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Norepinephrine-induced hyperglycemia does not increase cortical lactate in brain-injured rats
John F Stover1, Oliver W Sakowitz, Ulrich W Thomale
1Department of Neurosurgery, Charité, Virchow Medical Center, Humboldt University Berlin, Germany. stover@mail.med.upenn.edu
Intensive Care Medicine
|October 10, 2002
Summary
Norepinephrine and dopamine increase brain glucose levels after injury, but do not worsen brain swelling or lactate levels. This suggests glucose enters the injured brain through a damaged blood-brain barrier.
Area of Science:
- Neuroscience
- Biochemistry
- Pathophysiology
Background:
- Hyperglycemia exacerbates ischemic brain damage.
- Catecholamines, like norepinephrine and dopamine, can increase blood glucose through hepatic gluconeogenesis.
- The direct impact of these catecholamines on brain glucose levels and edema formation post-injury is not fully understood.
Purpose of the Study:
- To investigate if norepinephrine and dopamine elevate arterial blood glucose.
- To determine if these catecholamines increase pericontusional cortical glucose and lactate concentrations.
- To assess the effect of norepinephrine and dopamine on brain edema in rats with focal cortical contusions.
Main Methods:
- A prospective, randomized, controlled animal study was conducted using male Sprague Dawley rats.
- Rats received intravenous infusions of physiological saline, norepinephrine, or dopamine for 90 minutes, starting 4.5 hours after inducing a focal cortical contusion.
- Blood glucose, lactate, and pericontusional cortical extracellular glucose and lactate were measured before, during, and after infusion. Brain water content was assessed post-mortem.
Main Results:
- Both norepinephrine and dopamine significantly increased pericontusional glucose concentrations, with norepinephrine having a more pronounced effect.
- Arterial blood glucose levels significantly increased only in norepinephrine-treated rats.
- The ratio of extracellular to blood glucose was significantly elevated in both dopamine- and norepinephrine-treated groups, while plasma and pericontusional lactate and brain edema remained unchanged.
Conclusions:
- Norepinephrine and dopamine administration leads to increased pericontusional glucose concentrations in brain-injured rats.
- These increases in glucose did not result in elevated extracellular lactate or aggravated posttraumatic brain edema.
- The elevated extracellular to blood glucose ratio suggests glucose entry via a damaged blood-brain barrier, potentially facilitated by increased endothelial transport.