Metabolische und histologische Veränderungen in Nieren nach 2 oder 3 Stunden Ischämie und Wiederdurchblutungszeiten bis zu 20 Tagen

Thorn, W.; Jacobs, Georg; Lapp, Harald; Wichert, P. v.

doi:10.1007/bf00362457

Cited by 32 publications

(5 citation statements)

References 5 publications

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“…Late regeneration of adenine nucleotide must occur by the slower de novo synthesis. With severe injury this may take several days [28] and presumably must await replacement of sloughed tubular epithelium.…”

Section: G M Collins Et Al: Kidney Preservationmentioning

confidence: 99%

Adenine nucleotide levels in preserved and ischemically injured canine kidneys

et al. 1977

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This study explored the relationship between adenine nucleotide levels in canine renal cortex and renal function following: (a) graded periods of warm ischemia; (b) 48 hours' flush cooling with electrolyte solutions and ice storage; and (c) continuous hypothermic perfusion. Exposure to normothermic ischemia resulted in a rapid (within 15 minutes) degradation of ATP to ADP and AMP as well as a slow decline in total adenine nucleotide (TAN) to levels which were proportional to the duration of the ischemie injury. No functional impairment was evident after 15 minutes' ischemia, but with longer times, both the extent of decline in TAN and the degree of recovery following restoration of blood flow could be used to predict the quality of renal function.The relationship between TAN levels and function was of less predictive value following cold storage or continuous perfusion. The efficacy of intracellular flush solutions could not be attributed solely to conservation of TAN, nor did the well-maintained TAN levels during continuous perfusion necessarily lead to significantly better 48-hour storage than flush cooling with C2 solution.

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Section: G M Collins Et Al: Kidney Preservationmentioning

confidence: 99%

Adenine nucleotide levels in preserved and ischemically injured canine kidneys

et al. 1977

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“…The increase in kidney weight during the early phase and the later decrease had been previously observed with this same method (18) and with other methods (11,6,25). At 48 h, the weight gain coincided with a minimal diuresis, a maximal occurrence of cast formation and an increased tissue water content, all suggesting the possibility of tubular obstruction and hydronephrosis.…”

Section: Discussionmentioning

confidence: 52%

Concentrating Mechanism and Histology During the Course of Unilateral Acute Renal Failure in the Dog

Arrizurieta¹,

Paz²,

Coelho³

et al. 1968

Nephron

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Unilateral acute renal failure was induced in dogs by a one hour clamping of the renal pedicle followed by an intravenous injection of acid hematin. The contralateral kidney remained largely unaffected and served as a control. The animals were then divided in four groups and studied at 2, 7, 12 and 21 days after the initial procedure. A diminished urine flow, urinary concentration and urea excretion were found in the damaged kidney, along with a decreased medullary content of sodium and urea, an increased medullary tissue water and histologic alterations. Concentrating capacity and tissue sodium and urea content were still reduced at the 12th day but were largely recovered after 21 days. Numerous distal intratubular casts, proximal tubular collapse and degeneration of proximal and distal convolutions and ascending loops of Henle were predominant at 48 h, followed later by progressive proximal and distal tubular dilatation and a decreasing number of casts. At 21 days the histologic picture was almost normal. The findings show that the urinary concentrating defect is mainly a consequence of a decreased medullary content of sodium and urea. Histologically evident damage to the ascending limb of Henle suggests that an impaired sodium transport at this level could be partly responsible for the decreased medullary sodium content. Other mechanisms contributing significantly to the medullary depletion of sodium and urea could be a primary fall in GFR and/or a massive backdiffusion of filtrate at the proximal tubules.

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“…In the intact animal, the nucleotide breakdown products released from the ischemic cells are available to the ischemic organ for only a short period after restoration of the circulation owing to their rapid utilization by the rest of the body and their removal from the substrate pool by conversion to uric acid [5,21,22]. In the absence of substrate for purine salvage pathways, adenine nucleotide regeneration must proceed by the slow de novo synthetic pathways, taking several days for completion [23]. Furthermore, even if substrate were freely available to the recovering kidney, adenine nucleotide regeneration might still be limited by prolongation into the recovery period of the effects of ischemic cell swelling.…”

Section: Discussionmentioning

confidence: 99%

In vitro regeneration of adenine nucleotide by ischemically injured kidney

1979

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Degradation of adenine nucleotide is a prominent feature of renal ischemic injury, the significance of which is still uncertain. In the present study, the conditions required for regeneration of adenine nucleotide by ischemically injured rabbit and dog kidneys were investigated using a slice incubation and isolated organ perfusion model. Regeneration in the whole organ was dependent on species, temperature, colloid concentration, and the presence of nucleoside as substrate. Under optimal conditions, slice incubation and perfusion yielded comparable results, and regeneration by ischemic tissue was equivalent to that of fresh tissue. These data suggest that the low adenine nucleotide levels after ischemic injury do not result from metabolic failure so much as from a local unavailability of substrate.

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Metabolische und histologische Veränderungen in Nieren nach 2 oder 3 Stunden Ischämie und Wiederdurchblutungszeiten bis zu 20 Tagen

Cited by 32 publications

References 5 publications

Adenine nucleotide levels in preserved and ischemically injured canine kidneys

Adenine nucleotide levels in preserved and ischemically injured canine kidneys

Concentrating Mechanism and Histology During the Course of Unilateral Acute Renal Failure in the Dog

In vitro regeneration of adenine nucleotide by ischemically injured kidney

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