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。     

血液动力学变化对血液流变学影响的研究进展

血液流变学是在流体力学基础上发展起来的一门关系到血液和循环两个系统生理功能的新兴边缘学科,是研究血液及其组成成分流变和变形规律的科学。近十几年来在我国发展十分迅猛,进行了许多研究,现综述如下:     

血液稀释对大鼠肺水肿保护作用的研究

本文观察等容血液稀释(HD)对大鼠氯化铵性肺水肿的防治作用。防治二组采用6%低分子右旋糖酐稀释。使血红蛋白值分别从130.5±1.2g/L,134.1±4.5g/L降至84.3±4.0g/L,88.6±4.5g/L。肺水肿组存活率为13.3%(2/15),预防组为42.1%(8/19),治疗组为60%(9/15),防治二组与肺水肿组比有非常显著差异(P<0.01)。肺系数肺水肿组为098±0.39,防治二组分别为0.70±0.16,0.69±0.07,与肺水肿组比有显著差异(P<0.05)。肺病理组织学与超微结构改变,防治二组均明显减轻。实验结果表明;HD对大鼠氯化铵引起的急性肺水肿有明显保护作用。     

山莨菪碱对氧在血浆中扩散影响的初步报道

<正> 山莨菪碱的作用与某些传统的活血化瘀药物类同。关于“活血化瘀”本质的研究,近年来主要集中在血液动力学(特别是微循环)及血液流变学等方面,而对血液的最重要的生理功能之一,氧的运载传输功能的研究甚少。我们设想活血化瘀药可能也影响氧由大气向组织细胞传输的诸过程(不同的药物可能作用于不同的某个或某几个过程)。为了验证我们这个设想,我们初步观测了山莨菪碱对氧在血浆中扩散的影响。     

局部脑血栓形成对心脏血液动力学的影响

本文采用静注孟加拉红(lmg/100g体重)与滤过的氙灯光源(λ560nm,△λ60nm)反应诱导大鼠血栓性局部脑缺血,并以局部脑血流(regional cerebral blood flow,rCBF)、每搏输出量(stroke volume,SV)、心输出量(cardiac output,CO)、心率(heart rate,HR)及心、肝、脾、肾、肾上腺血流量(blood flow,BF)为指标,探讨光化学反应后不同时间脑血液动力学改变对心脏功能的影响。结果表明,光化学反应后rCBF明显减小(P<0.05);SV、CO亦明显降低(P<0.05);部份器官血液重新分布;但光化学反应后5天,梗塞区rCBF明显增加(P<0.01),SV、CO及心肌血流恢复至对照水平。初步证明脑梗塞与心功能改变之间具有明显的因果关系。     

血液流变性对椎动脉血流动力学的影响

目的探讨血液流变性对椎动脉血流动力学的影响。方法对２６例椎基底动脉供血不足患者的椎动脉ＣＤＦＩ参数与血液流变学指标作多元回归相关分析。结果Ｖｍ、Ａ、Ｑ、ＰＩ与部分流变学指标显著相关,其中Ｖｍ与 ηｂ（８０ｓ~(－１)）,Ａ与ηｂ（２０ｓ~(－１)）,Ｑ与ηｂ（８０ｓ~(－１)）分别是独立相关性（ｒ为－０.３３、－０．３３、－０．３１,Ｐ<０．０５）;ＰＩ则与Ｒηｂ（８０ｓ~(－１)）、ηｂ（８０ｓ~(－１)）、ηｐ、ＨＣＴ、Ｆｎ多项指标密切相关。Ｖｍ、Ｑ、ＰＩ均成功建立对１２项流变学指标的多元拟合模型。结论①血液流变性变化可改变椎动脉血流内部阻力和流速,从而影响其血流动力学状态;②Ｖｍ、ＰＩ等ＣＤＦＩ参数是综合反映椎动脉血流动力学和流变学两方面状态的较灵敏指标。     

川芎嗪对不同状态大鼠胃粘膜血液动力学的影响

用反射光谱法探讨了川芎嗪对不同状态大鼠胃粘膜表层微循环血液量(AEr),Hb氧饱和度(F)的影响,用氢气清除法测定了川芎嗪对胃粘膜微循环障碍大鼠胃粘膜血流量(GMBF)的影响,同时也观察了川芎嗪对出血应激性溃疡形成的作用。结果表明①川芎嗪对正常麻醉大鼠胃粘膜△Er和F值无显著影响,较大剂量时呈一过性下降;②川芎嗪(4mg·100~(-1)g,j.v.)使失血性休克大鼠胃粘膜F值明显增加,注后10分钟时由注前13±10((?)±SD)增至22±5(P<001),△Er不变,表明胃粘膜表层血液灌注明显增加;③川芎嗪能提高LTC_4诱导的胃粘膜微循环障碍时的胃粘膜血流量,注后10分钟时由注前0.521±0.079增至0.979±0.174ml.min~(-1)·100~(-1)g。④川芎嗪对急性失血应激性胃粘膜损伤有保护作用。     

