ArticleCritical care (London, England)2006
Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia.
Article in Critical care (London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- DNA-PKcs Phosphorylates Cofilin2 to Induce Endothelial Dysfunction and Microcirculatory Disorder in Endotoxemic Cardiomyopathy.Research (Washington, D.C.) · 2024Article
- Furosemide exacerbated the impairment of renal function, oxygenation and medullary damage in a rat model of renal ischemia/reperfusion induced AKI.Intensive care medicine experimental · 2023Article
- Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development.Biology · 2023Review
- Kidney Microcirculation as a Target for Innovative Therapies in AKI.Journal of clinical medicine · 2021Review
- Septic acute kidney injury: a review of basic research.Clinical and experimental nephrology · 2020Review
- The effects of acute renal denervation on kidney perfusion and metabolism in experimental septic shock.BMC nephrology · 2017Article
- Physiological aspects of Toll-like receptor 4 activation in sepsis-induced acute kidney injury.Acta physiologica (Oxford, England) · 2017Review
- THE ENDOTHELIUM IN SEPSIS.Shock (Augusta, Ga.) · 2016Review
- Mitochondrial function and disturbances in the septic kidney.Seminars in nephrology · 2015Review
- Activated protein C ameliorates impaired renal microvascular oxygenation and sodium reabsorption in endotoxemic rats.Intensive care medicine experimental · 2013Article
- Renal macro- and microcirculation autoregulatory capacity during early sepsis and norepinephrine infusion in rats.Critical care (London, England) · 2013Article
- PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice.The Journal of clinical investigation · 2011Article
- The impact of crystalloid and colloid infusion on the kidney in rodent sepsis.Intensive care medicine · 2010Article
- Renal haemodynamic, microcirculatory, metabolic and histopathological responses to peritonitis-induced septic shock in pigs.Critical care (London, England) · 2008Article
- Mechanisms of critical illness--classifying microcirculatory flow abnormalities in distributive shock.Critical care (London, England) · 2006Review
- Iloprost as an acute kidney injury-triggering agent in severely atherosclerotic patients.Cardiovascular journal of AfricaArticle
- Renal hypoxia and dysoxia after reperfusion of the ischemic kidney.Molecular medicine (Cambridge, Mass.)Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSeptic renal failure is often seen in the intensive care unit but its pathogenesis is only partly understood. This study, performed in a normotensive rat model of endotoxemia, tests the hypotheses that endotoxemia impairs renal microvascular PO2 (microPO2) and oxygen consumption (VO2,ren), that endotoxemia is associated with a diminished kidney function, that fluid resuscitation can restore microPO2, VO2,ren and kidney function, and that colloids are more effective than crystalloids.
methodsMale Wistar rats received a one-hour intravenous infusion of lipopolysaccharide, followed by resuscitation with HES130/0.4 (Voluven), HES200/0.5 (HES-STERIL 6%) or Ringer's lactate. The renal microPO2 in the cortex and medulla and the renal venous PO2 were measured by a recently published phosphorescence lifetime technique.
resultsEndotoxemia induced a reduction in renal blood flow and anuria, while the renal microPO2 and VO2,ren remained relatively unchanged. Resuscitation restored renal blood flow, renal oxygen delivery and kidney function to baseline values, and was associated with oxygen redistribution showing different patterns for the different compounds used. HES200/0.5 and Ringer's lactate increased the VO2,ren, in contrast to HES130/0.4.
conclusionThe loss of kidney function during endotoxemia could not be explained by an oxygen deficiency. Renal oxygen redistribution could for the first time be demonstrated during fluid resuscitation. HES130/0.4 had no influence on the VO2,ren and restored renal function with the least increase in the amount of renal work.
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