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Dynamic responses of renal oxygenation at the onset of cardiopulmonary bypass in sheep and man.
Evans, Roger G; Cochrane, Andrew D; Hood, Sally G; Iguchi, Naoya; Marino, Bruno; Bellomo, Rinaldo; McCall, Peter R; Okazaki, Nobuki; Smith, Julian A; Zhu, Michael Zl; Ngo, Jennifer P; Noe, Khin M; Martin, Andrew; Thrift, Amanda G; Lankadeva, Yugeesh R; May, Clive N.
Afiliação
  • Evans RG; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
  • Cochrane AD; Department of Cardiothoracic Surgery, Monash Health and Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Melbourne, Victoria, Australia.
  • Hood SG; Pre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia.
  • Iguchi N; Pre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia.
  • Marino B; Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
  • Bellomo R; Cellsaving and Perfusion Resources, Melbourne, Victoria, Australia.
  • McCall PR; Department of Intensive Care, Austin Health, Heidelberg, Victoria, Australia.
  • Okazaki N; Department of Anaesthesia, Austin Health, Heidelberg, Victoria, Australia.
  • Smith JA; Pre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia.
  • Zhu MZ; Department of Anesthesiology and Resuscitology, Okayama University, Okayama, Japan.
  • Ngo JP; Department of Cardiothoracic Surgery, Monash Health and Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Melbourne, Victoria, Australia.
  • Noe KM; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
  • Martin A; Department of Cardiothoracic Surgery, Monash Health and Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Melbourne, Victoria, Australia.
  • Thrift AG; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
  • Lankadeva YR; Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan.
  • May CN; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
Perfusion ; 37(6): 624-632, 2022 09.
Article em En | MEDLINE | ID: mdl-33977810
ABSTRACT

INTRODUCTION:

The renal medulla is susceptible to hypoxia during cardiopulmonary bypass (CPB), which may contribute to the development of acute kidney injury. But the speed of onset of renal medullary hypoxia remains unknown.

METHODS:

We continuously measured renal medullary oxygen tension (MPO2) in 24 sheep, and urinary PO2 (UPO2) as an index of MPO2 in 92 patients, before and after induction of CPB.

RESULTS:

In laterally recumbent sheep with a right thoracotomy (n = 20), even before CPB commenced MPO2 fell from (mean ± SEM) 52 ± 4 to 41 ±5 mmHg simultaneously with reduced arterial pressure (from 108 ± 5 to 88 ± 5 mmHg). In dorsally recumbent sheep with a medial sternotomy (n = 4), MPO2 was even more severely reduced (to 12 ± 12 mmHg) before CPB. In laterally recumbent sheep in which a crystalloid prime was used (n = 7), after commencing CPB, MPO2 fell abruptly to 24 ±6 mmHg within 20-30 minutes. MPO2 during CPB was not improved by adding donor blood to the prime (n = 13). In patients undergoing cardiac surgery, UPO2 fell by 4 ± 1 mmHg and mean arterial pressure fell by 7 ± 1 mmHg during the 30 minutes before CPB. UPO2 then fell by a further 12 ± 2 mmHg during the first 30 minutes of CPB but remained relatively stable for the remaining 24 minutes of observation.

CONCLUSIONS:

Renal medullary hypoxia is an early event during CPB. It starts to develop even before CPB, presumably due to a pressure-dependent decrease in renal blood flow. Medullary hypoxia during CPB appears to be promoted by hypotension and is not ameliorated by increasing blood hemoglobin concentration.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ponte Cardiopulmonar / Injúria Renal Aguda Limite: Animals / Humans Idioma: En Revista: Perfusion Assunto da revista: CARDIOLOGIA Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Austrália

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ponte Cardiopulmonar / Injúria Renal Aguda Limite: Animals / Humans Idioma: En Revista: Perfusion Assunto da revista: CARDIOLOGIA Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Austrália