p38 MAPK在吗啡预处理对缺血-再灌注损伤心脏保护中的作用

目的 丝裂原活化蛋白激酶（MAPK）p38（p38 MAPK）是MAPK家族中重要成员之一，在缺血预处理（IPC）的保护作用信号传导机制中起着一定的作用，本研究旨在探讨p38 MAPK在吗啡预处理（MPC）对心脏缺血-再灌注损伤保护中的角色.方法 在麻醉开胸大鼠在体心脏模型，随机将54只雄性大鼠分为八组：所有心脏都经历30 min缺血和120 min再灌注，对照组（CON组，n=9）；缺血预处理组（IPC组，n=9）：在缺血-再灌注前经历3次5 min缺血，3次5 min再灌注；吗啡预处理组（MPC组，n=6）：在缺血和再灌注前5 min内分别静注吗啡100 μg/kg，再停止5 min共三个循环；SB＋MPC组（n=6）和SB＋IPC组（n=6）分别于MPC或IPC前15 min给予p38 MAPK选择性拮抗药（SB 203580）0.2 mg/kg静注.MPC＋SB组（n=6）或IPC＋SB组（n=6）分别于缺血前5min给予SB 203580 0.2 mg/kg静注.以及SB组（n=6）：缺血-再灌注前静脉给予SB 203580 0.2mg/kg.观察血流动力学指标、心肌缺血梗死区（IS/AAR）、p38 MAPK和磷酸化的p38 MAPK（pp38 MAPK）的表达.结果 MPC或IPC前应用SB 203580可以明显消除IPC的作用，但并没有消除MPC的作用.而30 min缺血前给予SB 203580可以消除MPC和IPC降低心脏IS/AAR的作用IPC组pp38 MAPK分别在缺血5 min和再灌注30 min蛋白表达密度明显高于CON组（P＜0.01）.然而在MPC组pp38 MAPK仅在再灌注30 min明显高于CON组（P＜0.01）.结论 p38 MAPK的激活是MPC对大鼠缺血后心肌保护信号机制中的介导因子而不是触发因子.     

脑阿片受体在侧脑室注射吗啡预处理减轻大鼠心肌缺血再灌注损伤中的作用

Objective To investigate the role of cerebral opioid receptors in the protective effects of intracerebro-ventricular (ICV) morphine preconditioning (MPC) against myocardial ischemia-reperfusion (I/R) injury in rats. Methods Male SD rats weighing 320-370 g were used in this study. A needle was inserted through a surgically created hole into the cerebro-ventricle using a stereotactic instrument and fixed. Sixty male SD rats in which ICV needle was successfully placed without complication were randomly divided into 10 groups of 6 animals each. In group I sham operation was performed (S). In group]] myocardial I/R was produced (I/R) . In group Ⅲ (ischemic preconditioning), the animals were subjected to 3 episodes of 5 min myocardial ischemia at 5 min intervals before ischemia (IPC) . In group IV morphine was given ICV in 3 repeated doses of 1 μg/kg at 5 min intervals before ischemia (MPC). Three types of opioid receptor antagonists -nor-binaltorphimine (nor-BNI) (κ receptor antagonist), D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2(CTOP) (μ receptor antagonist) and naltrindole (NTD) (S receptor antagonist) 15 nmol were given ICV in group V . VI and VIⅡI respectively at 10 min before MPC. In group VIII,IX and X , nor-BNI, CTOP and NTD 15 nmol were given ICV respectively at 40 min before ischemia. Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion. At the end of 120 min, femoral venous blood samples were taken for determination of lactate dehydrogenase ( LDH) and creatine kinase (CK) activities and calcitonin gene-related peptide (CGRP) concentration. The animals were then killed and hearts removed for measurement of area at risk (AAR) and infarct area (IA) . IA/AAR ratio was calculated. Results The size of IA was smaller and IA/AAR ratio lower and significantly less LDH and CK and more CGRP were released in group IPC and MPC ( group Ⅲ and IV) than in group I/R (group II ) . The protective effects of MPC were abolished by pretreatment with nor-BNI, CTOP and NTD. Conclusion Cerebral μ, k and δ opioid receptors are involved in the protective effects of ICV morphine preconditioning against myocardial I/R injury through CGRP released from peptidergic nerve fibers of heart.     

《药理学进展》(TiPS)受体名称——1991年元月增刊(续四)

<正> 续中国药理学通报,1993;9(5):400通道类型电导阻断剂特性部位/功能其它K通道——ATP-敏感性K~+通20～100(伏降糖在[ATP]_1抑制依赖于β-细胞静息电位/胰岛素分泌道[J_(k(ATPI))](ATP—pS nmol·L~(-1)浓[ATP]_1与[ADP]_1 比率的调节;可能是对抗心肌、骨骼依赖性或ATP-调度水平.甲糖通道开放。一些通道表现肌和CNS缺血的保护作用。节性K~+通道.K_G:宁)、TEA出弱电压依赖性.表明内     

临床应用Vit C有哪些不合理现象？

临床应用Ｖｉｔ　Ｃ有哪些不合理现象？ＶｉｔＣ作用广泛，临床上多联合应用，似可与任何药物配伍使用，其实不然，不合理联合应用，不仅降低药效，产生浪费，还可产生许多不良反应，因此①ＶｉｔＣ不宜与ＶｉｔＢ２、Ｋ３合用，因为不仅ＶｉｔＣ被氧化成去氢抗坏血酸，失...     

