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41.
T. Kullmer G. Kneissl T. Katova H. Kronenberger A. Urhausen W. Kindermann W. M?rz J. Meier-Sydow 《European journal of applied physiology and occupational physiology》1995,70(2):169-174
To clarify whether or not systolic and diastolic function of the human left ventricle (LV) were decreased during acute hypoxia, at rest and with exercise, 14 healthy male volunteers [age 25.9 (SD 3.0) years, height 182.9 (SD 7.1) cm, body mass 75.9 (SD 6.9)kg] were examined using M-mode and 2D-mode echocardiography to determine the systolic LV function as well as Doppler-echocardiography for the assessment of diastolic LV function on 2 separate test days. In random order, the subjects breathed either air on 1 day (N) or a gas mixture with reduced oxygen content on the other (H; oxygen fraction in inspired gas 0.14). Measurements on either day were made at rest, several times during incremental cycle exercise in a supine position (6-min increments of 50 W, maximal load 150 W) and in 6th min of recovery. Corresponding measurements during N and H were compared statistically. Arterial O2 tension (P
aO2) was normal on N-day. All subjects showed a marked acute hypoxia at rest [P
aO2, 54.5 (SD 4.6) mmHg], during exercise and recovery on H-day. The latter was associated with tachycardia compared to N-day. All echocardiographic measurements at rest were within the limits of normal values on both test days. Ejection time, end-systolic and end-diastolic left ventricular dimensions as well as the thickness of left posterior wall and of interventricular septum showed no statistically significant influence of H either at rest or during exercise. Stroke volume and cardiac output were always higher on H-day, which could be attributed to a slight reduction in end-systolic volume with unaffected end-diastolic volume as well as to increased heart rates. Among the indices of systolic LV function the fractions of thickening in the left ventricular posterior wall and interventricular septum showed no differences between H and N at rest or during exercise. However, fibre shortening, ejection fraction and mean circumferential fibre shortening were increased on H-day on all occasions. The mitral-valve-Doppler ratio, the index of diastolic LV function, was decreased with H at rest, showed a more pronounced reduction during exercise and was still lower in 6th min of recovery compared to N-day. It was concluded that with acute hypoxia of the severity applied in this study left ventricular systolic function in our healthy subjects showed a pronounced improvement and left ventricular diastolic function was reduced, both at rest and with exercise. 相似文献
42.
缺氧促进热休克蛋白70在肺动脉平滑肌细胞中的表达 总被引:2,自引:0,他引:2
缺氧性肺动脉高压中肺动脉结构重组,中膜平滑肌细胞增殖并迁移,但机制不明。本研究观察缺氧对肺动脉平滑肌细胞(PASMC)细胞周期、DNA合成及细胞增殖的影响,并通过观察缺氧对PASMC热休克蛋白70(HSP70)表达的影响,初步探讨缺氧的作用是如何介导的。结果表明缺氧可直接或协同内皮质-1促进PASMC DNA合成及细胞增殖,并可增加HSP70在PASMC中的表达。 相似文献
43.
内皮衍生舒张因子对缺血(缺氧),再灌注(复氧)心肌的保护作用 总被引:13,自引:1,他引:12
血管内皮产生的内皮衍生舒张因子(endothelium-derived relaxing factor,EDRF)即一氧化氮(nitric oxide,NO)本工作分别在大鼠Langendorff离体心脏灌流模型和培养的大鼠心肌细胞上观察了NO、NO的前体物质L-精氨酸(L-Arg)、NO的前体物质L-精氨酸(L-Arg)、NO的合成阻断剂L-硝基精氨酸(L-NNA)对心肌缺血(缺氧)再灌注(复氧 相似文献
44.
