吸入麻醉药预处理对心肌保护的作用机制

吸入麻醉药对心肌具有预处理作用,这为术中心肌保护的研究和应用提供了新的方向.目前有关吸入麻醉药预处理的机制尚未完全阐明,本文简要综述了吸入麻醉药在ATP敏感性钾通道开放、细胞膜受体-抑制性G蛋白-PKC信号通路激活、心肌微血管保护等方面的研究进展.     

吸入麻醉药心肌保护临床应用进展

大量的动物研究显示,除了对心肌的间接保护作用,吸入麻醉药还具有直接的对抗心肌缺血损伤的作用.这可能为临床提供了一种预防围手术期缺血心肌功能紊乱的技术.吸入麻醉药预处理、后处理技术应用于临床,可能会改善缺血/再灌注心肌的功能,并最终提高患者的愈后.吸入麻醉药心肌保护临床实验研究较少,现主要讨论近几年吸入麻醉药预处理临床应用的进展.     

吸入麻醉药心肌预处理的信号转导机制

吸入麻醉药预处理有IPC样的心肌保护作用,其作用机制目前尚未完全阐明。吸入麻醉药预处理的信号转导机制可能与IPC的信号转导途径相似,吸入麻醉药可能刺激心肌产生触发因子,然后启动级联反应,激活效应因子,发挥预处理效应。目前为止,研究已证实ROS、G蛋白耦联受体、蛋白激酶、线粒体和肌膜KATP通道（Mito KATP and Sarc KATP）介导APC。现就吸入麻醉药心肌预处理信号转导机制方面的最新进展作一综述。     

吸入麻醉药预处理对心肌保护的作用机制

吸入麻醉药对心肌具有预处理作用，这为术中心肌保护的研究和应用提供了新的方向。目前有关吸人麻醉药预处理的机制尚未完全阐明，本文简要综述了吸人麻醉药在ATP敏感性钾通道开放、细胞膜受体一抑制性G蛋白-PKC信号通路激活、心肌微血管保护等方面的研究进展。     

异氟醚预处理通过激活蛋白激酶C-δ诱发心肌纤维膜ATP敏感性钾通道持久敏感化

背景：吸入麻醉药预处理的心肌保护作用机制涉及到心肌纤维膜A胛敏感性钾通道（sarcKATP）的激活，本实验通过研究短暂麻醉药预处理是否能产生持久sarcKATP敏感化，及其是否是通过蛋白激酶C（PKC）介导，进而研究麻醉药预处理的记忆时相。     

七氟醚在不停跳冠脉搭桥病人心肌保护效果优于异丙酚

大量的离体和在体动物实验都证实卤代吸入麻醉药对缺血心肌具有保护作用。吸入麻醉药可促进缺血后心肌功能的恢复和减少心肌梗死面积。其机制有模拟缺血预处理的作用。静脉麻醉药如异丙酚无此种心肌保护作用的特性。其机制尚未阐明,但     

吸入异氟醚或地氟醚预处理对心内直视手术小儿围术期心肌的保护作用

吸入性麻醉药具有与缺血预适应相仿的效应,使心肌梗死范围减小,产生直接的心脏保护作用,这种现象称之为“吸入性麻醉药预处理”。异氟醚和地氟醚是卤族氟类吸入麻醉药,在临床麻醉上广泛使用,特别是用于小儿的麻醉诱导和维持。但异氟醚或地氟醚预处理对小儿围术期心肌的保护作用尚未定论,本研究拟观察吸入异氟醚或地氟醚预处理对体外循环(CPB)下心内直视手术小儿围术期心肌的保护作用。     

七氟醚在不停跳冠脉搭桥病人心肌保护效果优于异丙酚

大量的离体和在体动物实验都证实卤代吸入麻醉药对缺血心肌具有保护作用。吸入麻醉药可促进缺血后心肌功能的恢复和减少心肌梗死面积。其机制有模拟缺血预处理的作用。静脉麻醉药如异丙酚无此种心肌保护作用的特性。其机制尚未阐明，但对心肌细胞的保护效应是通过蛋白激酶C耦联的     

