Urinary Bladder incarceration and Infarction by an Intra-Abdominal Fat Pad in a Virginia Opossum (Didelphis Virginiana)

A 2.5-year-old, female opossum had acute stranguria. Based on radiography and ultrasonographic examination a cystic structure was identified in the caudal abdomen associated with bilateral hydroureter and hydronephrosis. This structure contained a neutrophilic fluid, determined to be urine. There was a neutrophilic leukocytosis. Serum chemistry values were within normal limits. The opossum was euthanized. An intra-abdominal fat pad incarceration of the urinary bladder above the trigone was present, resulting in complete obstruction of the urinary bladder and partial obstruction of the ureters. Vessels to the bladder were involved in the incarceration which resulted in vascular compromise and infarction of the bladder. Mild to moderate hydroureter and hydronephrosis were present.     

Effect of hypoxia on persistent sodium current in ventricular myocytes from 3-week infarcted rat heart

AIM: To investigate the effect of hypoxia on persistent sodium current (INap) in single ventricular myocyte isolated from acute myocardial infarction (AMI) heart of rats and to study the mechanisms of cardiac arrhythmias that occur after AMI. METHODS: AMI model was induced by ligating the left anterior descending coronary artery in rats. The whole-cell patch clamp technique was used to record the current in epicardial myocytes in infarcted region from rats at 3 week after AMI. RESULTS: In normoxic conditions, the current density of INap in cardiomyocytes of fake operation (FO) and AMI hearts was 0.144±0.022 pA/pF (n=9), 0.121±0.013 pA/pF (n=9，P<0.01)， respectively, which was blocked by tetrodotoxin (TTX). The amplitude of INap was gradually increased with the prolongation of hypoxia time, but the increase in extent of INap in FO cells was significant bigger than that in AMI cells. The INap was blocked by 1 mmol/L glutathione. CONCLUSIONS: After AMI, the amplitude of INaP in infarcted and noninfarcted myocardium showed differences both in normoxic and hypoxic conditions, which increased dispersion of repolarization. This may be one of the reasons of reentrant ventricular arrhythmias that occur after AMI.     

Nitric oxide opens the second window of protection in ischemic preconditioning via induction of heat shock protein 72

AIM:To examine the inhibition of nitric oxide (NO) synthesis during ischemic preconditioning (IP) on the induction of heat shock protein 72 (HSP72) and infarct size-limiting effect of the second window of protection. METHODS:Rabbits were subjected to 4 cycles of 5 min of coronary artery occlusion separated by 10 min reperfusion, or received a sham operation. During this procedure, N^G-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthase) was injected intravenously 5 min before IP followed by its continuous infusion. Twenty-four hours later, the hearts were rapidly excised for assaying HSP72 expression or were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion and then measured infarct size (IS). RESULTS:Twenty-four hours later, immunoblotting revealed an increase in HSP72 protein levels in the IP group, and this was blocked by L-NAME. IS of the IP rabbits was reduced as compared with the control (29.8%±3.7% vs 50.8%±4.3%, P＜0.01). IS in the IP rabbits was elevtated as a result of L-NAME treatment (46.0%±5.1%). Administration of L-arginine reversed the effects of L-NAME on the induction of HSP72 and IS (33.5%±4.0%). The intravenous administration of S-nitroso-N-acetylpenicillamine (SNAP, a NO donor) increased the induction of HSP72 and reduced IS (31.3%±5.7%, P＜0.01vs control) 24 h later. CONCLUSION:These findings suggest that NO may be involved in the induction of HSP72 and the opening of the second window of protection of IP.     

三九舒血宁(银杏叶)注射液治疗急性脑梗死的临床观察

目的:观察三九舒血宁(银杏叶)注射液治疗急性脑梗死的疗效与安全性。方法:438例急性脑梗死患者随机分为治疗组(n=220)和对照组(n=218)。治疗组予生理盐水250mL 三九舒血宁(银杏叶)注射液12mL静脉滴注,1次/d,连用15d;对照组予低分子右旋糖酐注射液500mL 复方丹参注射液12mL静脉滴注,1次/d,连用15d。根据入院当日和治疗15d后神经功能缺损评分的减少、血液流变学及脑梗死灶的变化,并结合患者的生活能力进行评定疗效。结果:治疗组与对照组的临床疗效差异有统计学意义(H c=22.49,P<0.01);两组治疗前后的全血粘度、血浆粘度、红细胞聚集指数、甘油三酯、胆固醇、纤维蛋白原、脑梗死灶体积差异均有统计学意义(P<0.01),治疗后治疗组的指标优于对照组(P均<0.01)。治疗组无不良反应发生,对照组出现过敏性皮疹3例。结论:三九舒血宁(银杏叶)注射液治疗急性脑梗死疗效显著、安全。     

冠状动脉结扎制备大鼠心肌梗死模型及血流动力学检测

目的 探讨大鼠心肌梗死模型制备及血流动力学检测方法.方法 60只雄性SD大鼠随机分为模型组、假手术组,分别行左冠状动脉前降支结扎术和假手术,术后2周行血流动力学检测及心脏组织病理学检查.结果 模型组大鼠左室收缩压(LVSP)、左室压最大上升和下降速率(±dp/dtmax)明显低于假手术组(P＜0.05或0.01),左室...     

