地佐辛用于术后硬膜外镇痛的临床观察

目的 观察地佐辛用于术后硬膜外镇痛的临床效果.方法 D组镇痛泵配方地佐辛0.3 mg/kg＋1%罗哌卡因100 mg＋地塞米松5 mg＋生理盐水至100 mL,F组芬太尼3 μg/kg＋1%罗哌卡因100 mg＋地塞米松5 mg＋生理盐水至100 mL.镇痛泵参数：持续输注2 mL/h,PCA量0.5 mL/次,锁定时间15 min.记录术后3 h、6 h、9 h、12 h、24 h、36 h各个时间点的VAS、Ramsay、BCS评分及恶心呕吐、尿潴留、皮肤瘙痒、呼吸抑制等不良反应的发生情况.结果 2组各个时间点VAS、Ramsay比较,差异无统计学意义（P＞0.05）,2组舒适度评分D组高于F组,F组不良反应发生率高于D组,差异有统计学意义（P＜0.05）.结论 地佐辛可安全有效的用于术后硬膜外镇痛,且不良反应少.     

咪唑安定、芬太尼联合布比卡因用于妇产科术后硬膜外自控镇痛的临床观察

目的 探讨咪唑安定、芬太尼联合布比卡因用于妇产科术后硬膜外自控镇痛(PCEA)的临床效果观察.方法 对我院2008-11 2012-03收治的ASAI～Ⅱ级采用连续硬膜外麻醉且术后采用PCEA镇痛的病人78例,随机分为观察组和对照组各39例,观察组应用咪唑安定、芬太尼联合布比卡因进行镇痛;对照组应用芬太尼和布比卡因进行镇痛.分别观察2组患者的镇痛效果、疼痛评分、生命体征及不良反应.结果 观察组优良率为97.43％,明显高于对照组的69.23％,2组镇痛,比较差异有统计学意义(P＜0.05).观察组中恶心呕吐3例,皮肤瘙痒2例;对照组中恶心呕吐4例,皮肤瘙痒1例,2组间比较差异无统计学意义(P＞0.05),2组中均无尿潴留及呼吸抑制的发生.结论 眯唑安定、芬太尼复合布比卡因用于妇产科术后是安全有效的,且不良反应轻微,值得临床推广应用.     

Electroacupuncture and morphine analgesia potentiated by bestatin and thiorphan administered to the nucleus accumbens of the rabbit

The endogenous opioid peptide enkephalin (EK) is known to be degraded mainly by two enzymes, the depeptidyl car☐ypeptidase ‘enkephalinase’ and aminopeptidase. Microinjection of the enkephalinase inhibitor thiorphan or the aminopeptidase inhibitor bestatin into the nucleus accumbens of the rabbit produced a dose-dependent analgesic effect. This analgesic effect was totally reversed by the narcotic antagonist naloxone or by antibodies against [Met⁵]enkephalin (MEK) administered to the same site. Antibodies against [Leu⁵]enkephalin were not effective. Moreover, microinjection of thiorphan or bestatin into the nucleus accumbens resulted in a marked potentiation of the aftereffect of electroacupuncture (EA) produced analgesia, as well as the analgesia induced by a small dose of morphine. It is concluded that the analgesic effect elicited by EA and morphine is mediated, at least in part, by MEK-like immunoreactive substance(s) in the nucleus accumbens.     

吗啡对糖奖赏剥夺所致大鼠挫折反应的抑制作用

In this study,a T-maze-based frustration model in rats was established using sucrose-reward de-privation.The results revealed that rats maintained a 75% preference for the sucrose-reward arm in the reward phase.During the sucrose-deprivation frustration phase,both the preference for the sucrose-deprivation arm (62.5%) and time spent waiting in the sucrose-deprivation arm decreased.Acute injection of morphine increased the preference in a dose-dependent fashion,and prolonged the waiting duration in the sucrose-deprivation arm.These findings indicate that morphine specifically inhibited the frustration response induced by sucrose reward deprivation.To further elucidate the pharmacological mechanisms involved,the opioid receptor antagonist naloxone was given to model rats prior to the injection of morphine.The results revealed that naloxone administration markedly attenuated the anti-frustration-like effects of 3 mg/kg morphine treatment.These findings suggest that morphine attenuates the frustration-like response to reward deprivation in rats through the opioid receptor.     

Morphine antagonizes inhibitory controls of nociceptive reactions, triggered by visceral pain in the rat

The interaction between morphine analgesia and the heterotopic hypoalgesic effects induced by visceral pain was investigated using a behavioral approach in the rat. Both systemic morphine and a dull pain of peritoneal-visceral origin (induced by i.p. phenylbenzoquinone, PBQ) increase the threshold for vocalization to tail-shock. The question of the interaction between these two factors was assessed by administering morphine during the period of increase in threshold induced by PBQ. Not only did we find that morphine did not increase the threshold further, but, indeed, very significantly decreased it, with the more obvious effect being observed for a moderate dose (0.33 mg/kg, i.v.). It is concluded that morphine antagonizes the heterotopic hypoalgesic effects of visceral pain. These results do not support the hypothesis that morphine increases inhibitory controls of pain triggered by noxious inputs.     

