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  • 1
    Electronic Resource
    Electronic Resource
    Immature renal tubules are resistant to prolonged anoxia (1994)
    Springer
    Pediatric nephrology 8 (1994), S. 784-784 
    Details
    ISSN: 1432-198X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00869125
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Immature tubules are tolerant of oxygen deprivation (1997)
    Springer
    Pediatric nephrology 11 (1997), S. 757-760 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Immature renal tubules ; Glycolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The tolerance of immature tissues to injury has been noted over the past several decades. Traditional teaching relates this tolerance to energy derived from anaerobic glycolysis. This mini-review describes investigations of the hypothesis that the immature kidney is less susceptible to oxygen deprivation than the mature kidney. Utilizing proximal tubule suspensions from immature and mature rats, studies assessing ATP levels as an index of cellular energy and lactate dehydrogenase (LDH) release as a determinant of plasma membrane damage demonstrate the developing kidney is resistant to prolonged anoxia. ATP is maintained at twofold higher levels during anoxia in the immature tubule compared with the mature tubule. The contribution of anaerobic glycolysis to the tolerance of the immature renal tubules is investigated by two inhibitors of the glycolytic pathway, L-glucose and iodoacetate. Following 70% – 90% inhibition of glycolysis, ATP is decreased to similar levels in immature and mature tubules. However, immature tubules remain resistant to anoxic damage with no significant change in LDH release. Therefore, enhanced glycolytic activity does not play a dominant role in the tolerance of the developing kidney to anoxia, and this tolerance is not primarily dependent on preservation of cellular ATP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050384
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Beneficial effect of thyroxin in the treatment of ischemic acute renal failure (1988)
    Springer
    Pediatric nephrology 2 (1988), S. 1-7 
    Details
    ISSN: 1432-198X
    Keywords: Acute renal failure ; Thyroxin-Ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To evaluate the effect of thyroxin (T4) on recovery from ischemic acute renal failure, rats were treated with T4 (10 or 20 μg/100 g body wt.) or normal saline (NS) either immediately prior to, immediately after or 24 h after 45 min of renal ischemia. Animals given T4 prior to ischemia had no significant increase in Inulin clearance (Cin) (377±40 μl/min per 100 g body wt.) as compared with saline-treated ischemic controls (306±54). In contrast, animals treated immediately after ischemia with either dose of T4 demonstrated significantly better kidney function (Cin 515±59 μl/min per 100 g body wt., Uosm 842±88 mosmol/kg, FENa 0.52%±0.12% and Cin 543±71, Uosm 939±103, FENa 0.48±0.12, for 10 and 20 μg/100 g body wt., respectively). Moreover, the improvement in renal function was sustained and Cin was significantly better at day 3 (748±70) and day 7 (990±75) compared with saline controls (560±30 and 732±45, respectively). Animals which received T4 24 h after ischemia showed significantly higher Cin when compared with ischemic controls. To assess the impact of T4 on recovery of renal ATP,31P-NMR was used. T4-treated rats demonstrated 90%±5% recovery of renal ATP by 120 min of reflow, whereas NS animals had only 64%±1%. In addition, cellular morphology was better preserved in T4 animals. These data indicate that animals treated postischemically with T4 showed accelerated and sustained recovery from acute renal failure. This beneficial effect appears to be related to cellular mechanisms which are essential for the restoration of sublethally injured cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00870370
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  • 4
    Electronic Resource
    Electronic Resource
    Redistribution of cellular energy following renal ischemia (1991)
    Springer
    Pediatric nephrology 5 (1991), S. 591-596 
    Details
    ISSN: 1432-198X
    Keywords: Acute renal failure ; Na/K-ATPase activity ; Adenosine triphosphate ; Oxygen consumption ; Cellular respiration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to elucidate the pattern of redistribution of cellular energy and the restoration of basic cellular metabolism following an ischemic renal insult, suspensions enriched in proximal tubule segments were studied after 45 min of bilateral artery occlusion and 15 min and 2 h of reflow from rats given either normal saline (control), ATP-MgCl2 (which enhances postischemic recovery of ATP), or α, β-methyl adenosine diphosphate (AMPCP), which inhibits nucleotide degradation during ischemia. In non-ischemic control animals, approximately half of the energy is distributed to functional pump activity and half directed for non-transport purposes. When cellular ATP is reduced to 56% of control values, functional pump activity is significantly reduced to 61% of control, while energy delegated for non-transport purposes is decreased by a significantly smaller increment to only 78% of control at 15 min of reflow. In animals given ATP-MgCl2, the cellular and metabolic profile at 15 min of reflow was no different from ischemic control animals with cellular ATP levels similar at 58%. However, by 2 h, cellular ATP levels had increased significantly to 74%, and this was associated with a redistribution of cellular energy to functional pump activity (119% of control) with little change in non-transport function (76%). In animals treated with AMPCP, the cellular ATP levels were 74% of controls, similar to ATP-MgCl2-treated rats after 2 h of reflow. Despite the differences in reflow interval, the distribution of cellular energy was similar (functional pump activity 120% and non-transport activity 79%). By 2 h, cellular ATP was at 95% and both functional pump activity and non-transport activity were 100%. This early restoration of pump activity, followed by repletion of energy available for non-transport activity, is associated with minimal histological evidence of ischemic injury. These studies have shown: (1) a hierarchy of distribution of energy and maintenance of cellular metabolism; (2) there appears to exist a threshold requirement of ATP that is necessary to replete functional pump activity prior to redirecting energy for non-transport purposes; (3) energy redistribution following ischemia is not dependent upon time of reflow but upon replenishment of cellular energy; (4) repletion of transport and non-transport activities limits the degree of cellular damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00856647
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    An acellular human amnionic membrane model for in vitro culture of type ii pneumocytes: The role of the basement membrane in cell morphology and function (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 121 (1984), S. 215-225 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: To determine whether a preformed basement membrane contributes to the maintenance of morphology and function of type II pneumocytes, we cultured isolated adult rat type II pneumocytes on the basement membrane and stromal surfaces of an acellular human amnionic membrane and on plastic. The presence of lamellar bodies on transmission electron microscopy and epithelial morphology in culture and a characteristic phospholipid profile after incubation with 3H-acetate identified the cells as type II. When type II cells were cultured on a preexisting basement membrane, they formed a well-organized monolayer with polarity, centrally located surface microvilli, and more basally located nuclei. Individual cells maintained a cuboidal morphology for 8-10 days. Intracellularly, there were numerous mitochondria, endoplasmic reticulum (ER), and lamellar bodies. The cells secreted a new basal lamina of their own. When cultured on the stromal side of the amnion, the cells became flattened within 48-60 hours, formed small lamellar bodies, and had scanty surface microvilli; they formed clumps and appeared less ordered. These cells did not secrete a visible basement membrane, and the majority detached from the stromal surface after 7-8 days in culture. In addition, culture on the basement membrane aspect of the amnion prevented the rapid decline in the percentage of 3H-acetate label incorporated in phosphatidylcholine after 72 hours of culture. We conclude that a preformed basement membrane influences the function and morphology of type II pneumocytes, organizes them into a monolayer in culture, and influences deposition of a visible basal lamina. Thus, the acellular human amnion provides an excellent model for the systematic study of basement membrane influence on the biology and pathology of these cells.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041210127
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