高原肺水肿——动物模型的复制(摘要)

高原肺水肿多发生在到达高原后12—72小时。其发生机制多数学者认为是由于缺氧所引起的肺血管非一致性收缩,造成肺灌流不均,在局部肺循环毛细血管内压增高并合并过渡灌流的部位,液体从毛细血管渗出引起。但直到目前尚不能复制出满意的动物模型。因此我们采取事先切除动物一侧肺,从而增加剩余肺的血液灌流量,以试图复制高原肺水肿模型。实验前两周,外科手术方法切除大白鼠左肺,左肺平均占总肺重35％,这就意味着在心     

急性高原病患者支气管肺泡灌洗前后肺功能及血气的改变

目的:探讨急性高原反应(HAAR)及高原肺水肿(HAPE)的发病机理。方法:对10例HAAR患者及6例HAPE患者灌洗前和灌洗后进行肺功能和动脉血气检测, 并与10例高原健康者进行对比。结果:HAAR患者及HAPE患者灌洗前动脉血氧分压明显低于对照组, HAAR同HAPE均存在弥散功能障碍;HAPE肺弥散功能(DLCO%)由灌洗前的(76.01±6.29)%, 上升到灌洗后的(103.31±9.23)%;气体转化因子(DLCO/VA%)由灌洗前的(150.30±15.20)%, 上升到灌洗后的(176.04±16.10)%;动脉血氧分压(PaO₂)由(31.73±3.01)mmHg上升到(45.31±3.56)mmHg。而HAAR及对照组灌洗后上述指标差异不显著。结论:HAPE患者肺泡内大量的液体渗出是HAPE病情恶化的主要原因之一。HAAR属HAPE发展的初级阶段, 存在着间质性肺水肿。     

机械通气缓解高原肺水肿患者舌下微循环和改善右心功能

目的探讨机械通气对高原肺水肿(HAPE)患者舌下微循环和右心功能的影响。方法将30例HAPE患者随机分为HAPE组(14例常规治疗)和MV组(16例机械通气治疗),随机选择平原急进高原未发生高原肺水肿健康志愿者20名为对照组。对MV组和HAPE组治疗前、治疗后、治愈后及对照组行总血管密度(TVD)、灌注血管密度(PVD)、灌注血管比例(PPV)、微循环流动指数(MFI)及右心房左右径、右心室前后径、主肺动脉内径、肺动脉收缩压、血气分析的检测。同时观察MV组、HAPE组肺部啰音、肺部阴影消失时间、临床治愈时间。结果与对照组相比,MV组、HAPE组治疗前pH值增高;血氧饱和度(SaO_2)下降;二氧化碳分压(PaCO_2)下降;血乳酸(Lac)增高(P0.01)。与HAPE组相比,MV组治疗后2 h和6 h能更快的缓解低氧血症、呼吸性碱中毒及降低血乳酸(P0.05或P0.01)。与对照组相比,MV组、HAPE组治疗前TVD、PVD、PPV、MFI值明显降低(P0.01)。MV组治疗后24 h TVD、PVD、PPV、MFI值升高,优于HAPE组(P0.05)。与对照组相比,MV组、HAPE组治疗前右心房左右径增大、右心室前后径增大、主肺动脉内径增宽、肺动脉收缩压增高(P0.01)。MV组、HAPE组治疗后右心房左右径、右心室前后径、主肺动脉内径缩小、肺动脉收缩压降低,与治疗后24 h相比,MV组优于HAPE组(P0.05)。与HAPE组相比,MV组能缩短肺部啰音及肺部阴影消失时间和临床治愈时间(P0.01)。结论机械通气能迅速缓解低氧血症,明显改善微循环障碍及右心功能衰竭,从而缩短HAPE患者的临床治愈时间。     

缺氧对培养的肺血管内皮细胞单层通透性的影响

缺氧对培养的肺血管内皮细胞单层通透性的影响第三军医大学基础部病理生理教研室高原医学研究室（重庆６３００３８）陈黎明罗德成血管壁通透性增高是高原肺水肿的重要发生机制之一，内皮屏障是血管壁最重要的通透性屏障。本实验探讨了缺氧的直接作用对培养的肺动脉内皮细...     

山莨菪碱、川芎嗪预防肺水肿大鼠动脉血浆及BALF中6-酮-PGF_1α、TXB_2含量变化

神经源性肺水肿(NPE)是颅脑创伤、脑血管病变、高原缺氧等常见的并发症,发病急剧凶险.在我国没有引起临床与基础应有的重视。我们用大量注射肾上腺素造成致死性肺水肿,病理过程与NPE+分相似,而程度上更剧烈,具有动力性与非动力性双重机制,既有肺毛细血管流体静压增高,又有毛细血管通透性增高.用山莨菪碱与川芎嗪进行预防,绝大部份动物不形成肺水肿并长期存活,效果明显.     