Electroacupuncture ameliorates cerebrovascular impairment in Alzheimer's disease mice via melatonin signaling

Aims

Cerebrovascular impairment contributes to the pathogenesis of Alzheimer's disease (AD). However, it still lacks effective intervention in clinical practice. Here, we investigated the efficacy of electroacupuncture (EA) in cerebrovascular repair in 3xTg-AD mice and its mechanism.

Methods

3xTg-AD mice were employed to evaluate the protective effect of EA at ST36 acupoint (EAST36). Behavioral tests were performed to assess neurological disorders. Laser speckle contrast imaging, immunostaining, and Western blot were applied to determine EAST36-boosted cerebrovascular repair. The mechanism was explored in 3xTg mice and endothelial cell cultures by melatonin signaling modulation.

Results

EAST36 at 20/100 Hz effectively alleviated the olfactory impairment and anxiety behavior and boosted cerebrovascular repair in AD mice. EAST36 attenuated cerebral microvascular degeneration in AD mice by modulating endothelial cell viability and injury. Consequently, the Aβ deposits and neural damage in AD mice were reversed after EAST36. Mechanistically, we revealed that EAST36 restored melatonin levels in AD mice. Melatonin supplement mimicked the EAST36 effect on cerebrovascular protection in AD mice and endothelial cell cultures. Importantly, blockage of melatonin signaling by antagonist blunted EAST36-induced cerebrovascular recovery and subsequent neurological improvement.

Conclusions

These findings provided strong evidence to support EAST36 as a potential nonpharmacological therapy against cerebrovascular impairment in AD. Further study is necessary to better understand how EAST36 treatment drives melatonin signaling.     

迟发性硬脑膜外血肿所致的术中急性脑膨出

目的 分析急性颅脑损伤后开颅血肿清除术中急性脑膨出的原因。方法 对发生于近5年内开颅血肿清除术中发生的急性脑膨出患者进行统计,总结其中迟发性硬脑膜外血肿发生情况。结果 5年中发生于颅脑损伤后开颅血肿清除术中的急性脑膨出患者75例,其中迟发性外伤性硬脑膜外血肿25例(25/75),占同期外伤性硬脑膜外血肿的5.1％。死亡6例,死亡率为24％(6/25)。结论 颅脑损伤后减压术中出现原因不明的颅内压增高、脑膨出时,应首先排除迟发性硬脑膜外血肿的可能,以防漏诊,延误治疗。     

Morphine suppression of bradycardia induced by electrical stimulation of gigantocellular reticular nucleus in the cat

In chloralose-urethane-anesthetized cats, intravertebral injection of morphine (1,2 and 4 mg/kg) promoted a drastic suppression of the bradycardia elicited by stimulating the medullary gigantocelular reticular nucleus (GRN). The degree of blockadge of GRN-induced cardioinhibition was directly dependent upon the dose of morphine and inversely related to the reticular stimulus train intensity and pulse frequency. The possibility that the GRM may be a site of action for morphine in its production of hypotension and bradycardia was discussed.     

Intracerebral interleukin-1β impairs response to tumor invasion: involvement of adrenal catecholamines

Interleukin-1β (IL-1β) is released within the brain following stress, trauma, infection, and in specific brain disorders. This centrally acting IL-1β has recently been shown to impair peripheral immunity. Central administration of IL-1β suppresses natural killer (NK) cell activity impairs lung clearance of tumor cells and enhances tumor colonization. Using an in vivo model of tumor colonization (lung clearance of NK-sensitive MADB106 adenocarcinoma cells), this study examined the role of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) in mediating these effects. We demonstrate that adrenalectomy significantly attenuated the impaired lung clearance of MADB106 tumor cells induced by intracerebroventricular (i.c.v.) administration of IL-1β (20 ng). Supplementing adrenalectomized animals with corticosterone did not reinstate the effect. The effect of IL-1β on lung clearance was blocked by pretreatment with the β-adrenergic antagonist, nadolol (0.5 mg/kg), but not by the α-antagonist phentolamine (5 mg/kg). Peripheral noradrenergic pathways are not implicated given that systemic administration of the noradrenergic neurotoxin, 6-hydroxydopamine, did not block the effect of IL-1β. Taken together, these findings indicate that IL-1β impairs lung clearance of MADB106 tumor cells via the actions of adrenal catecholamines, most likely epinephrine, acting at β-adrenergic receptors in the periphery.     

幕上骨瓣开颅清除骑跨横窦硬膜外血肿

目的探讨骑跨横窦的硬膜外血肿的手术治疗方法。方法对我科2003年12月至2005年12月收治的6例骑跨横窦硬膜外血肿病人均采用枕部幕上马蹄形皮骨瓣开颅,先清除幕上血肿,再经静脉窦与颅骨内板之间的空隙清除幕下硬膜外血肿。结果6例患者平均手术时间80min,术中失血少。术后5例血肿基本清除,1例幕上残留少量硬膜外血肿。出院时5例恢复良好,1例中残。结论采用枕部幕上马蹄形皮骨瓣开颅,能够顺利清除幕上、下硬膜外血肿,且手术时间短,清除血肿迅速,操作简单,出血少,术后不遗留颅骨缺损。