Neurochemical mechanism of the gastrointestinal interdigestive migrating motor complex in rats with acute inflammatory stomach ache

The normal gastrointestinal interdigestive migrating motor complex cycle was interrupted, and paroxysmal contraction appeared after formaldehyde-induced stomach ache. Activities of nitric oxide synthase, acetylcholinesterase and vasoactive intestinal peptide neurons were significantly reduced, whereas activities of calcitonin gene-related peptide neurons were significantly increased in the pyloric sphincter muscular layer, myenteric nerve plexus and submucous nerve plexus. Electroacupuncture at Zusanfi （ST36） suppressed paroxysmal contraction in rats with formaldehyde-induced stomach ache, and neurons in the enteric nervous system were normal. These results indicated that nitrergic neurons, cholinergic neurons, vasoactive intestinal peptide neurons and calcitonin gene-related peptide neurons in the enteric nervous system may be involved in changes to the gastrointestinal interdigestive migrating motor complex following stomach ache, and that electroacupuncture can regulate this process.

EFECT OF ERYTHROMYCIN ON INTERDIGESTIVE MIGRATING MOTOR COMPLEX IN HUMANS

Objective To investigate the effect of erythromycin (EM) on interdigestive migrating motor complex (MMC) in healthy volunteers. Methods 20 healthy volunteers were randomly divided into 2 groups: EM group (n=11) and placebo group (n=9). The changes of MMC were observed by gastrointestinal manometry before and after oral administration of EM or placebo. Results Gastric antral MMCs that evoked by EM were similar to spontaneous MMCs. EM orally intaking decreased MMC cycle duration significantly (P<0.05). EM orally intaking decreased the percentage of phase Ⅱ duration to MMC cycle duration significantly (P<0.05). But EM orally intaking increased the percentage of phase Ⅲ duration to MMC cycle duration significantly (P<0.05). The amplitude of antral waves of phase Ⅲ increased significantly after EM orally intaking (P<0.05). Placebo orally intaking didn't affect MMC cycle duration, propagation velocity of phase Ⅲ and percentages of phase Ⅰ, phase Ⅱ, phase Ⅲ duration to MMC cycle duration. Conclusion EM has stimulating effect on gastrointestinal motor activity.

THE ROLE OF NITRIC OXIDE IN SMALL INTESTINAL MIGRATING MOTOR COMPLEX

The main objective is to study the role or nitric oxide (NO) in small Intestinal migratingmotor complex (MMC). Rats were implanted with strain gauges in the duobenum and jejunum forrecording the motor action of the small intestine in fasting and red states arter intravenous infusionof N'-nitro-L-arginine methyl ester (L-NAME ), L-arginin., D-arglnine, sodium nitropusside(NaNP) and angiotensin 1 respectively. The results showed that intravenous inrusion or L-NAME,a NO synthase inhibitor, induced a fasting-like MMC motor pattern in fed rats. Infusion of NaNP, aNO donor, disrupted small intestinal MMC in fasting rats, inducing a postprandial-like motor pattern. Both fasting and postprandial, infusion of L-NAME shortened the duration or Phase I andphase Ⅱ,but didn't chang. the duration, frequency, amplitude and s,eed or Propogatiou of thephaSe, Ⅲ-argining, not D-arginine infused together with L-NAME, prevented the effect of LNAME infusion. Infusion of L-arginine, D-arginine or angioteusin Ⅰ alone didn't modify the smallintestinal motor pattern. It suggests that an inhibition of NO synthesis may be involved in the initiation of the MMC motor pattern during fasting, whereas an increase of NO output relates to the occurrence of the fed motor pattern

Xiangbinfang granules enhance gastric antrum motility via intramuscular interstitial cells of Cajal in mice

BACKGROUND Interdigestive migrating motor complexes(MMC)produce periodic contractions in the gastrointestinal tract,but the exact mechanism of action still remains unclear.Intramuscular interstitial cells of Cajal(ICC-IM)participate in gastrointestinal hormone and neuromodulation,but the correlation between ICCIM and MMC is also unclear.We found that xiangbinfang granules(XBF)mediated the phase III contraction of MMC.Here,the effects of XBF on gastric antrum motility in W/Wv mice and the effects of ICC-IM on gastric antrum MMC are reported.AIM To observe the effects of ICC-IM on gastric antrum motility and to establish the mechanism of XBF in promoting gastric antrum motility.METHODS The density of c-kit-positive ICC myenteric plexus(ICC-MP)and ICC-IM in the antral muscularis of W/Wv and wild-type(WT)mice was examined by confocal microscopy.The effects of XBF on gastric antrum slow waves in W/Wv and WT mice were recorded by intracellular amplification recording.Micro-strain-gauge force transducers were implanted into the gastric antrum to monitor the MMC and the effect of XBF on gastric antrum motility in conscious W/Wv and WT mice.RESULTS In the gastric antrum of W/Wv mice,c-kit immunoreactivity was significantly reduced,and no ICC-IM network was observed.Spontaneous rhythmic slow waves also appeared in the antrum of W/Wv mice,but the amplitude of the antrum slow wave decreased significantly in W/Wv mice(22.62±2.23 mV vs 2.92±0.52 mV,P<0.0001).MMCs were found in 7 of the 8 WT mice but no complete MMC cycle was found in W/Wv mice.The contractile frequency and amplitude index of the gastric antrum were significantly increased in conscious WT compared to W/Wv mice(frequency,3.53±0.18 cpm vs 1.28±0.12 cpm;amplitude index,23014.26±1798.65 mV·20 min vs 3782.16±407.13 mV·20 min;P<0.0001).XBF depolarized smooth muscle cells of the gastric antrum in WT and W/Wv mice in a dose-dependent manner.Similarly,the gastric antrum motility in WT mice was significantly increased after treatment with XBF 5 mg(P<0.05).Atropine(0.1 mg/kg)blocked the enhancement of XBF in WT and W/Wv mice completely,while tetrodotoxin(0.05 mg/kg)partially inhibited the enhancement by XBF.CONCLUSION ICC-IM participates in the regulation of gastric antrum MMC in mice.XBF induces MMC III-like contractions that enhance gastric antrum motility via ICCIM in mice.

Changes of gastrointestinal myoelectric activity and bile acid pool during cholesterol gallstone formation in guinea pig

It has been known that enterohepatic circulation of bile acids is essential for regular cycling of migrating motor complex （MMC）. An important component of the enterohepatic circulation is the active reabsorption of conjugated bile acids in the terminal ileum, with special reference to bile acid pool size that may be defined as the total mass of bile acids in the enterohepatic circulation. However, because of technical difficulties in measuring of bile acid pool size in human being, the role of the bile acid pool has little been investigated, and the exact mechanism of change in bile acid pool size has not yet been clear. Therefore, were there two changes of small intestinal motility and bile acid pool size in cholesterol gallstone patients？ and, if so, was there correlated relationship between both alterations require further investigation？