamate transporters play an important role in maintaining extracellular glutamate homeostasis. The authors studied the effects of volatile anesthetics on one type of glutamate transporters, excitatory amino acid transporter type 3 (EAAT3), and the role of protein kinase C in mediating these effects.

Methods: Excitatory amino acid transporter type 3 was expressed in Xenopus oocytes by injection of EAAT3 mRNA. Using two-electrode voltage clamp, membrane currents were recorded before, during, and after application of l-glutamate. Responses were quantified by integrating the current trace and are reported as microcoulombs. Data are mean +/- SEM.

Results: l-Glutamate-induced responses were increased gradually with the increased concentrations of isoflurane, a volatile anesthetic. At 0.52 and 0.70 mm isoflurane, the inward current was significantly increased compared with control. Isoflurane (0.70 mm) significantly increased Vmax (maximum velocity) (3.6 +/- 0.4 to 5.1 +/- 0.4 [mu]C;P < 0.05) but not Km (Michoelis-Menten Constant) (55.4 +/- 17.0 vs. 61.7 +/- 13.6 [mu]m;P > 0.05) of EAAT3 for glutamate compared with control. Treatment of the oocytes with phorbol-12-myrisate-13-acetate, a protein kinase C activator, caused a significant increase in transporter current (1.7 +/- 0.2 to 2.5 +/- 0.2 [mu]C;P < 0.05). Responses in the presence of the combination of phorbol-12-myrisate-13-acetate and volatile anesthetics (isoflurane, halothane, or sevoflurane) were not greater than those when volatile anesthetic was present alone. Oocytes pretreated with any of the three protein kinase C inhibitors alone (chelerythrine, staurosporine, or calphostin C) did not affect basal transporter current. Although chelerythrine did not change the anesthetic effects on the activity of EAAT3, staurosporine or calphostin C abolished the anesthetic-induced increase of EAAT3 activity.     

Oxygenation of Liver Transplants as a Predictor of Success

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