吸入麻醉药预处理对心肌缺血“第二保护窗”的作用机制

吸入麻醉药预处理对心肌缺血侑罐注损伤具有急性期和“第二保护窗”两个时间段的保护作用。“第二保护窗”起效缓慢而持久,临床上有充分的时间在手术前给予,能更方便有效地预防围术期心肌缺血的并发症。它可诱导一些触发因子如腺苷、一氧化氮的产生,通过信号转导通路蛋白激酶C、核因子-κB等,作用于ATP敏感性钾通道及活性氧族等终末效应离子通道或保护蛋白而发挥迟发性心肌保护。现就近年来关于吸入麻醉药预处理对心肌“第二保护窗”的作用机制作一综述。     

吸入麻醉药后处理心肌保护作用机制的研究进展

背景 吸入麻醉药后处理(inhalational anesthetics postconditioning,APO)是指在缺血后冉灌注早期给予一定浓度吸入麻醉药处理.APO具有心肌保护作用,其作用机制目前尚未完全阐明.目的 对APO心肌保护作用机制的研究进展进行回顾和总结.内容 APO的心肌保护的信号转导机制与缺血后处...     

Phylogenetic, ontogenetic, and pathological aspects of the urine-concentrating mechanism

The urine-concentrating mechanism is one of the most fundamental functions of avian and mammalian kidneys. This particular function of the kidneys developed as a system to accumulate NaCl in birds and as a system to accumulate NaCl and urea in mammals. Based on phylogenetic evidence, the mammalian urine-concentrating mechanism may have evolved as a modification of the renal medulla's NaCl accumulating system that is observed in birds. This qualitative conversion of the urine-concentrating mechanism in the mammalian inner medulla of the kidneys may occur during the neonatal period. Human kidneys have several suboptimal features caused by the neonatal conversion of the urine-concentrating mechanism. The urine-concentrating mechanism is composed of various functional molecules, including water channels, solute transporters, and vasopressin receptors. Abnormalities in water channels aquaporin (AQP)1 and AQP2, as well as in the vasopressin receptor V2R, are known to cause nephrogenic diabetes insipidus. An analysis of the pathological mechanism involved in nephrogenic diabetes insipidus suggests that molecular chaperones may improve the intracellular trafficking of AQP2 and V2R, and, in the near future, such chaperones may become a new clinical tool for treating nephrogenic diabetes insipidus.     

What makes cells grow larger and how do they do it? Renal hypertrophy revisited.

Hypertrophy, defined as an increase in cell size without an increase in cell number, occurs in a number of conditions, including compensatory renal growth, diabetes mellitus, protein feeding, chronic metabolic acidosis, and chronic potassium deficiency. In vitro cell culture studies have been used to characterize the mechanisms involved in the development of hypertrophy. Two mechanisms have been identified and characterized. One mechanism involves regulation of processes that are also associated with the initial events of the hyperplastic growth process, and is referred as a cell cycle-dependent mechanism. The other mechanism occurs independently of these particular cell cycle processes, but involves regulation of protein degradation by lysosomal enzymes. This latter mechanism is referred to as a cell cycle-independent mechanism. In vivo studies suggest that both compensatory renal hypertrophy following uninephrectomy and diabetes mellitus-induced hypertrophy involve the cell cycle-dependent mechanism.     

Management of extensor mechanism deficit as a consequence of patellar tendon loss in total knee arthroplasty: a new surgical technique

Extensor mechanism disruption is an uncommon but devastating complication of total knee arthroplasty. A new technique of extensor mechanism reconstruction for patellar tendon loss, after total knee arthroplasty, with the help of extensor mechanism composite allograft is described. Four patients with chronic extensor mechanism-deficient total knee arthroplasty were undertaken for revision surgery along with reconstruction of extensor mechanism with an innovative technique using an extensor mechanism composite allograft consisting of a patella-patellar tendon-tibial tubercle. On final follow-up, none of the patients had extensor lag but for 10 degrees of extensor lag in 1 patient only. Providing an environment for bone-to-bone healing both proximally as well as distally and supervised postoperative rehabilitation led to encouraging results in the management of a failed extensor mechanism after total knee arthroplasty.     

