TY - JOUR
T1 - Haemodynamic influences on kidney oxygenation: clinical implications of integrative physiology
AU - Evans, Roger G
AU - Ince, Can
AU - Joles, Jaap A
AU - Smith, David W
AU - May, Clive N
AU - O'Connor, Paul M
AU - Gardiner, Bruce S
PY - 2013
Y1 - 2013
N2 - Renal blood flow, local tissue perfusion and blood oxygen content are the major determinants of oxygen delivery to kidney tissue. Arterial pressure and segmental vascular resistance influence kidney oxygen consumption through effects on glomerular filtration rate and sodium reabsorption Diffusive shunting of oxygen from arteries to veins in the cortex, and from descending to ascending vasa recta in the medulla, limits oxygen delivery to renal tissue. Oxygen shunting depends on the vascular network, renal haemodynamics and kidney oxygen consumption. Consequently, the impact of changes in renal haemodynamics on tissue oxygenation cannot necessarily be predicted intuitively, and instead requires the integrative approach offered by computational modelling and multiple measuring modalities Tissue hypoxia is a hallmark of acute kidney injury (AKI) arising from multiple initiating insults, including ischaemia-reperfusion injury, radio-contrast administration, cardiopulmonary bypass surgery, shock and sepsis. Its pathophysiology is defined by inflammation and/or ischaemia resulting in alterations in renal tissue oxygenation, nitric oxide bioavaliability and oxygen radical homeostasis. This sequence of events appears to cause renal microcirculatory dysfunction, which might then be exacerbated by inappropriate use of therapies common in peri-operative medicine such as fluid resuscitation Development of new ways to prevent and treat AKI requires an integrative approach which considers not just the molecular mechanisms underlying failure of filtration and tissue damage, but also the contribution of haemodynamic factors which determine kidney oxygenation. Development of bedside monitors allowing continuous surveillance of renal haemodynamics, oxygenation, and function should facilitate better prevention, detection and treatment of AKI (c) 2012 The Authors Clinical and Experimental Pharmacology and Physiology (c) 2012 Wiley Publishing Asia Pty Ltd.
AB - Renal blood flow, local tissue perfusion and blood oxygen content are the major determinants of oxygen delivery to kidney tissue. Arterial pressure and segmental vascular resistance influence kidney oxygen consumption through effects on glomerular filtration rate and sodium reabsorption Diffusive shunting of oxygen from arteries to veins in the cortex, and from descending to ascending vasa recta in the medulla, limits oxygen delivery to renal tissue. Oxygen shunting depends on the vascular network, renal haemodynamics and kidney oxygen consumption. Consequently, the impact of changes in renal haemodynamics on tissue oxygenation cannot necessarily be predicted intuitively, and instead requires the integrative approach offered by computational modelling and multiple measuring modalities Tissue hypoxia is a hallmark of acute kidney injury (AKI) arising from multiple initiating insults, including ischaemia-reperfusion injury, radio-contrast administration, cardiopulmonary bypass surgery, shock and sepsis. Its pathophysiology is defined by inflammation and/or ischaemia resulting in alterations in renal tissue oxygenation, nitric oxide bioavaliability and oxygen radical homeostasis. This sequence of events appears to cause renal microcirculatory dysfunction, which might then be exacerbated by inappropriate use of therapies common in peri-operative medicine such as fluid resuscitation Development of new ways to prevent and treat AKI requires an integrative approach which considers not just the molecular mechanisms underlying failure of filtration and tissue damage, but also the contribution of haemodynamic factors which determine kidney oxygenation. Development of bedside monitors allowing continuous surveillance of renal haemodynamics, oxygenation, and function should facilitate better prevention, detection and treatment of AKI (c) 2012 The Authors Clinical and Experimental Pharmacology and Physiology (c) 2012 Wiley Publishing Asia Pty Ltd.
UR - http://www.ncbi.nlm.nih.gov/pubmed/23167537
U2 - 10.1111/1440-1681.12031
DO - 10.1111/1440-1681.12031
M3 - Article
SN - 0305-1870
VL - 40
SP - 106
EP - 122
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
IS - 2
ER -