Pulmonary arterial systolic pressure and susceptibility to high altitude pulmonary edema

There is evidence that pulmonary arterial hypertension plays a major role in the occurrence of high altitude pulmonary edema (HAPE). We tested the hypothesis that the pulmonary arterial systolic pressure response to a challenge associated with hypoxia and mild exercise may be considered a predictive factor of HAPE. Pulmonary arterial systolic pressure was measured by Doppler echocardiography in 8 HAPE susceptible (HAPE-S) subjects and 8 HAPE resistant mountaineers (HAPE-R) during a hypoxic exercise challenge established by the French Association for Sport Medicine (Richalet's test). Pulmonary arterial systolic pressure during hypoxic exercise allowed a significant discrimination between the groups, although an overlap of values was observed. When expressed as individual variations from baseline to hypoxic exercise level however, we found a highly significant difference. No overlap was observed between HAPE-R (range: 6.7-18.5 mmHg) and HAPE-S (range: 19.2-30.4 mmHg) groups, with a cut-off value at 19 mmHg. Plasma Vascular Endothelial growth factor (VEGF) and malondialdehyde (MDA) increased in response to hypoxic exercise only in HAPE-S group. Individual increases in pulmonary arterial systolic pressure during hypoxic exercise from basal resting normoxic values seem relevant to estimate HAPE susceptibility when measured during the Richalet's test.     

Changes in pulmonary hemodynamics in acute pulmonary edema

Summary Experiments were made on dogs to study the hemodynamic changes following intravenous injections of chloramine and adrenaline. Chloramine injections were followed by the development of a severe pulmonary edema in an of the dogs. In most of them, however, the capillary pressure in the pulmonary circulation increased, but insignificantly. The great increase in the pulmonary capillary pressure following adrenaline injection did not culminate in the development of edema or caused very slight edema. The conclusion is drawn that increase of filtration pressure is not an indispensable decisive factor for the development of pulmonary edema, even if it is concurrent with considerable disturbances in the pulmonary circulation.(Presented by Academician V. V. Parin) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 60, No. 8, pp. 25–29, August, 1965     

山茛菪硷及川芎嗪对肺水肿大鼠的生存率、肺指数及形态学观察

静脉注射肾上腺素可造成大鼠剧烈的致死性肺水肿,动物于5分钟内全部死亡,类似于临床上中枢性肺水肿,属混合性肺水肿。用中药山茛菪硷及川芎嗪进行预防,效果十分明显。以正常组、肺水肿组、山茛菪组、川芎嗪组为序,存活率为100%、0%、96%、80%。生存时间为30分、4分5秒±27秒、28分43秒±4分36秒、25分12秒±9分36秒。((?) SD,生存时间计算,正常组30分钟处死,预防组30分钟不死者亦处死,均算30分钟。)肺指数为0.48±0.06、1.70±0.47、0.74±0.39、0.83±0.55。上述指标各组与肺水肿组相比,均P<0.01。病理镜检见肺水肿组肺组织的正常结构破坏,间质及肺泡充满大片水肿液,充血、出血,间质增宽、两预防组均接近正常组。结果表明两种药对大鼠肺水肿有明显预防作用。     

山茛菪碱与川芎嗪预防肺水肿时大鼠血气及红细胞超氧化物歧化酶的变化

肾上腺素所致肺水肿类似中枢性肺水肿,具有动力性及非动力性双重机制。此时,动脉血中PaO_2、O_2Sat明显下降、PaCO_2明显上升,pH下降,红细胞超氧化物歧化酶含量下降,654-2与川芎嚓能防止上述异常变化,并使之趋于正常。实验显示了654-2及川芎嗪对肺水肿防止作用的部分机理。     

Role of alveolar epithelial sodium transport in high altitude pulmonary edema (HAPE)

Alveolar edema results from an imbalance between fluid filtration into the alveolar space and removal by reabsorption. Hypoxia increases filtration by raising pulmonary capillary pressure and increasing endothelial and epithelial permeability allowing fluid and blood cells to access the alveoli. Active Na-reabsorption drives the fluid reabsorption from the alveolar space, but hypoxia inhibits reabsorption by inhibition of epithelial Na-channels (ENaC) and Na/K-ATPase. A (genetically determined) low activity of alveolar reabsorption in normoxia and further inhibition by hypoxia might cause HAPE-susceptibility, since at some point the depressed reabsorption may not keep pace with increased filtration. Na-reabsorption might even prove totally inefficient in the presence of large leaks of the alveolar barrier. Alveolar Na-reabsorption has not been measured in HAPE. Nasal epithelial Na-transport has been used as surrogate marker based on similarities in subunit expression of ENaC in nasal, airway, and alveolar epithelium. At high altitude cold, dryness, and nasal infections affect the nasal potential making any extrapolation to processes at the alveolar epithelium unreliable. The variability in nasal Na- and Cl-transport reduces the usefulness of nasal potentials to diagnose HAPE-susceptibility.