心肌缺血后处理对急性ST段抬高型心肌梗死再灌注心律失常的影响

目的探讨缺血后处理对STEMI心肌再灌注心律失常的影响.方法 2006年10月—2009年1月在北华大学附属医院心内科住院的STEMI患者且于12 h内行直接PCI者共64例,随机分为两组：对照组（34例）和缺血后处理组（30例）.对照组给予单纯再灌注治疗,缺血后处理组采用再灌注30 s/再缺30 s,交替3次后再持续灌注的方法.对比观察再灌注心律失常的发生频率.结果与对照组相比,缺血后处理组再灌注心律失常的发生率显著减少.结论急性心肌缺血后处理能够显著减少再灌注心律失常的发生.     

体温与急性脑梗死临床关系的探讨

目的：探讨体温与急性脑梗死的临床关系。方法：分析１９９例急性脑梗死患者的体温与神经功能缺损程度、梗塞灶大小、梗塞部位及急性期预后的关系。结果：体温升高组最初的神经功能缺损程度、梗塞灶大小及预后与体温正常组比较,差异有极显著性（Ｐ〈０．０１）,体温升高组的梗塞部们以脑叶居多。结论：体温升高可能加重脑缺血损害。     

不同剂量纳洛酮治疗脑梗死临床疗效对比分析

目的分析不同剂量纳洛酮在急性期脑梗死患者治疗中的临床效果．方法选取住院后确诊为急性期脑梗死患者156例作为研究对象,按随机原则将其分成观察组和对照组．每天分别给予小剂量（1．2mg）和较大剂量（4．0mg）纳洛酮静脉滴注,每10d为1个治疗周期．观察治疗后的总有效率及呕吐、恶心、呼吸抑制等并发症的发生情况．结果治疗后,两组患者的总有效率比较没有统计学意义（P〉0．05）;呕吐、恶心、呼吸抑制和低血压等并发症的发生率比较,观察组明显低于对照组,差异具有统计学意义．结论在对急性期脑梗死患者的治疗中,运用较低剂量的纳洛酮临床效果并不低于较高剂量的纳洛酮,并且并发症较少,值得临床关注．     

丹红注射液对急性脑梗死患者神经功能及血清hs-CRP、TNF-á和IL-6水平的影响

目的探讨丹红注射液对急性脑梗死患者神经功能及血清超敏C反应蛋白（hs-CRP）、TNF-和IL-6水平的影响。方法 80例急性脑梗死患者随机分为观察组和对照组,均使用脑梗死常规治疗;观察组加用丹红注射液,对照组加用低分子胞磷胆碱。比较两组患者神经功能及血清hs-CRP、TNF-、IL-6水平。结果两组患者治疗后日常生活能力（Barthel指数）明显升高,而卒中量表（NIHSS）评分和血清hs-CRP、TNF-、IL-6水平均明显下降,观察组改变更显著,差异均有统计学意义（P〈0.01）。结论丹红注射剂可抑制炎性细胞因子表达,具有抗脑损伤作用。     

Wistar rats from different suppliers have a different response in an acute myocardial infarction model

The Wistar rat is a commonly used strain for experimental animal models. Recently it was shown that results vary between studies using Wistar rats of different suppliers. Therefore we studied whether Wistar rats obtained from Harlan Laboratories (Ha, n = 24) and Charles River (CR, n = 22) had a different outcome in an acute myocardial infarction (AMI) model. AMI was induced in both Ha and CR Wistar rats by one operator. This resulted in a significantly higher survival rate for Ha (79.2 ± 10.2%) compared with CR rats (54.2 ± 10.2%, p < 0.05). Furthermore, CR rats had lost significantly more weight after 7 days (−5.9 ± 3.1%) compared with Ha rats (−0.8 ± 1.7%; p < 0.001), indicating a worse health status of the CR rats. Paradoxically, the induced infarct was smaller in CR rats (7.3 ± 3.6% of the heart) compared with Ha rats (12.1 ± 4.7%, p < 0.05). This indicates that CR rats were less sensitive for the cardiomyocyte damage subsequent to AMI induction, but remarkably showed more clinical side effects indicating that Wistar rats from two suppliers had a different response within the same AMI model.