Abstract
G A A b st ra ct s recovery. Then the rats were fed with 1.5ml phenol red solution mixed with methycellulose and EA was performed for 30min immediately after feeding. Gastric retention of phenol red was calculated by the spectrophotometric method. In the control session, no EA was performed. In another study, a gastric balloon was chronically implanted in 5 rats. Gastric accommodationwasmeasured by barostat with ramp distension before and after the induction of diabetes, and with and .without EA at ST36. Results: 1. EA improved gastric dysrhythmia in diabetic rats. The normal percentage of slow wave was 54.7 ± 4.0% at baseline and significantly increased to 68.4 ± 3.6% with EA (P < 0.01) and sustained at 67.8 ± 2.3% during recovery period and 67.1 ± 5.2 after the test meal (P < 0.01). 2. EA resulted in a 21.4% increase in gastric emptying in diabetic rats. Gastric emptying at 30minwas 75.1±5.0% in the control diabetic animals and 91.2±1.5% in the diabetic animals with EA (P=0.01). 3. EA improved impaired gastric accommodation. The confirmed diabetic rats showed a significantly decreased gastric accommodation (0.85 ± 0.14ml with diabetes vs. 0.69 ± 0.12ml before STZ injection, P = 0.05). EA at ST36 resulted in a striking effect on gastric accommodation with a mean increase of 87.8 ± 25.8% (P < 0.05). 4. EA significantly increased vagal activity and sympathovagal balance in diabetic rats. The high frequency (vagal component) was 0.55±0.05 at baseline and increased to 0.61 ± 0.03 during EA (P = 0.03); the LF/HF (sympathovagal balance) was 0.85 ± 0.13 at baseline and significantly decreased to 0.67 ± 0.08 during EA. Conclusion: EA at ST 36 improves impaired gastric accommodation, gastric dysrhythmia and delayed gastric emptying and the improvement may be mediated via the vagal pathway. EA may have a promising therapeutic potential for diabetic gastroparesis.
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