Elbow dislocation with ipsilateral diaphyseal fractures of radius and ulna in an adult is it type 1 or type 2 Monteggia equivalent lesion？

Elbow dislocation with concomitant diaphyseal fractures of radius and ulna has been reported rarely.This injury could be included in Monteggia equivalent lesions based on the mechanism of injury,radiog...     

Mechanism of injury and morphology of the greater tuberosity fracture

Only a few publications discuss the mechanism of injury and morphology of the greater tuberosity fracture. Often, it is described as an avulsion fracture of the rotator cuff. The exact pathobiomechanics is uncertain. We performed a retrospective study and evaluated the mechanism of injury, fracture morphology, and displacement in 103 patients over a 16-year period. Fifty-nine patients sustained a greater tuberosity fracture as part of a traumatic shoulder dislocation. In 44 cases, an isolated greater tuberosity fracture was diagnosed. Of the patients, 47.6% reported a direct mechanism of injury and 32% reported an indirect mechanism of injury. There was one abduction-external rotation injury thought to be the cause of the greater tuberosity fracture. Of the patients, 20.4% were unable to reconstruct the mechanism of injury. Radiologic evaluation revealed an inferior displacement of the fracture on the anteroposterior view in 25% of cases. Our data contradict the theory that this fracture is the result of a bony avulsion of the rotator cuff. Potential mechanisms of injury are discussed. We conclude that there has to be a specific mechanism of injury for greater tuberosity fractures. Further investigations would be beneficial.     

重症急性胰腺炎相关性肾损伤的发病机制及防治

重症急性胰腺炎相关性肾损伤的发病机制尚未完全明确,目前主要有肾脏血流动力学异常、炎性递质与细胞因子释放、肾小管细胞凋亡、肠道细菌和内毒素移位等学说,文中就近年来其发病机制及防治研究进展作一综述.     

男性性活动相关的脑机制

本文从正常性功能的脑机制、性功能障碍的脑机制以及药物治疗机制等几个方面综述了近年来男性性相关的脑成像研究。研究发现男性性活动兴奋期、平台期和高潮期由不同脑区构成的神经网络控制。其中,间脑转换区在男性射精中发挥了关键的启动作用。男性性功能障碍患者在性唤起时存在眶额回和额下回的异常激活模式。血清睾酮和脱水吗啡等药物治疗性功能障碍时,主要通过改变眶额回、脑岛、屏状核和颞下回的激活状态来发挥作用。     

Extensor mechanism failure associated with total knee arthroplasty: prevention and management

Extensor mechanism complications are the most commonly reported reasons for revision surgery after total knee arthroplasty and are a frequent source of postoperative morbidity. Patellofemoral instability is the most commonly reported extensor mechanism complication and has multiple etiologies, including prosthetic malalignment and soft-tissue imbabalce. Patellar fracture or rupture of either the quadriceps or patellar tendon can cause catastrophic disruption of the extensor mechanism. Although some stable fractures can be successfully managed nonsurgically, displaced fractures or tendon rupture often lead to poor results. Other complications include patellar clunk and soft-tissue adhesions, prosthetic wear or loosening, and osteonecrosis. Increased understanding of implant alignment, rotation, and soft-tissue balance, as well as improved design of the trochlear groove of femoral implants and patellar components, has resulted in a decline in extensor mechanism complications. Appropriate prosthetic selection and meticulous surgical technique remain the keys to avoiding unsatisfactory results and revision surgery.     

Fractures of the trochlear notch of the ulna in children. Biomechanical and morphological differentiation from the typical injury picture in adults

Various fractures of the trochlear notch of the ulna seen in children are presented and discussed below. Anatomical differences in bone density and cartilage surfaces as well as a different fracture mechanism make it possible to differentiate these fractures from those in adults. A causal relationship between fracture mechanism, bone density distribution and common fractures of the trochlear notch is discussed.