内皮素-1对缺氧肺动脉平滑肌细胞的增殖作用 总被引:2,自引:0,他引:2
内皮素(ET)是至今所发现的最强的内源性血管收缩肽,近年来发现ET-1能促进血管平滑肌细胞增殖。本研究表明ET-1对缺氧培养的肺动脉平滑肌细胞(PASMC)有剂量依赖的增殖作用,缺氧可促进PASMC的DNA合成且增加ET-1的丝裂原作用。ET-1的丝裂原作用主要由其A型受体(ETR_A)所介导,ETR_A的特异拮抗剂BQ123可显著抑制缺氧以及缺氧与ET-1协同所产生的增殖作用,而且发现ETR_A在缺氧培养的PASMC中的表达显著高于常氧对照组PASMC。本研究表明ET-1参与了缺氧性肺动脉结构重组,而缺氧可增强PASMC对ET-1的增殖反应性。 相似文献
45.
46.
Robert L. Vender 《In vitro cellular & developmental biology. Animal》1992,28(6):403-409
Summary The development of pulmonary hypertension in a wide variety of human disease states and experimental animal models characterized
by chronic alveolar hypoxia is mediated by two pathologic vascular processes, a) vasoconstriction and b) vasoconstruction
(structural remodeling). The anatomic changes seen within the pulmonary circulation include a) increased deposition of collagen
and elastin in the adventitial layer and b) aberrant pulmonary vascular smooth muscle cell proliferation and maturation in
the medial segments. Despite the demonstrated ability of pharmacologic manipulation in the experimental animal to ameliorate
both the structural and hemodynamic changes, the actual etiologic mechanisms are only beginning to be explored. Using the
cell culture technique of co-cultivation, we have investigated the potential role of bovine pulmonary arterial endothelial
cell-derived factors in mediating abnormal bovine smooth muscle cell growth under conditions of reduced oxygen tension. We
have demonstrated that these cultured endothelial cells exposed in vitro to reduced levels of atmospheric oxygen concentrations
of 5.0% and 2.5% O2 for durations of 24 to 72 h produce and secrete soluble growth factor(s) which stimulate smooth muscle cell proliferation
when compared to cells maintained under standard tissue culture oxygen conditions of 95% room air. This growth-stimulatory
effect required the concomitant presence of serum factors (0.5% fetal bovine serum), was inhibited by heparin, was distinct
from platelet-derived growth factor, and seemed to have a molecular weight greater than 14 000 Da. We conclude that reduced
levels of oxygen tension in vitro can selectively induce pulmonary arterial endothelial cells to release mitogen(s) which
can stimulate vascular smooth muscle replication. Furthermore, we speculate that this in vitro finding may be of importance
as an etiologic mechanism to explain the accelerated smooth muscle cell growth characteristic of hypoxic pulmonary arteriopathy. 相似文献
47.
《Cell metabolism》2020,31(1):115-130.e6
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48.
49.
Nirvana Sadaghianloo Julie Contenti Maeva Dufies Julien Parola Matthieu Rouleau Shinrong Lee Jean-François Peyron Lucilla Fabbri Réda Hassen-Khodja Jacques Pouysségur Frédéric Bost Elixène Jean-Baptiste Alan Dardik Nathalie M. Mazure 《Journal of cellular and molecular medicine》2020,24(5):2931-2941
Arteriovenous fistulas (AVFs) are the preferred vascular access for haemodialysis of patients suffering from end-stage renal disease, a worldwide public health problem. However, they are prone to a high rate of failure due to neointimal hyperplasia and stenosis. This study aimed to determine if osteopontin (OPN) was induced in hypoxia and if OPN could be responsible for driving AVF failure. Identification of new factors that participate in remodelling of AVFs is a challenge. Three cell lines representing the cells of the three layers of the walls of arteries and veins, fibroblasts, smooth muscle cells and endothelial cells, were tested in mono- and co-culture in vitro for OPN expression and secretion in normoxia compared to hypoxia after silencing the hypoxia-inducible factors (HIF-1α, HIF-2α and HIF-1/2α) with siRNA or after treatment with an inhibitor of NF-kB. None of the cells in mono-culture showed OPN induction in hypoxia, whereas cells in co-culture secreted OPN in hypoxia. The changes in oxygenation that occur during AVF maturation up-regulate secretion of OPN through cell-cell interactions between the different cell layers that form AVF, and in turn, these promote endothelial cell proliferation and could participate in neointimal hyperplasia. 相似文献
50.