急性脑出血综合治疗的几个问题探讨：附死亡80例分析

通过对８０例急性脑出血死亡组分析,发现死于脑疝的占６２．５％,脑疝与一种或二种以上合并症同存者占７７．５％,显著高于存活组（Ｐ＜０．０１）．它们互为因果,加速死亡。因此,应重视早期或超早期采用简易定向锥颅脑内血肿碎吸术吸除血肿,同时注意维持生命体征稳定,加强脱水降颅压,预防、控制合并症等综合治疗。且要全面分析,相互兼顾,正确处置。这是帮助机体渡过调控障碍难关,挽救生命的有效治疗措施。     

Acetazolamide alleviates sequelae of hyperglycaemic intracerebral haemorrhage by suppressing astrocytic reactive oxygen species

Abstract

Hyperglycaemia is associated with the poor outcome after intracerebral haemorrhage (ICH). Acetazolamide (AZA), a kind of carbonic anhydrogenase (CA) inhibitor, its effectiveness in ICH had been reported. However, the connections between AZA and ICH, especially in hyperglycaemia condition had never been defined. In this study, adult Sprague–Dawley rats were administered with vehicle or streptozotocin (STZ) to render them into normoglycaemic (NG) or hyperglycaemic (HG), respectively. Collagenase was then injected into the striatum. The NG or HG ICH rats treated with vehicle control or 5?mg/kg AZA (oral gavage) underwent haemorrhagic area assessments on the 1st, 4th, and 7th day after ICH. The coverage of pericytes was examined by immunohistochemistry. Reactive oxygen species (ROS) levels were assessed in mouse astrocyte cell line treated with vehicle or 20?μmol/L of AZA in culture media according to two different glucose concentrations. AZA reduced the haematoma size, improved neurobehavioral functions, suppressed astrocytic ROS production in vitro, and preserved cerebral pericytes coverage, which are even more remarkable in HG conditions. The present study indicates that AZA may alleviate some sequelae after ICH, especially in poorer prognostic HG rats through the suppression of astrocytic ROS production.     

Colitis por citomegalovirus en paciente anciano inmunocompetente

Gastrointestinal tract involvement due to cytomegalovirus infection is a condition that usually occurs in immunocompromised patients, but is uncommon in immunocompetent patients. In a review of 33 cases, the median age was 68 years, and the accompanying symptoms were diarrhoea (76%), abdominal pain (52%), and haematochezia, or melena (27%)^.The case is presented of ctyomegalovirus colitis in an 85 year-old man with no previously identified immunocompromised states.     

尖吻蝮蛇凝血酶治疗消化性溃疡出血的有效性和安全性评价

目的:评价尖吻蝮蛇凝血酶治疗消化性溃疡出血的有效性和安全性。方法:选取2014年4月~2015年4月我院消化科收治的消化性溃疡出血患者100例为研究对象,根据病情程度分为轻度、中度和重度,将入选患者随机分为观察组和对照组,每组各50例。对照组在抑酸、消炎和保护胃黏膜等常规治疗基础上采用垂体后叶素止血,观察组在上述常规治疗基础上采用尖吻蝮蛇凝血酶止血,比较观察两组不同病情程度患者的临床疗效和有既往心脑血栓病史患者再次发生血栓的情况。结果:观察组中度、重度患者的疗效明显优于对照组中、重度患者,且差异有统计学意义(P0.05),观察组中有既往心脑血栓病史的患者无再次发生血栓。结论:尖吻蝮蛇凝血酶治疗消化性溃疡出血具有较好的疗效和安全性。     

The autophagy–lysosomal system in subarachnoid haemorrhage

The autophagy–lysosomal pathway is a self‐catabolic process by which dysfunctional or unnecessary intracellular components are degraded by lysosomal enzymes. Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most devastating forms of stroke. Multiple pathogenic mechanisms, such as inflammation, apoptosis, and oxidative stress, are all responsible for brain injury and poor outcome after SAH. Most recently, accumulating evidence has demonstrated that the autophagy–lysosomal pathway plays a crucial role in the pathophysiological process after SAH. Appropriate activity of autophagy–lysosomal pathway acts as a pro‐survival mechanism in SAH, while excessive self‐digestion results in cell death after SAH. Consequently, in this review article, we will give an overview of the pathophysiological roles of autophagy–lysosomal pathway in the pathogenesis of SAH. And approaching the molecular mechanisms underlying this pathway in SAH pathology is anticipated, which may ultimately allow development of effective therapeutic strategies for SAH patients through regulating the autophagy–lysosomal machinery.     

Identification and Determination of 1-Methylimidazole-4-Acetic Acid in Human Cerebrospinal Fluid by Gas Chromatography-Mass Spectrometry

Abstract: A method for the quantification of 1-methylimidazole-4-acetic acid in human CSF was developed. Methylimidazole-acetic acid was identified and quantitated in CSF. The method involves concentration of the compound on a cation exchanger, extraction of the methyl ester with ethyl acetate, and preparation of a heptafluorobutyryl derivate of the methyl ester, which is finally purified by chromatography on silica gel and quantitated by gas chromatography-mass spectrometry with the deuterated analogue as internal standard. The coefficient of variation at 1 ng/ml was 13%. The limit of sensitivity was about 0.2 ng/ml. The concentration of methylimidazole-acetic acid in lumbar CSF from healthy volunteers was below 1 ng/ml. Ventricular CSF contained higher concentrations than lumbar fluid. The existence of a rostrocaudal concentration gradient was established. There was a correlation between the concentration of methylimidazole-acetic acid and tele-methylhistamine in CSF. The concentration of methylimidazole-acetic acid in lumbar CSF from schizophrenic patients, patients with subarachnoidal haemorrhage, or patients with rheumatic disease was in the range of that in healthy volunteers.     

Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans

Free radical toxicity is considered as a key mechanism in the neuronal damage occurring after aneurysmal subarachnoid haemorrhage (SAH). We measured markers of DNA and RNA damage from oxidation (8-oxodG and 8-oxoGuo, respectively) in cerebrospinal fluid from 45 patients with SAH on day 1–14 after ictus and 45 age-matched healthy control subjects. At baseline, both markers were significantly increased in patients compared to controls (p values?20-fold above control levels) from day 5–14. None of the markers predicted the occurrence of vasospasms or mortality, although there was a trend that the 8-oxoGuo marker was more strongly associated with mortality than the 8-oxodG marker. We conclude that SAH leads to a massive increase in damage to nucleic acids from oxidative stress, which is likely to play a role in neuronal dysfunction and death. As only patients in need of a ventriculostomy catheter were included in the study, the findings cannot necessarily be extrapolated to all patients with SAH.     

GFAP and antibodies against NMDA receptor subunit NR2 as biomarkers for acute cerebrovascular diseases

We studied whether the serum levels of glial fibrillary acidic protein (GFAP) and of antibodies against the N‐methyl‐d ‐aspartate receptor subunit NR2 (NR2 R_NMDA) can discriminate between intracerebral haemorrhage (ICH) and ischaemic stroke (IS) in stroke patients. We prospectively recruited patients with suspected stroke (72 confirmed) and 52 healthy controls. The type of brain lesion (ICH or IS) was established using brain imaging. The levels of GFAP and of antibodies against NR2 R_NMDA were measured in blood samples obtained within 12 hrs after stroke onset and 24, 48 and 72 hrs and 1 and 2 weeks later using ELISA immunoassay. Improvement in diagnostic performance was assessed in logistic regression models designed to predict the diagnosis and the type of stroke. GFAP peaks early during haemorrhagic brain lesions (at significantly higher levels), and late in ischaemic events, whereas antibodies against NR2 R_NMDA have significantly higher levels during IS at all time‐points. Neither of the two biomarkers used on its own could sufficiently discriminate patients, but when they are used in combination they can differentiate at 12 hrs after stroke, between ischaemic and haemorrhagic stroke with a sensitivity and specificity of 94% and 91%, respectively.     

痛血康胶囊对早孕大鼠不完全流产模型的治疗作用

目的：探讨痛血康胶囊治疗早孕SD大鼠不完全流产模型产后出血的疗效及作用机制。方法：1）受孕7 d予米非司酮和米索前列醇,造成早孕不完全流产模型,痛血康治疗7 d观察并记录SD大鼠离体子宫平滑肌活动情况及病理组织学改变。2）用小鼠尾尖取血法,观察痛血康对小鼠出凝血时间的影响。3）用小鼠耳廓肿胀和SD大鼠棉球肉芽肿两个模型,观察痛血康的抗炎作用。4）用皮下注射肾上腺素加冰水刺激所致SD大鼠血瘀模型,观察痛血康的活血化瘀作用。结果：痛血康能增强早孕不完全流产SD大鼠子宫平滑肌收缩强度,促进残存的胚囊组织排出;能降低血瘀模型SD大鼠全血和血浆黏度,缩短小鼠出凝血时间;对二甲苯所致小鼠耳廓肿胀和SD大鼠棉球肉芽肿有明显抑制作用。结论：痛血康在早孕SD大鼠中具有治疗产后出血的作用,可能与增强流产SD大鼠的子宫收缩强度、促进残留在宫腔的绒毛或蜕膜组织排出、缩短出凝血时间、抑制炎症等有关。     

The vascular protective role of oestradiol: a focus on postmenopausal oestradiol deficiency and aneurysmal subarachnoid haemorrhage

The steroid hormone, oestradiol, has pleiotropic functions. The protective effects of oestradiol are attributed to its anti‐inflammatory, antioxidant, anti‐atherogenic, anti‐apoptotic, vasodilatory activities and regulation of micro RNA. Oestradiol upregulates endothelial nitric oxide synthase gene expression and increases the production of nitric oxide, an important vasodilator. It suppresses the renin–angiotensin system and monitors haemodynamic stress. The hormone maintains the integrity of blood vessels by reducing oxidative stress while upregulating the expression of antioxidant enzymes and prevents vascular inflammation by regulating pro‐ and anti‐inflammatory cytokines. Aneurysmal subarachnoid haemorrhage (aSAH) occurring as a consequence of the rupture of an intracranial aneurysm is a devastating cerebrovascular event, representing 5–7% of all strokes. Postmenopausal women are more susceptible to aSAH compared to men in the same age group. This gender disparity has been attributed to reduced levels of the vascular protective hormone oestradiol following menopause. This review is focused on the protective role of oestradiol on vasculature and how the drop in oestradiol levels after menopause dramatically increases the incidence of aSAH in women. During menopause, oestradiol deficiency may affect vascular integrity causing dysregulation of vascular homeostasis by affecting the renin–angiotensin–aldosterone system (RAAS) and inflammatory and apoptotic cascades, resulting in the weakening of the cerebral arterial wall and potentially to development of an aneurysm and its rupture. In view of the role of oestradiol in maintaining vascular integrity, treatments involving hormone replacement could be a promising approach in postmenopausal women who are at risk of developing or rupturing an intracranial aneurysm.