卡托普利异氟醚联合预处理对心脏瓣膜置换术患者的心肌保护作用

探讨卡托普利与异氟醚联合预处理对心肌缺血再灌注损伤的保护作用.选择100例瓣膜置换术惠者分为五组,分别给以不同的药物预处理.观察各组心肌酶、心肌蛋白、炎症因子的变化,以及心脏复跳率和血管活性药物使用.结果显示,卡托普利与异氟醚联合处理组的心肌酶、心肌蛋白、炎症因子以及心脏复跳率和血管活性药物用量与其他三组相比有显著性差异(P<0.05).认为卡托普利延迟相或早期相复合异氟醚预处理对心脏瓣膜置换术患者的心肌缺血再灌注损伤均具有更强保护作用,并以卡托普利延迟相组为优.     

盐酸戊乙奎醚对心脏瓣膜置换术患者NF-κB表达的影响

为研究盐酸戊乙奎醚对心脏瓣膜置换术患者心肌NF-κB转录活性的影响,选取择期瓣膜置换术患者60例,随机分为对照组(C)、盐酸戊乙奎醚组1(P1)、盐酸戊乙奎醚组2(P2),每组20例.结果心肌缺血再灌注后,P1、P2组NF-κB的转录活性明显下降,可见盐酸戊乙奎醚可以抑制心肌NF-κB的激活,在一定程度上具有心肌保护作用.     

盐酸戊乙奎醚对心脏瓣膜置换术患者NF-κB表达的影响

为研究盐酸戊乙奎醚对心脏瓣膜置换术患者心肌NF-κB转录活性的影响,选取择期瓣膜置换术患者60例,随机分为对照组（C）、盐酸戊乙奎醚组1（P1）、盐酸戊乙奎醚组2（P2）,每组20例。结果心肌缺血再灌注后,P1、P2组NF-κB的转录活性明显下降,可见盐酸戊乙奎醚可以抑制心肌NF-κB的激活,在一定程度上具有心肌保护作用。     

血管紧张素转换酶抑制剂与心肌缺血再灌注的细胞凋亡

随着心脏外科手术和介入治疗技术的进展以及心肌缺血患者的增加,心肌缺血再灌注损伤成为临床工作一种常见的病理生理过程。如何采用有效的治疗手段进行心肌保护,防治或降低缺血再灌注所造成的损伤,一直是心脏科学探索的一个重要课题。血管紧张素转化酶抑制剂对很多心脏疾病的治疗特别是拟行心脏手术患者的治疗都取得了良好的效果。随着对其研究的进展,其预处理可为临床预防治疗心肌缺血再灌注损伤提供思路与方法。     

血管紧张素转换酶抑制剂与心肌缺血再灌注的细胞凋亡

随着心脏外科手术和介入治疗技术的进展以及心肌缺血患者的增加,心肌缺血再灌注损伤成为临床工作一种常见的病理生理过程.如何采用有效的治疗手段进行心肌保护,防治或降低缺血再灌注所造成的损伤,一直是心脏科学探索的一个重要课题.血管紧张素转化酶抑制剂对很多心脏疾病的治疗特别是拟行心脏手术患者的治疗都取得了良好的效果.随着对其研究的进展,其预处理可为临床预防治疗心肌缺血再灌注损伤提供思路与方法.     

舒芬太尼和七氟烷不同剂量组合对创伤患者心肌损伤的协同保护作用

创伤失血性休克患者在接受液体复苏和输血治疗时,由于再灌注可导致心肌和心脏功能进一步受损.在再灌注前应积极采取临床措施以保护心脏.阿片类药物和吸入麻醉药物后处理对创伤失血性休克患者心肌缺血-再灌注损伤具有良好的保护作用.此研究中,笔者将不同剂量的舒芬太尼和七氟烷联合应用,通过对患者心肌酶检测相比较,发现两种药物组对后处理是否对失血性休克患者心肌缺血-再灌注损伤具有协同保护作用.     

心肌保护新靶点——线粒体钙激活钾通道研究进展

心肌缺血再灌注损伤与线粒体有密切的关系.其中,位于线粒体的钾通道受到了人们的广泛关注.除了已被许多研究证明的线粒体ATP敏感钾通道参与心肌缺血再灌注的保护作用外,近年来研究发现的线粒体内膜钙激活钾通道也参与心肌保护作用,而国内相关研究报道很少.本文拟就心肌细胞线粒体上的钙激活钾通道结构、生物学特性和心脏缺血再灌注中的心肌保护作用进行简要阐述.     

