Early Metabolic Effects of Hypotension on Rat Kidney

Freeman, Dominique M.; Chan, Laurence; Yahaya, Haliru; Holloway, Paul; Ross, Brian D.

doi:10.1159/000173199

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…In this combina tion, renal CrP is very low [14] and thus contributes little. ADP in tissues consists of a bound (immobile) and an (mobile) unbound fraction [15,16].…”

Section: Discussionmentioning

confidence: 88%

Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?

Lambalgen¹,

Kraats²,

Bos³

et al. 1993

Nephron

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Endotoxin shock not only causes renal failure, endotoxemia also leads to metabolic impairment, resulting in energy shortage and loss of cellular integrity; therefore, we tested the hypothesis that early changes in renal metabolism contribute to the development of acute renal failure during endotoxin shock. Endotoxin (Escherichia coli127B8; 8 mg/kg from t = 0 to 60 min) was infused in three groups of 8 rats, in which renal biopsies were taken at t = 30,50 and 90 min, respectively; a fourth group (n – 8) served as control. In the biopsies, glucose, lactate, ATP, ADP, AMP and creatine phosphate concentrations were determined. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured from the clearances of ¹³¹I-hippurate and ¹²⁵I-thalamate, respectively. We also assayed urine flow (V; catheter in the bladder), cardiac output (CO), blood pressure (MAP), heart rate (HR) and arterial lactate, glucose and creatinine concentrations. During the first 30 min of endotoxemia, we found no systemic hemodynamic or biochemical changes. From t = 30 to t = 90, CO and MAP decreased to 59 and 70%, respectively, while HR and serum levels rose to 110 and 800%, respectively (p < 0.05), indicating progression of shock. Renal function clearly deteriorated from t = 30: at t = 90 RPF, GFR and V had decreased by 86, 84 and 86%, respectively, plasma creatinine being 193% of the baseline value (p < 0.05). In the t = 30 biopsies, the only change was an increase in glucose concentration (by 21% vs. control value; p < 0.05), which peaked at t = 50 (by 63%; p < 0.05), and was still elevated at t = 90 (by 43%; p < 0.05). The rise in renal lactate concentration paralleled that in serum lactate. There were, however, no differences in energy-rich phosphates between the four groups. Thus, our results show that endotoxemia causes early changes in RPF, GFR, V and renal glucose metabolism, but no early decrease in energy status.

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“…In this combina tion, renal CrP is very low [14] and thus contributes little. ADP in tissues consists of a bound (immobile) and an (mobile) unbound fraction [15,16].…”

Section: Discussionmentioning

confidence: 88%

Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?

Lambalgen¹,

Kraats²,

Bos³

et al. 1993

Nephron

View full text Add to dashboard Cite

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Renal corticomedullary metabolite gradients during graded arterial occlusion

Parivar

Narasimhan²,

Ross³

1991

Journal of the American Society of Nephrology

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In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.

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Early Metabolic Effects of Hypotension on Rat Kidney

Cited by 2 publications

References 10 publications

Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?

Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?

Renal corticomedullary metabolite gradients during graded arterial occlusion

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