Role of hydrogen sulfide in subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is a common acute and severe disease worldwide, which imposes a heavy burden on families and society. However, the current therapeutic strategies for SAH are unsatisfactory. Hydrogen sulfide (H₂S), as the third gas signaling molecule after carbon monoxide and nitric oxide, has been widely studied recently. There is growing evidence that H₂S has a promising future in the treatment of central nervous system diseases. In this review, we focus on the effects of H₂S in experimental SAH and elucidate the underlying mechanisms. We demonstrate that H₂S has neuroprotective effects and significantly reduces secondary damage caused by SAH via antioxidant, antiinflammatory, and antiapoptosis mechanisms, and by alleviating cerebral edema and vasospasm. Based on these findings, we believe that H₂S has great potential in the treatment of SAH and warrants further study to promote its early clinical application.     

Massive ovarian edema mimicking an ovarian neoplasm in a patient with IVC web

Massive ovarian edema is an uncommon benign condition affecting young females predominantly those in the child bearing age group and preadolescent girls. Its clinical and radiologic overlap with ovarian neoplasms and torsion which require surgical intervention makes it imperative for the radiologist to consider this entity preoperatively as preserving fertility is vital in this young age group. We report a case of massive ovarian edema, a rare presentation in a patient with inferior vena cava web and consequent Budd Chiari Syndrome, an association previously unreported in literature.     

大剂量甲基泼尼松龙对急性外伤性脑水肿的治疗作用

目的：探讨大剂量甲基泼尼松龙治疗急性外伤性脑水肿的效果。方法将80例急性外伤性脑水肿患者随机分为两组各40例,对照组应用常规综合治疗,包括止血、脱水、利尿、抗感染、钙拮抗、神经营养等,研究组在此基础上加用甲基泼尼松龙,对比两组疗效。结果研究组患者脑水肿Ⅰ度比例明显高于对照组,Ⅲ度明显低于对照组;研究组患者恢复良好率明显高于对照组,死亡率明显低于对照组(P<0.05)。结论大剂量甲基泼尼松龙治疗急性外伤性脑水肿具有较好抗炎作用和临床疗效,可有效改善脑水肿。     

孕酮对大鼠脑缺血再灌注后脑水肿的影响

目的观察孕酮对脑缺血后脑水肿的影响,并从孕酮对血-脑屏障通透性的影响和抗氧自由基两方面进一步探讨其可能的作用机制。方法雄性SD大鼠72只随机分为假手术组、I／R组、孕酮组。进行脑组织含水量测定,伊文思蓝渗透法血-脑屏障通透性定量分析,电镜下血-脑屏障超微结构形态学观察,脑组织SOD活性和MDA含量测定。结果孕酮能明显减轻脑水肿,降低血-脑屏障通透性,抑制SOD活性的降低和MDA含量的增高。结论孕酮抑制氧自由基的损害,降低血-脑屏障通透性,减轻脑缺血后脑水肿。     

高血压性脑出血后迟发性脑水肿患者B型脑钠肽变化及临床意义

目的观察高血压性脑出血后迟发性脑水肿患者B型脑钠肽(B-type natriuretic peptide,BNP)水平的动态变化,探讨BNP水平与迟发性脑水肿的关系。方法收集40例高血压脑出血患者[其中迟发性脑水肿者18例(DE组),无迟发性脑水肿者22例(MDE组)]和19例健康人群(对照组)。在入院后当天和治疗第10天CT扫描动态检查,且在入院当天、治疗第3天和第10天,收集血浆样本测定BNP含量,同时根据美国国立卫生研究院卒中量表(NIHSS)评估神经功能损伤程度。结果入院当天DE组及NDE组BNP含量高于对照组(P<0.01);入院后DE和NDE组BNP含量均有缓慢上升;治疗第10天NDE组BNP水平较入院时显著增加(P<0.01),NDE组则较入院时显著下降(P<0.01)。血浆BNP水平变化与NIHSS评分呈正相关(r=0.706,P<0.05)。结论动态观察血浆BNP含量是早期诊断和监测高血压性脑出血后迟发性脑水肿的有效指标。     

丙泊酚和硫喷妥钠对光化学诱导树血栓性脑缺血脑水含量和心功能的影响

目的探讨两种静脉麻醉药抗光化学诱导树局部脑缺血的脑保护作用.方法观察两种静脉麻醉药丙泊酚和硫喷妥钠在光化学诱导树血栓性脑缺血后4、24h对缺血中心区和半暗带脑水含量及心率（HR）、平均动脉压（MAP）、左室收缩压（LVSP）、心室内压变化最大速率（±dp/dtmax）、左室舒张末期压力（LVEDP）等指标的影响.结果光化学反应后4h丙泊酚组和硫喷妥钠组缺血半暗带脑水含量分别为（80.95±1.04）%和（83.44±1.33）%,光化学反应后24h则分别为（81.02±0.51）%和（84.04±0.97）%,说明丙泊酚可使缺血半暗带脑水含量的升高程度明显减轻;同时丙泊酚组的心功能变化趋势基本与硫喷妥钠组一致,但抑制程度稍轻.结论丙泊酚具有一定的脑保护作用,且较硫喷妥钠更为明显,亦更为安全.     