SAFE通路参与缺血后处理心肌保护作用机制的探讨

缺血后处理(ischemic postconditioning,IPost)是在心肌缺血后持续再灌注前给予多次短暂的再灌注/缺血处理的处理方法,对心肌缺血/再灌注损伤有着重要的保护作用.其心肌保护的具体机制十分复杂,尚未完全阐明.生存活化因子增强(survivor activating factor enhancement,SAFE)途径是IPost中新近发现的保护通路,阐明其在IPost心肌保护中的作用,将为寻找新的药物治疗靶点提供新思路.     

SAFE通路参与缺血后处理心肌保护作用机制的探讨

缺血后处理(ischemic postconditioning,IPost)是在心肌缺血后持续再灌注前给予多次短暂的再灌注/缺血处理的处理方法,对心肌缺血/再灌注损伤有着重要的保护作用。其心肌保护的具体机制十分复杂,尚未完全阐明。生存活化因子增强(survivor activating factor enhancement,SAFE)途径是IPost中新近发现的保护通路,阐明其在IPost心肌保护中的作用,将为寻找新的药物治疗靶点提供新思路。     

心肌保护新靶点——线粒体钙激活钾通道研究进展

心肌缺血再灌注损伤与线粒体有密切的关系。其中,位于线粒体的钾通道受到了人们的广泛关注。除了已被许多研究证明的线粒体ATP敏感钾通道参与心肌缺血再灌注的保护作用外,近年来研究发现的线粒体内膜钙激活钾通道也参与心肌保护作用,而国内相关研究报道很少。本文拟就心肌细胞线粒体上的钙激活钾通道结构、生物学特性和心脏缺血再灌注中的心肌保护作用进行简要阐述。     

ACE与体外循环后心肌损伤的关系

观察体外循环后血管紧张素转换酶（ACE）及心肌标志物的变化,探讨ACE与心肌损伤之间的关系。20例择期CPB心脏手术患者分别于术前（T1）、CPB60rain（T2）、CPB后30min（T3）、4h（T4）、24h（T5）及48h（T6）各时间点测定静脉血中下列各指标的水平：ACE、肌钙蛋白I（cTnI）、肌红蛋白（...     

预防性应用盐酸氟桂利嗪对高血糖SD大鼠局部脑缺血再灌注模型bcl-2表达的影响

探讨预防性应用盐酸氟桂利嗪对高血糖Sprague-Dawley(SD)大鼠局部脑缺血再灌注后bcl-2表达的影响,采用高血糖条件下SD大鼠局灶性脑缺血再灌注模型,36只雄性健康SD大鼠,建立高血糖模型后随机分为2组:高血糖组(n=18)、盐酸氟桂利嗪+高血糖组(简称氟桂利嗪组n=18),各组按脑缺血90min再灌注3h(n=6)、6h(n=6)、24h(n=6)分为3个亚组。应用免疫组织化学方法观察bcl-2的表达。结果氟桂利嗪组bcl-2于再灌注3h可见阳性表达,再灌注6h达高峰,至24h逐渐下降,各时间点之间比较差异显著,P0.01。氟桂利嗪组与高血糖组各再灌注时间点比较,缺血区bcl-2表达增加,差异显著,各时间点均为P0.01。证实预防性应用盐酸氟桂利嗪能使损伤脑区bcl-2表达上调,减轻高血糖条件下的局灶性脑缺血再灌注损伤。     

腹内压的变化对肠道氧合及功能的影响

以胃黏膜pH值及血浆D-乳酸为监测指标,观察腹高压患者的腹内压变化前后胃肠道氧合及功能的变化。本研究提示胃黏膜pH值可以反映胃肠道的缺血,且早于腹腔间隙综合征出现,可敏感反映腹高压时肠道氧舍情况;血浆D-乳酸可反映肠缺血再灌注时肠屏障功能状态。以上观察为临床提供简便易行的监测手段及治疗思路。     

The effect of acute stress exposure on ischemia and reperfusion injury in rat heart: role of oxytocin

Previous studies showed the protective effects of oxytocin (OT) on myocardial injury in ischemic and reperfused rat heart. Moreover, exposure to various stressors not only evokes sudden cardiovascular effects but also triggers the release of OT in the rat. The present study was aimed to evaluate the possible cardioprotective effects of endogenous OT released in response to stress (St), and effects of administration of exogenous OT on the ischemic-reperfused isolated heart of rats previously exposed to St. Wistar rats were divided into six groups: ischemia/reperfusion (IR); St: rats exposed to swim St for 10?min before anesthesia; St+atosiban (ATO): an OT receptor antagonist, was administered (1.5?mg/kg?i.p.) prior to St; St+OT: OT was administered (0.03?mg/kg?i.p.) prior to St; OT: OT was administrated prior to anesthesia; ATO was given prior to anesthesia. Isolated hearts were perfused with Krebs buffer solution by the Langendorff method and subjected to 30?min of regional ischemia followed by 60?min of reperfusion. The infarct size (IS) and creatine kinase MB isoenzyme (CK-MB) and lactate dehydrogenase (LDH) in coronary effluent were measured. Hemodynamic parameters were recorded throughout the experiment. The plasma concentrations of OT and corticosterone were significantly increased by St. Unexpectedly St decreased IR injury compared with the IR alone group. OT administration significantly inhibited myocardial injury, and administration of ATO with St abolished recovery of the rate pressure product, and increased IS and levels of CK-MB and LDH. These findings indicate that activation of cardiac OT receptors by OT released in response to St may participate in cardioprotection and inhibition of myocardial IR injury.     

