Differential responses of cerebral and renal oxygenation to altered perfusion conditions during experimental cardiopulmonary bypass in sheep

Author:

Evans Roger G.12ORCID,Cochrane Andrew D.3,Hood Sally G.2,Marino Bruno4,Iguchi Naoya25,Bellomo Rinaldo167,McCall Peter R.78,Okazaki Nobuki29,Jufar Alemayehu H.12,Miles Lachlan F.278,Furukawa Taku2,Ow Connie P. C.2,Raman Jaishankar610,May Clive N.27,Lankadeva Yugeesh R.27

Affiliation:

1. Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology Monash University Melbourne Victoria Australia

2. Pre‐clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health University of Melbourne Melbourne Victoria Australia

3. Department of Cardiothoracic Surgery, Monash Health and Department of Surgery (School of Clinical Sciences at Monash Health) Monash University Melbourne Victoria Australia

4. Cellsaving and Perfusion Resources Melbourne Victoria Australia

5. Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medicine Osaka University Osaka Japan

6. Department of Intensive Care, Austin Health Heidelberg Victoria Australia

7. Department of Critical Care, Melbourne Medical School University of Melbourne Victoria Australia

8. Department of Anaesthesia, Austin Health Heidelberg Victoria Australia

9. Department of Anesthesiology and Resuscitology Okayama University Okayama Japan

10. Faculty of Medicine, Dentistry and Health Sciences University of Melbourne Victoria Australia

Abstract

AbstractWe tested whether the brain and kidney respond differently to cardiopulmonary bypass (CPB) and to changes in perfusion conditions during CPB. Therefore, in ovine CPB, we assessed regional cerebral oxygen saturation (rSO2) by near‐infrared spectroscopy and renal cortical and medullary tissue oxygen tension (PO2), and, in some protocols, brain tissue PO2, by phosphorescence lifetime oximetry. During CPB, rSO2 correlated with mixed venous SO2 (r = 0.78) and brain tissue PO2 (r = 0.49) when arterial PO2 was varied. During the first 30 min of CPB, brain tissue PO2, rSO2 and renal cortical tissue PO2 did not fall, but renal medullary tissue PO2 did. Nevertheless, compared with stable anaesthesia, during stable CPB, rSO2 (66.8 decreasing to 61.3%) and both renal cortical (90.8 decreasing to 43.5 mm Hg) and medullary (44.3 decreasing to 19.2 mm Hg) tissue PO2 were lower. Both rSO2 and renal PO2 increased when pump flow was increased from 60 to 100 mL kg−1 min−1 at a target arterial pressure of 70 mm Hg. They also both increased when pump flow and arterial pressure were increased simultaneously. Neither was significantly altered by partially pulsatile flow. The vasopressor, metaraminol, dose‐dependently decreased rSO2, but increased renal cortical and medullary PO2. Increasing blood haemoglobin concentration increased rSO2, but not renal PO2. We conclude that both the brain and kidney are susceptible to hypoxia during CPB, which can be alleviated by increasing pump flow, even without increasing arterial pressure. However, increasing blood haemoglobin concentration increases brain, but not kidney oxygenation, whereas vasopressor support with metaraminol increases kidney, but not brain oxygenation.

Funder

National Heart Foundation of Australia

National Health and Medical Research Council

State Government of Victoria

Publisher

Wiley

Reference73 articles.

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