AUGMENTATION OF ANGIOTENSIN II RELEASE FROM ISOLATED MESENTERIC ARTERIES OF WISTAR-KYOTO AND SPONTANEOUSLY HYPERTENSIVE RATS FOLLOWING NEPHRECTOMY

1. We previously reported that angiotensin II release from the mesenteric arteries of Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) increased in a time-dependent manner as a result of the isolation of the arteries and perfusion. This phenomenon appeared to be due to the withdrawal of circulating angiotensin II (AII). 2. The purpose of the present study was to test the hypothesis that vascular AII generation may be negatively regulated by circulating AII in WKY and SHR, and to clarify the role of this vascular angiotensin II in the sustained hypertension of SHR following nephrectomy. 3. The mesenteric arteries from kidney-intact and nephrectomized WKY and SHR were perfused and the amount of AII released into the perfusate was measured. The effects of the angiotensin converting enzyme inhibitor, captopril, and the effects of supplementation of renal renin and circulating angiotensins to nephrectomized rats, by blood exchange between kidney-intact and nephrectomized rats, on AII release were examined to clarify the pathway of vascular AII generation after nephrectomy. 4. Nephrectomy caused augmentation of vascular AII release both in WKY and SHR in spite of the abolishment of circulating renin. Captopril reduced this enhanced release of AII, but blood exchange did not affect it. There was no significant difference in these responses between WKY and SHR. 5. These results suggest that WKY and SHR have in common a potent pathway for production of vascular AII in response to the withdrawal of circulating AII, although this pathway is not responsible for the sustained hypertension of SHR after nephrectomy. The precise pathophysiological role of this pathway remains to be elucidated.     

甲状腺功能亢进性呕吐(附2例报告)

本文报告2例系非甲亢危象及危象前期的甲状腺功能亢进(简称甲亢)患者,临床突出的症状是:频繁而又顽固的呕吐,例1导致了Mallory-Weiss征,服他巴唑60小时后呕吐明显缓解,96小时后呕吐完全停止。例2由于呕吐误诊为胃神经官能症,服他巴唑治疗一周后呕吐停止。甲亢性呕吐国内未见报告,本文对呕吐的机制进行了分析探讨。     

高血压脑出血患者血肿周围血-脑屏障葡萄糖转运蛋白1表达的研究

目的观察高血压脑出血(ICH)患者血肿周围血-脑屏障葡萄糖转运蛋白1(GLUT1)表达的变化。方法采用免疫组化方法检测28例高血压ICH患者不同病程血肿周围脑组织GLUT1的表达情况。结果与对照组相比,ICH组发病12 h GLUT1表达开始增强,24 h、48 h表达最强(均P<0.01);72 h表达明显下降(P<0.01)。结论ICH早期血肿周围GLUT1表达增多,有助于恢复脑的能量代谢。     

从SARS流行看医院危机管理

医院是一个高风险的组织，在复杂、多变的市场环境中，危机是一种连续发生的常态。要借鉴SARS危机管理的经验教训，树立预警性反危机理念，尽量减少危机发生。要提高医院危机管理能力和水平，尽量减少危机造成的损害。要善于把危机变成推动医院发展的契机。     

三维重建单(双)靶点定向置管引流术治疗高血压壳核出血

目的回顾性分析三维重建单(双)靶点定向置管引流术治疗高血压壳核出血的疗效,验证该方法的有效性和可行性。方法将133例壳核脑出血病人的CT定位扫描资料输入计算机工作站,对血肿进行三维重建,根据血肿量的大小和形状设计1～2个靶点和引流管路径。应用立体定向技术将引流管(外径5mm,内径3mm)送至颅内预定靶点,术中应用10ml注射器轻柔抽吸血肿液化部分,术后将尿激酶(1～2万IU)注入血肿腔内,夹闭引流管2h后自然引流,每12h重复1次。复查CT证实剩余血肿量为最初的10%~15%时拔除引流管。结果平均置管1.5 d(1～3d),平均血肿排空率92.8%。术后1个月病死率6.0%,远期随访(平均22个月)病死率11.3%,优良率74.4%。结论该方法治疗高血压壳核脑出血,血肿排空较彻底,疗效可靠,尤其适用于血肿量较大(>25ml)且形态不规则的颅内血肿。     

复方麝香注射液联合脑血肿引流术治疗中老年高血压脑出血疗效观察及费用对比

目的:探讨复方麝香注射液联合微创手术治疗中老年高血压脑出血的临床疗效.方法:将78例接受微创治疗的患者随机分组,两组均采用内科综合治疗.手术对照组在综合治疗基础上加用微创手术进行脑血肿引流;中西医结合组在微创手术治疗后加用复方麝香注射液(10～20 ml/d)静脉滴注1周.结果:中西医结合组显效率(66.67%)、有效率(82.05%)均明显高于手术对照组(46.15%和69.23%,P均<0.05),存活患者日常生活能力也明显优于手术对照组(P<0.05),意识恢复时间明显短于手术对照组(P<0.05),并发症的发生率(15.38%)明显低于手术对照组(38.46%,P<0.01),病死率(5.13%)明显低于手术对照组(10.26%,P<0.01),平均住院天数[(18.29±4.93)d]明显少于手术对照组[(26.23±5.82)d,P<0.05],平均住院费用[(5 916.23±826.39)元]明显少于手术对照组[(8 168.35±1 021.21)元,P<0.05].结论:脑血肿引流术后加用复方麝香注射液治疗中老年高血压脑出血,可降低病死率,减少并发症,降低病残程度,提高生存患者的生活质量,缩短住院时间,降低治疗费用.     

高血压脑出血微创外科治疗的预后因素分析

目的探讨影响高血压脑出血（HICH）微创外科治疗预后的相关因素。方法回顾性分析经微创手术治疗的HICH病人106例,总结其临床特点和疗效,并采用单因素和Logistic多因素回归分析,总结影响预后的有关因素。结果单因素分析显示：平均动脉压（MAP）、术前意识状态、血肿形态、出血部位、血肿量、血肿与脑室关系、血肿再发及术后并发症等因素与HICH微创外科治疗临床预后有关（P〈0.05）。多因素回归分析显示：术前意识状态、术后并发症及出血部位与HICH微创外科治疗预后密切相关（P〈0.01）。结论微创外科手术治疗HICH具有简单、安全、疗效好等优点;术前意识状态、术后并发症、出血部位是影响其预后的重要因素。     

The battering syndrome: A poor record of detection in the emergency department

A review of recent studies shows that physicians have a poor record in detection of cases of domestic violence, with only one battered woman in twenty-five diagnosed on physical examination. Emergency physicians who are more aware of the distinguishing features of the battering syndrome and provide appropriate crisis intervention may help victims to seek early legal and social aid, thereby preventing development of a chronic situation or a personal tragedy.     

Presynaptic α2-adrenoceptor-mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats

The present study was designed to investigate the presynaptic alpha 2-adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na-loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na-loaded HT and normotensive control rats (NT-control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na-loaded HT than in NT-control. Yohimbine, a potent alpha 2-adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na-loaded HT compared with NT-control. These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na-loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na-loaded HT could partially depend on impaired presynaptic alpha 2-adrenoceptor-mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt-dependent hypertension.