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Received for publication April 25, 2003.
Revised May 19, 2003.
Accepted for publication August 21, 2003.
Acute hyperglycemia evokes gastric slow wave dysrhythmias via endogenous prostaglandin generation. Ginger exhibits slow wave antiarrhythmic effects in other models, but its actions on hyperglycemia-evoked gastric dysrhythmias are unexplored. We hypothesized that ginger prevents disruption of slow wave rhythm by acute hyperglycemia via inhibition of prostaglandin production but not its actions. 22 healthy humans underwent fasting electrogastrography (EGG) during hyperglycemic clamping to 250-290 mg/dl after double-blind placebo or ginger root (1 gm). Responses were compared to the prostaglandin E1 analog misoprostol (400 µ g). Dominant frequencies (DF) and the % recording times in the bradygastric (0.5-2 cycles per min), normal (2-4 cpm), and tachygastric (4-9 cpm) frequency ranges were analyzed. After placebo, hyperglycemia reduced normal 2- 4 cpm activity from 94.4±2.6 to 66.0± 10.4%, increased the DF from 2.96±0.04 to 4.09 ±0.45 cpm, and increased tachygastria from 2.0 ±1.4 to 29.3±10.7% (P<0.05). Hyperglycemia effects on normal activity (77.3± 8.3%), DF (3.46±0.37 cpm), and tachygastria (15.6 ±8.6%) were significantly reduced by ginger (P<0.05). Misoprostol evoked decreases in normal activity from 95.4±2.0 to 81.7±3.0%, rises in DF from 2.98±0.06 to 3.16±0.11 cpm, and increases in tachygastria from 3.1±1.6 to 11.2±2.4 % (P<0.05). However, ginger did not correct these abnormalities versus placebo (P=NS). In conclusion, acute hyperglycemia evokes gastric slow wave dysrhythmias which are prevented by ginger root. Conversely, the compound has no effect on dysrhythmias elicited by a prostaglandin E1 analog indicating that ginger likely acts to blunt production of prostaglandins rather than inhibiting their action. These findings suggest novel mechanisms for the traditional Chinese herbal remedy ginger.
Key words:
diabetes, gastric slow wave, gastrointestinal motility, ginger, hyperglycemia, prostaglandins
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