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Cerebral blood flow and cerebral edema in rats with diabetic ketoacidosis

Natalie Yuen1, Steven E Anderson, Nicole Glaser

  • 1Department of Physiology and Membrane Biology, University of California, Davis, California, USA.

Diabetes
|July 18, 2008
PubMed

Insights

Cerebral edema in diabetic ketoacidosis (DKA) is linked to reduced cerebral blood flow (CBF). Blocking ion transport with bumetanide may help reduce brain swelling during DKA treatment.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Pediatrics

Background:

  • Cerebral edema (CE) is a serious complication of diabetic ketoacidosis (DKA) in children.
  • Traditionally, osmotic shifts during DKA treatment were blamed, but recent evidence suggests cerebral hypoperfusion and ion transporter activation may play a role.
  • Diminished cerebral blood flow (CBF) in DKA has not been previously demonstrated.

Purpose of the Study:

  • To investigate CBF and edema formation in a rat model of DKA.
  • To determine the effects of bumetanide, an inhibitor of Na-K-Cl cotransport, on CE and CBF during DKA treatment.

Main Methods:

  • Juvenile rats with streptozotocin-induced DKA were treated with intravenous saline and insulin.
  • CBF was measured using MR perfusion-weighted imaging.
  • CE was assessed by MR diffusion-weighted imaging to determine apparent diffusion coefficients (ADCs).

Main Results:

  • CBF was significantly reduced in DKA rats and responsive to pCO(2) changes.
  • Reduced ADC values indicated cell swelling, correlating with dehydration.
  • Bumetanide increased ADCs without altering CBF, while saline/insulin increased CBF and gradually increased ADCs.
  • Combined bumetanide and saline/insulin treatment showed a trend toward faster ADC increases and greater CBF rise.

Conclusions:

  • CE in DKA is associated with cerebral hypoperfusion prior to treatment.
  • Inhibiting Na-K-Cl cotransport with bumetanide may reduce cerebral cell swelling in DKA.
Abstract

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