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Renal hypoxia and lactate metabolism in hemorrhagic shock in dogs.
Crit Care Med. 1984 Aug; 12(8):656-60.CC

Abstract

Central and renal hemodynamics, renal cortical and medullary oxygen tension, and renal lactate metabolism were investigated in hemorrhagic shock in dogs. During graded hemorrhage, renal tissue PO2 decreased in parallel with renal blood flow, whereas renal lactate uptake remained virtually unchanged. During shock, below a mean arterial pressure (MAP) of 72 mm Hg, renal lactate utilization declined in parallel with tissue PO2. Renal lactate was produced at an MAP of 38 mm Hg. Reinfusion of shed blood increased renal tissue PO2 above its preshock value but did not restore baseline renal oxygen consumption and lactate uptake levels. These results suggest that renal lactate utilization is not limited by oxygen delivery under moderate hemorrhagic hypotension but decreases linearly with renal tissue PO2 during shock.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

6744906

Citation

Nelimarkka, O, et al. "Renal Hypoxia and Lactate Metabolism in Hemorrhagic Shock in Dogs." Critical Care Medicine, vol. 12, no. 8, 1984, pp. 656-60.
Nelimarkka O, Halkola L, Niinikoski J. Renal hypoxia and lactate metabolism in hemorrhagic shock in dogs. Crit Care Med. 1984;12(8):656-60.
Nelimarkka, O., Halkola, L., & Niinikoski, J. (1984). Renal hypoxia and lactate metabolism in hemorrhagic shock in dogs. Critical Care Medicine, 12(8), 656-60.
Nelimarkka O, Halkola L, Niinikoski J. Renal Hypoxia and Lactate Metabolism in Hemorrhagic Shock in Dogs. Crit Care Med. 1984;12(8):656-60. PubMed PMID: 6744906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal hypoxia and lactate metabolism in hemorrhagic shock in dogs. AU - Nelimarkka,O, AU - Halkola,L, AU - Niinikoski,J, PY - 1984/8/1/pubmed PY - 1984/8/1/medline PY - 1984/8/1/entrez SP - 656 EP - 60 JF - Critical care medicine JO - Crit Care Med VL - 12 IS - 8 N2 - Central and renal hemodynamics, renal cortical and medullary oxygen tension, and renal lactate metabolism were investigated in hemorrhagic shock in dogs. During graded hemorrhage, renal tissue PO2 decreased in parallel with renal blood flow, whereas renal lactate uptake remained virtually unchanged. During shock, below a mean arterial pressure (MAP) of 72 mm Hg, renal lactate utilization declined in parallel with tissue PO2. Renal lactate was produced at an MAP of 38 mm Hg. Reinfusion of shed blood increased renal tissue PO2 above its preshock value but did not restore baseline renal oxygen consumption and lactate uptake levels. These results suggest that renal lactate utilization is not limited by oxygen delivery under moderate hemorrhagic hypotension but decreases linearly with renal tissue PO2 during shock. SN - 0090-3493 UR - https://www.unboundmedicine.com/medline/citation/6744906/Renal_hypoxia_and_lactate_metabolism_in_hemorrhagic_shock_in_dogs_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=6744906.ui DB - PRIME DP - Unbound Medicine ER -