坎地沙坦致血管神经性水肿及骶髂关节疼痛

1例63岁女性患者因高血压给予坎地沙坦酯8mg/d,口服3天后,患者出现口腔咽部水肿,腰腿疼痛.停药7天后骶髂关节疼痛加剧后出现抽搐,半坐位后出现呼吸困难,意识丧失,大动脉波动消失,抢救后心跳恢复,无自主呼吸,支持治疗,肝肾功能进行性减弱,支持治疗5天死亡.     

Pharmacological characterization of the late phase reduction in lung functions and correlations with microvascular leakage and lung edema in allergen-challenged Brown Norway rats

Late phase airflow obstruction and reduction in forced vital capacity are characteristic features of human asthma. Airway microvascular leakage and lung edema are also present in the inflammatory phase of asthma, but the impact of this vascular response on lung functions has not been precisely defined. This study was designed to evaluate the role of increased lung microvascular leakage and edema on the late phase changes in forced vital capacity (FVC) and peak expiratory flow (PEF) in allergen-challenged Brown Norway rats using pharmacological inhibitors of the allergic inflammatory response. Rats were sensitized and challenged with ovalbumin aerosol and forced expiratory lung functions (FVC, PEF) and wet and dry lung weights were measured 48 h after antigen challenge. Ovalbumin challenge reduced FVC (63% reduction) and PEF (33% reduction) and increased wet (65% increase) and dry (51% increase) lung weights. The antigen-induced reduction in FVC and PEF was completely inhibited by oral treatment with betamethasone and partially attenuated by inhibitors of arachidonic acid metabolism including indomethacin (cyclooxygenase inhibitor), 7-TM and MK-7246 (CRTH2 antagonists) and montelukast (CysLT₁ receptor antagonist). Antagonists of histamine H₁ receptors (mepyramine) and 5-HT receptors (methysergide) had no significant effects indicating that these pre-formed mast cell mediators were not involved. There was a highly significant (P < 0.005) correlation for the inhibition of FVC reduction and increase in wet and dry lung weights by these pharmacological agents. These results strongly support the hypothesis that lung microvascular leakage and the associated lung edema contribute to the reduction in forced expiratory lung functions in antigen-challenged Brown Norway rats and identify an important role for the cyclooxygenase and lipoxygenase products of arachidonic acid metabolism in these responses.     

Protein Concentration and Hydrostatic Pressure in Subcutaneous Tissue of Rats in Hypoproteinemia

Protein concentration and hydrostatic pressure were measured in subcutaneous tissue of rats during development of aminonucleoside nephrosis. Samples of interstitial fluid for protein analysis were collected from subcutaneous tissue by a wick method, and hydrostatic pressure was measured by a modified Scholander technique. When the serum protein concentration was reduced from 6.1 to 4.8 g/100 ml, interstitial fluid protein concentration fell from 3.0 to 1.1 g/100 ml. This corresponds to a reduction of calculated oncotic pressures from 18.0 to 13.0 mm Hg and from 7.8 to 3.0 mm Hg in serum and interstitial fluid, respectively, thus leaving a nearly constant net transcapillary oncotic pressure. When serum protein concentration was further reduced to 3.8 g/100 ml, interstitial fluid protein concentration was reduced to 0.5 g/100 ml, reducing net transcapillary oncotic pressure by 2–3 mm Hg. The average hydrostatic pressure in subcutis was 1.0 mm Hg sub-atmospheric under control conditions and did not change during hypoproteinemia. The results indicate that a reduction of interstitial protein concentration is an important factor in preventing edema formation in hypoproteinemia.     

Cellular and humoral mediators of pulmonary edema

Pulmonary edema results from increases in pulmonary capillary hydrostatic pressure and microvascular protein permeability. Mediators that induce pulmonary edema can be subdivided into two classes: (1) mediators that alter pulmonary hydrostatic pressure such as serotonin and (2) mediators that increase capillary permeability and result in increased transport of protein. A recognized important permeability increasing factor in the pulmonary microcirculation is the process of neutrophil activation and concomitant mediator release subsequent to neutrophil sequestration. Increased pulmonary capillary pressure occurring concomitantly with increased permeability greatly enhances protein flux and extravascular fluid accumulation. The rise in capillary hydrostatic pressure is determined by precapillary and postcapillary vessel resistances. Recent data indicate that pulmonary veins are not inert conduits but possess active smooth muscle components which respond to vasoactive agents such as histamine and arachidonic acid metabolites through venoconstriction. It appears that few humoral factors acting independently actually increase pulmonary capillary permeability. In comparison to the systemic microcirculation, the lung microcirculation appears to be more resistant to agents such as histamine and bradykinin which are known permeability-increasing agents in systemic microvessels. This may be important teleologically as the pulmonary microcirculation receives the entire cardiac output.