Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi

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Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi. / Petersen, H K; Henriksen, Jens Henrik Sahl.

In: Clinical physiology (Oxford, England), Vol. 4, No. 1, 1984, p. 41-50.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Petersen, HK & Henriksen, JHS 1984, 'Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi', Clinical physiology (Oxford, England), vol. 4, no. 1, pp. 41-50.

APA

Petersen, H. K., & Henriksen, J. H. S. (1984). Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi. Clinical physiology (Oxford, England), 4(1), 41-50.

Vancouver

Petersen HK, Henriksen JHS. Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi. Clinical physiology (Oxford, England). 1984;4(1):41-50.

Author

Petersen, H K ; Henriksen, Jens Henrik Sahl. / Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi. In: Clinical physiology (Oxford, England). 1984 ; Vol. 4, No. 1. pp. 41-50.

Bibtex

@article{2a0d8d004b8c11df928f000ea68e967b,
title = "Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi",
abstract = "Peroperative measurements of renal blood flow (RBF), renal O2-uptake, and renal venous lactate/pyruvate (L/P) ratio were performed before and after a period of 30-71 min of hypothermic (10-15 degrees C) renal ischaemia in nine patients, undergoing surgery for renal calculi. Before ischaemia, RBF correlated inversely to arterial-renal venous O2-difference (r = -0.74, P less than 0.05, n = 9) and directly to the preoperatively estimated unilateral glomerular filtration rate (r = 0.76, P less than 0.05, n = 8). After hypothermic ischaemia RBF decreased on the average by 42% (P less than 0.01) immediately after re-established perfusion and 36% (P less than 0.02) 30 min later. In one additional patient, who had a short warm ischaemia (8 min), the flow pattern was the same. As arterial pressure remained constant, the reduced RBF signifies an increased renal vascular resistance. Renal O2-uptake and renal venous L/P ratio were almost constant, indicating no significant anaerobic processes being involved in the flow response. None of the patients showed any signs of reactive hyperaemia. It is concluded that hypothermic renal ischaemia may be followed by an increased renal vascular resistance even when signs of anaerobic metabolism are sparse or absent. This conception is in contrast to that gained from previous animal experiments where anaerobic processes are kept responsible for the changes. The mechanism behind the described response is unknown, but the changes are probably reversible.",
author = "Petersen, {H K} and Henriksen, {Jens Henrik Sahl}",
note = "Keywords: Adult; Female; Humans; Hypothermia, Induced; Ischemia; Kidney; Kidney Calculi; Lactates; Male; Middle Aged; Oxygen Consumption; Postoperative Period; Pyruvates; Regional Blood Flow; Renal Circulation; Vascular Resistance",
year = "1984",
language = "English",
volume = "4",
pages = "41--50",
journal = "Clinical Physiology",
issn = "0144-5979",
publisher = "Blackwell Science Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - Renal blood flow and metabolism after cold ischaemia: peroperative measurements in patients with calculi

AU - Petersen, H K

AU - Henriksen, Jens Henrik Sahl

N1 - Keywords: Adult; Female; Humans; Hypothermia, Induced; Ischemia; Kidney; Kidney Calculi; Lactates; Male; Middle Aged; Oxygen Consumption; Postoperative Period; Pyruvates; Regional Blood Flow; Renal Circulation; Vascular Resistance

PY - 1984

Y1 - 1984

N2 - Peroperative measurements of renal blood flow (RBF), renal O2-uptake, and renal venous lactate/pyruvate (L/P) ratio were performed before and after a period of 30-71 min of hypothermic (10-15 degrees C) renal ischaemia in nine patients, undergoing surgery for renal calculi. Before ischaemia, RBF correlated inversely to arterial-renal venous O2-difference (r = -0.74, P less than 0.05, n = 9) and directly to the preoperatively estimated unilateral glomerular filtration rate (r = 0.76, P less than 0.05, n = 8). After hypothermic ischaemia RBF decreased on the average by 42% (P less than 0.01) immediately after re-established perfusion and 36% (P less than 0.02) 30 min later. In one additional patient, who had a short warm ischaemia (8 min), the flow pattern was the same. As arterial pressure remained constant, the reduced RBF signifies an increased renal vascular resistance. Renal O2-uptake and renal venous L/P ratio were almost constant, indicating no significant anaerobic processes being involved in the flow response. None of the patients showed any signs of reactive hyperaemia. It is concluded that hypothermic renal ischaemia may be followed by an increased renal vascular resistance even when signs of anaerobic metabolism are sparse or absent. This conception is in contrast to that gained from previous animal experiments where anaerobic processes are kept responsible for the changes. The mechanism behind the described response is unknown, but the changes are probably reversible.

AB - Peroperative measurements of renal blood flow (RBF), renal O2-uptake, and renal venous lactate/pyruvate (L/P) ratio were performed before and after a period of 30-71 min of hypothermic (10-15 degrees C) renal ischaemia in nine patients, undergoing surgery for renal calculi. Before ischaemia, RBF correlated inversely to arterial-renal venous O2-difference (r = -0.74, P less than 0.05, n = 9) and directly to the preoperatively estimated unilateral glomerular filtration rate (r = 0.76, P less than 0.05, n = 8). After hypothermic ischaemia RBF decreased on the average by 42% (P less than 0.01) immediately after re-established perfusion and 36% (P less than 0.02) 30 min later. In one additional patient, who had a short warm ischaemia (8 min), the flow pattern was the same. As arterial pressure remained constant, the reduced RBF signifies an increased renal vascular resistance. Renal O2-uptake and renal venous L/P ratio were almost constant, indicating no significant anaerobic processes being involved in the flow response. None of the patients showed any signs of reactive hyperaemia. It is concluded that hypothermic renal ischaemia may be followed by an increased renal vascular resistance even when signs of anaerobic metabolism are sparse or absent. This conception is in contrast to that gained from previous animal experiments where anaerobic processes are kept responsible for the changes. The mechanism behind the described response is unknown, but the changes are probably reversible.

M3 - Journal article

C2 - 6538130

VL - 4

SP - 41

EP - 50

JO - Clinical Physiology

JF - Clinical Physiology

SN - 0144-5979

IS - 1

ER -

ID: 19345119