西红花苷对血管内皮细胞的保护作用研究

目的 研究西红花苷对过氧化氢所致牛内皮细胞（BAEC）损伤的保护作用，并初步探讨其可能的作用机制。方法 利用过氧化氢刺激BAEC，观察了西红苷对细胞培养液内MDA、SOD、LDH含量或活性的影响，并对细胞进行流式细胞分析和细胞内钙测定，观察了该药对细胞凋亡及胞内钙的影响。结果 西红花苷可剂量依赖性的减少MDA生成，提高SOD活性，阻止LDH的外漏，还能抑制过氧化氢所致细胞内钙升高，减少细胞凋亡百分率。结论 西红花苷对过氧化氢所致BAEC损伤有保护作用，其作用机制可能与其拮抗细胞内钙有关，值得在临床上推广应用治疗心血管疾病。     

1011例农村农药中毒分析

随着农村生产责任制的实行,出现了自购、自存、自用农药的新情况,使农药的使用量和接触人数增多,农药中毒不断发生。本文对我区1011例农药中毒事故进行分析,探讨农药中毒发生的规律,为制定防治措施提供科学依据。现报道如下: 一、材料和方法材料取自成都市的温江、蒲江、灌县、新津、新都、大邑、崇庆、邛崃、郫县、彭县等十县1986年(全年)农药中毒报告卡,进行相应的统计学处理。     

对伴有心律失常者施行扁桃体摘除术的体会：附14例报告

本文报告14例室性心律失常者施行扁桃体摘除术,结果13例顺利摘除并纠正了心律失常,改善了全身状况;另1例因手术刺激并室速而中止手术,无并发症。作者认为对伴有心律失常的扁桃体炎患者,应尽早积极地采取手术治疗。     

眼脉冲幅度增加提示动脉反流

目的:报道1例因双眼脉冲幅度(OPA)增加发现动脉反流的病例,而后者正是引起OPA增加的原因。设计:病例报道。方法:偶然发现双眼OPA增高,由此发现脉压增高和动脉反流。患者接受动脉瓣膜手术,待动脉脉压恢复正常后评价OPA。结果:动脉脉压高时的双眼OPA为9mmHg,动脉脉压恢复正常后的双眼OPA为3mmHg。结论:动脉脉压增高可以导致OPA增高。眼脉冲幅度增加提示动脉反流@McKee H.D.R.$Hull and East Yorkshire Eye Hospital, Fountain Street, Hull, Uni ted Kingdom @Saldaa M. @Ahad M.A. @张少娟…     

瘘口周围皮瓣Y—V成形尿道瘘修补术

瘘口周围皮瓣ＹＶ成形尿道瘘修补术罗汉宏何恢绪李清荣聂海波吕军曹启友１９８８年８月至１９９６年３月，对２１例尿道下裂尿道成形术后尿瘘患者施行瘘口周围皮瓣ＹＶ成形尿瘘修补术，２０例一次成功。报告如下。临床资料本组２１例，年龄１～２３岁，平均１１３岁...     

新疆维吾尔族成人颅底和蝶鞍X线测量

作者根据Ｘ线诊断测量标准，观察测量维吾尔族健康成人７６例，对照组汉族１０１例Ｘ线头颅正侧位片的颅底和蝶鞍１６例指标；并进行计算分析，与其它资料进行比较。     

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.

Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.

Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR.     

Morphine Enhances Pharmacological Preconditioning by Isoflurane: Role of Mitochondrial KATP Channels and Opioid Receptors

Background: Adenosine triphosphate-regulated potassium channels mediate protection against myocardial infarction produced by volatile anesthetics and opioids. We tested the hypothesis that morphine enhances the protective effect of isoflurane by activating mitochondrial adenosine triphosphate-regulated potassium channels and opioid receptors.

Methods: Barbiturate-anesthetized rats (n = 131) were instrumented for measurement of hemodynamics and subjected to a 30 min coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size was determined using triphenyltetrazolium staining. Rats were randomly assigned to receive 0.9% saline, isoflurane (0.5 and 1.0 minimum alveolar concentration [MAC]), morphine (0.1 and 0.3 mg/kg), or morphine (0.3 mg/kg) plus isoflurane (1.0 MAC). Isoflurane was administered for 30 min and discontinued 15 min before coronary occlusion. In eight additional groups of experiments, rats received 5-hydroxydecanoic acid (5-HD; 10 mg/kg) or naloxone (6 mg/kg) in the presence or absence of isoflurane, morphine, and morphine plus isoflurane.

Results: Isoflurane (1.0 MAC) and morphine (0.3 mg/kg) reduced infarct size (41 +/- 3%; n = 13 and 38 +/- 2% of the area at risk; n = 10, respectively) as compared to control experiments (59 +/- 2%; n = 10). Morphine plus isoflurane further decreased infarct size to 26 +/- 3% (n = 11). 5-HD and naloxone alone did not affect infarct size, but abolished cardioprotection produced by isoflurane, morphine, and morphine plus isoflurane.