External oxidation pathway in nerve tissue

Institute of Pharmacology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. V. Val'dman.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 4, pp. 431–433, April, 1989.     

High-altitude pulmonary edema

Lay summary: High Altitude Pulmonary Edema (HAPE) is a potentially fatal disease of altitude, in which the lungs can become filled with fluid. In this article we explore the mechanisms causing this condition and how it can be viewed as a condition of a mismatch between current environment and evolutionary experience.     

牛磺酸对培养乳鼠心肌细胞缺氧坏死的保护作用

目的　观察牛磺酸 (Tau)对缺氧引起的心肌细胞坏死有无直接保护作用。方法　将培养心肌细胞分为正常对照、Tau对照缺氧 Tau和缺氧 4个组。测定培养细胞上清液中肌酸磷酸激酶 (CPK)活性 ,用原子吸收法测定细胞内钙、镁含量 ,Annexin V- FITC/ PI双染流式细胞术和台盼蓝染色镜检检测坏死细胞。结果　 Tau可使缺氧时培养细胞上清液中CPK活性降低 30 % ,坏死细胞减少大约 2 0 %。减少细胞内钙超载和镁丢失。结论　 Tau对缺氧导致的心肌细胞坏死有直接保护作用 ,此作用可能与减少细胞内钙超载和镁丢失有关。     

缺氧预适应小鼠脑组织中缺氧诱导因子-1的表达

为探讨缺氧诱导因子 1 (HIF 1 )在缺氧预适应小鼠脑组织中的表达 ,用Western印迹法检测慢性缺氧 (H)和不缺氧 (C)HeLa细胞、急性重复性缺氧 0次 (H0 )、1次 (H1)、4次 (H4 )小鼠脑组织中的HIF 1α。结果 :慢性缺氧HeLa细胞中可检测到较多的HIF 1α,H0 组脑组织中检测不到HIF 1α ,H1组检测到微量HIF 1α,H4 组检测到较多HIF 1α。结果显示 :脑组织中HIF 1α的含量随缺氧预适应的产生而逐步增加 ,提示HIF 1可能参与缺氧预适应的形成。     

普鲁卡因对缺氧心肌细胞的影响

目的 探讨普鲁卡因对心肌细胞缺氧损伤的影响。方法 将原代培养成活48h的大鼠乳鼠心肌细胞分为三组：A组为对照组（氰化钠造成心肌细胞内缺氧模型）,B组为Prol组（缺氧＋7．4mg／L普鲁卡因）,C组为Pro2组（缺氧＋14．8mg／L普鲁卡因）。比较三组心肌细胞形态学（倒置相差显微镜、透射电镜观察）的变化及吸光度A值的改变。结果 缺氧12h后,对照组细胞搏动功能变化明显,呈散在细胞搏动,而实验组搏动频率减慢。随着时间的延长,细胞形态学变化逐渐明显,对照组较实验组变化更显著。结论 普鲁卡因对培养心肌细胞缺氧损伤有一定的保护作用。     

The Effect of Erigeron Breviscapus on Proliferation of Pulmonary Artery Smooth Muscle Cells in Hypoxic Porcines

Erigeron breviscapus can relax microarteries,improve microcirculation,increase tissue bloodstream,enhance heart function and decrease bloodviscosity.Presently,good curative effects on is-chemia has been achieved,but few studies have beenconducted on the treatment of hypoxic pulmonaryhypertension( HPH) .In this study,MTT and ex-pression of PCNA was used to examine the prolifera-tion of PASMC and investigate the mechanism of ef-fectof EB on HPH.1　 MATERIALSAND METHODS1 .1　 Cult…     