Neurocognitive outcomes following pediatric brain injury: A developmental approach

Developmental neuropsychologists postulate that “immaturity” of the cerebral cortex should no longer be perceived as a protective factor. They argue that injury to the young brain may affect new learning by disrupting the skills in the midst of being acquired and skills that are yet to be developed. Cognitive deficits or weaknesses that are not detectable in the acute phase following a traumatic brain injury (TBI) may emerge over development as more complex skills are needed, thereby creating a developmental lag between children who sustained a pediatric TBI and typical age peers. This literature review was conducted to evaluate the developmental perspective on neurocognitive recovery/development following a TBI. Overall, the described findings support a developmental view and suggest that predictions of prognosis should be based on the child's remaining ability to learn.     

Response Blocking with Guided Compliance and Reinforcement for a Habilitative Replacement Behavior: Effects on Public Masturbation and On-Task Behavior

ABSTRACT

There is limited empirical research regarding effective treatment for public masturbation. In the current study, the relative and combined effects of reinforcement of an incompatible habilitative replacement behavior and response blocking with guided compliance on masturbation and on-task behavior were evaluated for a seven year-old African-American female with a traumatic brain injury who masturbated in her regular and special education classrooms. Results indicated that response blocking with guided compliance was successful in reducing masturbation. However, response blocking with guided compliance and reinforcement of an incompatible response was most effective for reducing masturbation and simultaneously increasing on-task behavior.     

体外循环所致炎性肺损伤机制及保护进展

肺损伤是体外循环心内直视手术的主要并发症之一。肺损伤的机制十分复杂,主要是全身炎性反应和缺血/再灌注损伤所致。肺保护的方法多种多样,其目的是降低全身炎性反应,减轻或避免缺血/再灌注损伤。本文探讨体外循环肺损伤的机制和保护进展。     

神经生长因子对大鼠脑缺血再灌注后TGF-β1和IL-1β表达的影响及临床意义

探讨神经生长因子（NGF）的脑保护作用及临床意义。采用大鼠脑缺血再灌注（MCAO）模型,选取健康成年SD大鼠55只,随机分为假手术组（n=5）、对照组（n=30）,NGF组（n=10）和生理盐水对照组（n=10）进行造模,应用免疫组化方法检测TGF-β1和IL-1β的表达。可见NGF组神经功能障碍明显减轻,TGF-β1...     

罗红霉素对兔急性心肌缺血再灌注损伤的作用

研究罗红霉素对兔急性心肌缺血再灌注损伤的作用及机制。新西兰大白兔随机分三组。分别于缺血前、后及再灌注结束后测定MDA、IL-6、IL-8、IL-10、中性粒细胞凋亡率。缺血及再灌注后Apo、IR组较Sham组MDA升高(P0.01);再灌注结束后Apo组较IR组IL-6、IL-8减少,IL-10、中性粒细胞凋亡增加(P0.01)。罗红霉素能保护兔心肌缺血再灌注损伤,与减少致炎因子,诱导中性粒细胞凋亡有关。     

Determinants of depressive mood states in everyday life: An experience sampling study

This study tests relative contributions and time-course of proposed risk/protective factors (e.g., stress, coping, and lack of social interactions) for influencing depressed mood states in daily life. Seventy-three participants completed baseline measurement of major depressive disorder symptomatology, followed by smartphone app-based monitoring of momentary experiences of depressed mood and risk/protective factors for 7 days. All predictors had deteriorating impacts on mood as lag increased, and the optimal lag appears to be less than 120 min. Linear decay in effect sizes was found for physical activity, social interaction, and tiredness, whereas exponential decline in effect sizes was found for stress and coping ability. Stress, coping, and depressed mood at the prior time-point were the best predictors of subsequent mood. These effects did not differ as a function of trait depressive symptom severity. Findings highlight the influence of spacing of assessments in identification and magnitude of predictors of mood states, and provide insights into key drivers of change in mood and their time-course.