Oxygen deprivation-induced injury to isolated rabbit kidney tubules.
Oxygen deprivation-induced injury to isolated rabbit kidney tubules.
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缺氧引起的离体兔肾小管损伤。
DOI：
10.1172/jci112075
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Weinberg,JM
中科院分区：
文献类型：
--
作者：
Weinberg,JM
评价了新鲜分离的富含近端肾小管的兔肾小管悬液用于研究缺氧诱导的肾小管细胞损伤的发病机制的效用。氧合对照制剂在超过2小时的时间内表现出非常好的关键细胞损伤相关代谢参数的稳定性，包括耗氧量、细胞阳离子稳态和腺嘌呤核苷酸代谢。开发了高度可重复的缺氧诱导的损伤和恢复模型，并详细描述了这些模型中损伤相关代谢参数的变化。当缺氧条件下产生的氧剥夺，肾小管持续广泛的致死性细胞损伤和相关的代谢改变在15-30分钟内。然而，当缺氧条件下产生的模拟缺血性条件下，肾小管耐受30-60分钟，只有适量的致死性细胞损伤发生，类似于在体内缺血所看到的情况。与体内缺血一样，体外模拟缺血的特征在于缺氧期间pH值下降。在缺氧模型中没有发生这样的pH下降。为了测试这种pH值的下降是否有助于在体外模拟缺血期间观察到的保护，将肾小管在中等pH值范围从7.45至6.41下进行缺氧。当pH值降低时，可以看到对缺氧损伤的显著保护，其中在pH值低于7.0时缺氧的小管中发生最大保护。损伤相关的代谢参数的测量表明，pH值降低的保护作用可能是介导的pH值诱导的肾小管细胞Ca++代谢的改变。因此，本研究详细定义和表征了一种新的和非常通用的模型系统，用于研究缺氧诱导的肾脏细胞损伤，并确定pH值的改变在调节这种损伤中起着重要作用。
The utility of freshly isolated suspensions of rabbit tubules enriched in proximal segments for studying the pathogenesis of oxygen deprivation-induced renal tubular cell injury was evaluated. Oxygenated control preparations exhibited very good stability of critical cell injury-related metabolic parameters including oxygen consumption, cell cation homeostasis, and adenine nucleotide metabolism for periods in excess of 2 h. Highly reproducible models of oxygen deprivation-induced injury and recovery were developed and alterations of injury-related metabolic parameters in these models were characterized in detail. When oxygen deprivation was produced under hypoxic conditions, tubules sustained widespread lethal cell injury and associated metabolic alterations within 15-30 min. However, when oxygen deprivation was produced under simulated ischemic conditions, tubules tolerated 30-60 min with only moderate amounts of lethal cell injury occurring, a situation similar to that seen with ischemia in vivo. Like ischemia in vivo, simulated ischemia in vitro was characterized by a fall in pH during oxygen deprivation. No such fall in pH occurred in the hypoxic model. To test whether this fall in pH could contribute to the protection seen during simulated ischemia in vitro, tubules were subjected to hypoxia at medium pHs ranging from 7.45 to 6.41. Striking protection from hypoxic injury was seen as pH was reduced with maximal protection occurring in tubules made hypoxic at pHs below 7.0. Measurements of injury-associated metabolic parameters suggested that the protective effect of reduced pH may be mediated by pH-induced alterations of tubule cell Ca++ metabolism. This study has, thus, defined and characterized in detail a new and extremely versatile model system for the study of oxygen deprivation-induced cell injury in the kidney and has established that pH alterations play a major role in modulating such injury.
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大鼠肾近端小管刷状缘膜相关磷脂酰肌醇磷酸二酯酶的表征。
影响因子：
3.9
作者：
Schwertz,DW;Kreisberg,JI;Venkatachalam,MA
通讯作者：
Venkatachalam,MA
完整肾细胞中线粒体呼吸能力以及 Na 和 K 依赖性三磷酸腺苷酶介导的离子转运。
DOI：
--
发表时间：
1981
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Harris,SI;Balaban,RS;Barrett,L;Mandel,LJ
通讯作者：
Mandel,LJ
影响因子：
3.5
作者：
MAPES, JP;HARRIS, RA
通讯作者：
HARRIS, RA
影响因子：
--
作者：
STRUYVEN.A;MORRISON, RB;RELMAN, AS
通讯作者：
RELMAN, AS
影响因子：
5.4
作者：
W. Guder;O. Wieland;B. Stukowski
通讯作者：
B. Stukowski