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Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

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Cardiac function and tolerance to ischemia-reperfusion injury in chronic kidney disease

James M Kuczmarski1, Christopher R Martens2, Shannon L Lennon-Edwards3

  • 1Department of Kinesiology and Applied Physiology, University of Delaware, 25 N College Avenue, McDowell Hall, Newark, DE 19716, USA Department of Biological Sciences, University of Delaware, Newark, DE, USA.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|October 24, 2013
PubMed

Insights

Impaired cardiac function in chronic kidney disease (CKD) rats worsened outcomes after ischemia-reperfusion injury. This may be due to increased oxidative stress and nitric oxide pathway dysfunction.

Area of Science:

  • Cardiovascular Science
  • Nephrology
  • Biochemistry

Background:

  • Cardiac dysfunction is a significant risk factor for ischemic heart disease and mortality in chronic kidney disease (CKD) patients.
  • The impact of impaired cardiac function on ischemia-reperfusion (IR) injury tolerance in experimental CKD is not well understood.

Purpose of the Study:

  • To investigate the relationship between impaired cardiac function and tolerance to IR injury in a rat model of CKD.
  • To explore the underlying biochemical mechanisms, including oxidative stress and nitric oxide pathways.

Main Methods:

  • Assessed cardiac function in 5/6 ablation-infarction (AI) rats and sham controls using an isolated working heart system.
  • Measured left ventricular (LV) function curves during preload/afterload manipulation and post-ischemia reperfusion.
  • Performed biochemical analysis of LV tissue for oxidative stress markers and nitric oxide metabolites.

Main Results:

  • AI rats exhibited impaired cardiac function and reduced recovery post-ischemia, with 36% failing to achieve aortic overflow.
  • Lower urinary NOx excretion and reduced LV endothelial nitric oxide synthase in AI rats.
  • Decreased LV antioxidants (superoxide dismutase) and increased oxidative stress markers (NADPH-oxidase, H2O2) in AI rats.

Conclusions:

  • Impaired cardiac function in AI rats predisposes them to poor outcomes following ischemic insult.
  • Increased oxidative stress, involving both nitric oxide-dependent and -independent pathways, may mediate these adverse effects.
Abstract

Keywords:
cardiac dysfunctioncardiac ischemia–reperfusion injurychronic kidney diseasenitric oxideoxidative stress

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