人参皂甙Rg1对缺氧豚鼠心肌细胞游离钙浓度降低作用的研究

目的探讨人参皂甙(ginsentosides,Gin)单体Rgl及维拉帕米(verapamil,Ver)对豚鼠心肌细胞内游离钙浓度([Ca2+]i)变化的影响.方法采用离体豚鼠心脏Langendorff法灌注,胶原酶Ⅰ型分离心肌细胞,用荧光指示剂方法(Fura-2/AM)标记心肌([Ca2+]i)变化.将心肌细胞悬液分为3组对照组、Rgl组和Ver组.观察缺氧后心肌[Ca2+]i的变化.结果(1)正常氧状态心肌[Ca2+]i均值为(125.4±10.3)nmol/L(n=20).(2)缺氧状态下,心肌[Ca2+]i增加与缺氧时间(程度)直线相关,相关系数r为0.98左右.(3)Rgl对缺氧后心肌[Ca2+]i增加明显延缓.结论Rgl在缺氧条件下,使心肌[Ca2+]i明显下降,从而阻止心肌细胞内钙超载,其作用与Ver相似,我们认为Rgl具有心肌细胞的保护作用.     

不同抗炎药物对缺氧所致大鼠离体肺血管环张力变化的影响

为研究离体大鼠肺血管在缺氧时张力的变化,以及甾体、非甾体类抗炎药物对此变化影响的异同性,采用等长收缩技术,测定加入消炎痛或地塞米松前后张力改变的特点及两药作用的差异。结果发现Wistar大鼠与Sprague-Dawley大鼠肺血管环对缺氧的反应不同,后者仅出现收缩反应,而Wistar大鼠在收缩前出现一内皮依赖的舒张;COX非特异性抑制剂消炎痛对缺氧所致的舒张和收缩均有增强作用;COX-2特异性抑制剂地塞米松则在明显抑制舒张的同时轻度增强收缩反应。结果表明不同种属大鼠的肺血管缺氧反应可能存在差异;缩管性PGs和扩管性PGs分别调节急性肺血管缺氧的舒张和收缩反应,这一过程呈一定的内皮依赖性;非选择性和选择性的COX抑制剂对肺血管缺氧反应的作用不尽相同。     

Effects of cobalt and chromium ions on glycolytic flux and the stabilization of hypoxia‐inducible factor‐1α in macrophages in vitro

Implant wear and corrosion have been associated with adverse tissue reactions that can lead to implant failure. Wear and corrosion products are therefore of great clinical concern. For example, Co²⁺ and Cr³⁺ originating from CoCrMo‐based implants have been shown to induce a proinflammatory response in macrophages in vitro. Previous studies have also shown that the polarization of macrophages by some proinflammatory stimuli is associated with a hypoxia‐inducible factor‐1α (HIF‐1α)‐dependent metabolic shift from oxidative phosphorylation (OXPHOS) towards glycolysis. However, the potential of Co²⁺ and Cr³⁺ to induce this metabolic shift, which plays a determining role in the proinflammatory response of macrophages, remains largely unexplored. We recently demonstrated that Co²⁺, but not Cr³⁺, increased oxidative stress and decreased OXPHOS in RAW 264.7 murine macrophages. In the present study, we analyzed the effects of Co²⁺ and Cr³⁺ on glycolytic flux and HIF‐1α stabilization in the same experimental model. Cells were exposed to 6 to 24 ppm Co²⁺ or 50 to 250 ppm Cr³⁺. Glycolytic flux was determined by analyzing extracellular flux and lactate production, while HIF‐1α stabilization was analyzed by immunoblotting. Results showed that Co²⁺, and to a lesser extent Cr³⁺, increased glycolytic flux; however, only Co²⁺ acted through HIF‐1α stabilization. Overall, these results, together with our previous results showing that Co²⁺ increases oxidative stress and decreases OXPHOS, suggest that Co²⁺ (but not Cr³⁺) can induce a HIF‐1α‐dependent metabolic shift from OXPHOS towards glycolysis in macrophages. This metabolic shift may play an early and pivotal role in the inflammatory response induced by Co²⁺ in the periprosthetic environment.