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Erschienen in:
01.02.2003 | Experimental
Inhibitory effects of hyperglycemia on neural activity of the vagus in rats
Erschienen in: Intensive Care Medicine | Ausgabe 2/2003
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Objectives
Although it has been demonstrated that hyperglycemia inhibits gastrointestinal (GI) motility, its inhibitory mechanism remains unclear.
Design
Electrophysiological study.
Settings
As GI motility is under the influence of the vagus, we studied the effects of hyperglycemia on neural activity of the dorsal motor nucleus of vagi (DMV) in anesthetized rats.
Measurements and results
A tungsten electrode was placed in the left side of the DMV area and extracellular electrical signals from the electrode were recorded. Single unit nerve activity was identified by the discriminator. D-glucose infusion elevated the peripheral blood glucose concentration from 3.4–5.9 mm to 12.0–21.8 mm and the neural firing of the DMV was significantly reduced by D-glucose infusion. After the 30 min D-glucose infusion, saline was re-infused for 90 min. Blood glucose level returned to 6.5–7.8 mm and the neural firing partially recovered 90 min after the saline re-infusion. There was a significant negative correlation observed between the counts of neural spikes and blood glucose concentrations ( r =0.84, p <0.01).
Conclusion
It is suggested that hyperglycemia impairs GI motility by inhibiting vagal efferent activity. A recent study in intensive care unit (ICU) patients demonstrated that uncontrolled hyperglycemia is associated with poor outcomes. We propose that glycemia control is crucial in ICU patients to maintain the GI motility and vagus nerve activity.