脑阿片受体在侧脑室注射吗啡预处理减轻大鼠心肌缺血再灌注损伤中的作用

Objective To investigate the role of cerebral opioid receptors in the protective effects of intracerebro-ventricular (ICV) morphine preconditioning (MPC) against myocardial ischemia-reperfusion (I/R) injury in rats. Methods Male SD rats weighing 320-370 g were used in this study. A needle was inserted through a surgically created hole into the cerebro-ventricle using a stereotactic instrument and fixed. Sixty male SD rats in which ICV needle was successfully placed without complication were randomly divided into 10 groups of 6 animals each. In group I sham operation was performed (S). In group]] myocardial I/R was produced (I/R) . In group Ⅲ (ischemic preconditioning), the animals were subjected to 3 episodes of 5 min myocardial ischemia at 5 min intervals before ischemia (IPC) . In group IV morphine was given ICV in 3 repeated doses of 1 μg/kg at 5 min intervals before ischemia (MPC). Three types of opioid receptor antagonists -nor-binaltorphimine (nor-BNI) (κ receptor antagonist), D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2(CTOP) (μ receptor antagonist) and naltrindole (NTD) (S receptor antagonist) 15 nmol were given ICV in group V . VI and VIⅡI respectively at 10 min before MPC. In group VIII,IX and X , nor-BNI, CTOP and NTD 15 nmol were given ICV respectively at 40 min before ischemia. Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion. At the end of 120 min, femoral venous blood samples were taken for determination of lactate dehydrogenase ( LDH) and creatine kinase (CK) activities and calcitonin gene-related peptide (CGRP) concentration. The animals were then killed and hearts removed for measurement of area at risk (AAR) and infarct area (IA) . IA/AAR ratio was calculated. Results The size of IA was smaller and IA/AAR ratio lower and significantly less LDH and CK and more CGRP were released in group IPC and MPC ( group Ⅲ and IV) than in group I/R (group II ) . The protective effects of MPC were abolished by pretreatment with nor-BNI, CTOP and NTD. Conclusion Cerebral μ, k and δ opioid receptors are involved in the protective effects of ICV morphine preconditioning against myocardial I/R injury through CGRP released from peptidergic nerve fibers of heart.     

保和无糖颗粒剂助消化作用的研究

对中成药保和丸及其新剂型无糖颗粒剂的助消化作用进行了比较研究，发现两种剂型均能显著增加肠蠕动频率，无糖颗粒剂还能显著加速小肠推进运动。无糖颗粒剂促进胃酸分泌，提高胃蛋白酶和胰淀粉酶活性的作用比丸剂更佳。上述结果不仅解释了保和丸的药理作用，且说明无糖颗粒剂这一新剂型较传统的丸剂优越。     

黄蜀葵花总黄酮抗炎解热作用

目的 研究黄蜀葵花总黄酮(TFA)的抗炎、解热作用。方法 采用二甲苯致小鼠耳片肿胀的急性炎症模型和皮下埋植棉球致肉芽组织形成的慢性非特异性炎症模型观察TFA的抗炎作用；采用sc松节油或iv大肠杆菌液两种诱发家免发热的模型观察TFA的解热作用。结果 TFA(200、100、50mg／kg)均能有效减轻小鼠右耳肿胀程度，TFA50mg／kg可明显抑制大鼠新生肉芽组织形成；由sc松节油或iv大肠杆菌液诱发的家兔体温升高，TFA可产生不同程度地降低作用。结论 TFA具有良好的抗炎、解热作用。     

羟自由基致痛作用机制

目的 探讨羟自由基(OH)参与疼痛调控的机制。方法 分别用Ca2 通道阻滞剂维拉帕米(Ver)及N_-甲基-D-天(门)冬氨酸(NMDA)受体非竞争性拮抗剂氯氨酮(Ket)预处理观察OH的中枢致痛敏作用与Ca2 、NMDA受体之间的关系；并测定小鼠疼痛过程中脊髓、脑、血中前列腺素(PGs)的含量。结果 Ver(5mg／kg，ip)、Ket(30rag／0kg，ip；0．5mg／kg，ith)可拮抗*OH的致痛敏作用，但iev*OH后不影响PGs的含量。结论 *OH的中枢致痛敏作用的机制可能与细胞内高钙及NMDA受体的激活有关。     

金丝桃甙对大鼠缺血后脑细胞凋亡的影响

目的 研究金丝桃甙（Hyp)对脑缺血诱发细胞凋亡的抑制作用。方法 采用双侧颈总动脉（CCA）结扎法造成大鼠不完全脑缺血；采用TUNEL法和电镜法观察细胞凋亡；用二苯胺试剂法测定DNA片端含量。结果 结扎双侧CCA可显诱导脑皮质细胞凋亡；Hyp 100mg/kg可显改善凋亡细胞超微结构变化，并减少脑皮质中细胞凋亡数；Hyp50、100mg/kg可抑制脑缺血诱导DNA片端的增多。结论 Hyp对缺血诱导的脑皮质细胞凋亡有抑制作用。