缺氧性肺动脉高压发生机制的研究进展

缺氧性肺动脉高压是高原心脏病发生的中心环节,也是阻塞性肺疾患导致右心肥大以至衰竭的中心环节。此外,肺动脉高压还见于一此因素引起的急性肺损伤,而且还可能参与高原肺水肿的形成。对于缺氧性肺血管收缩机制的研究,其意义不仅限于理论上探讨,而且是     

高原低氧大鼠肺组织超微结构及其低氧诱导因子1α的表达

背景：低氧诱导因子1α可介导哺乳动物细胞适应低氧环境。 目的：观察高原低氧对大鼠肺组织超微结构的影响及其低氧诱导因子1α表达变化。 方法：将SD大鼠分别为进行高原低氧干预1,2,3和30 d,并设置对照组。4个高原低氧组由海拔5 m的西安地区途中耗时1 d带到海拔2 700 m的青海格尔木地区、途中耗时2 d带到海拔5 000 m的唐古拉地区,途中耗时3,30 d分别带到海拔4 500 m的西藏那曲地区。 结果与结论：光镜及电镜观察显示,急性高原低氧2 d组肺组织出现明显的高原肺水肿,急性高原低氧30 d组低氧诱导因子1α mRNA的表达明显增高(P < 0.01),高原肺水肿现象则明显减轻。结果证实,低氧习服后肺组织低氧诱导因子1α mRNA表达的提高有利于减轻高原肺水肿。     

高原肺水肿患者血流动力学变化及对吸氧反应的测定

目的:探讨高原肺水肿的发病机理。方法:采用右心漂浮导管检测法, 对9例高原肺水肿患者及9例同海拔高原健康人的血流动力学指标进行了检测, 同时也观察了吸入纯氧对高原肺水肿患者血流动力学的影响。结果:高原肺水肿患者发病时, 肺动脉平均压、肺血管阻力、心脏指数均明显高于同海拔高度健康人, 而患者肺动脉楔压, 右心房压力同对照组相比, 未见显著差异;吸氧后, 高原肺水肿患者心率、肺动脉平均压力, 肺血管阻力及心脏指数均较吸氧前明显下降, 特别是肺动脉平均压及肺血管阻力下降尤为明显, 肺动脉平均压力在吸氧1min后即明显下降, 吸氧5min后, 下降至最低值, 但吸氧20min后仍未达对照组水平。结论:高原肺水肿是非心源性肺水肿, 肺动脉高压在其发病中起重要作用。     

高原肺水肿患者凝血纤溶系统的变化

目的：探讨高原肺水肿（HAPE）患者治疗前后血液凝血与纤溶系统的变化。方法：对54例急进HAPE的患者治疗前后血浆中组织纤溶酶原激活剂（t-PA）、纤溶酶原激活剂抑制物-1（PAI-1）活性、纤维蛋白原（FG）、纤溶降解产物（FDP）和D-二聚体（DD）含量进行测定，并与20例高原健康人作对照比较。结果：HAPE患者治疗前血浆中t-PA活性高于正常对照组（P<0.05）；FG、FDP和DD含量及PAI-1活性高于正常对照组及临床治疗后水平（P<0.01或0.05），临床治疗后HAPE患者血浆中FG、DD含量及PAI-1活性与正常对照组无显著差异（P>0.05），但FDP含量仍高于正常对照组（P<0.05）。结论：HAPE患者存在纤溶抑制功能的亢进及凝血与纤溶系统的紊乱。     

实验性肺水肿大鼠血浆中内皮素,一氧化氮含量的变化以及硝普钠,川芎嗪？…

静脉注射大剂量肾上腺素引起肺水种,症状典型、剧烈,动物全部迅速死亡,其机理类似于临床上的中枢性肺水肿[1,2],为一种混合性肺水肿,此类肺水肿时肺动脉压[3]及肺楔压明显增高(以后者为主),肺泡通透性也明显增高[4],肺间质腔及肺泡腔内充满含有大量蛋白的水肿液.为进一步了解此类肺水肿发病机制,探讨儿茶酚胺与内皮素(ET-1)、一氧化氮(NO)释放的关系,我们对肺水肿及采用文献报道对肺水肿具有良好预防作用的硝普钠(NP)[2]、川芎嗪(TMP)[3]预防时大鼠血浆中的ET-1、NO含量及二者的增高倍数进行了测定与探讨.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

即早基因c-fos与脑血管病及学习记忆

即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.