| Numerous studies showed that, gastric motility hyperfunction and gastric acid over-secretionwere two key factors of gastric mucosal injury induced by the restraint water-immersion stressin peripheral in rats. The two factors were incited by the parasympathetic hyperactivity in stress.The parasympathetic nerves innervating the gastrointestinal tract are mainly originated from thedorsal motor nucleus of the vagus (DMV) and the nucleus ambiguous (NA) in the medullaoblongata, and the gastrointestinal sensory nerves are mostly projected to the nucleus of solitarytract (NTS) and area postrema (AP). So, the DMV, NTS, AP (the three parts are called thedorsal vagal complex, DVC) and NA constitute the primary center of the gastrointestinalfunction. As well we know, the senior center regulating the gastrointestinal function is in thehypothalamus and amygdaloid complex. Large number of papers reported the fibers linkbetween the two centers and gastrointestinal tract, and the regulatory mechanism in the restraintwater-immersion stress. But the most senior central pathway is not clear. The prefrontal cortexis the only cortex projecting directly to hypothalamus, and activities of the prefrontal cortex(especially PL and IL) neurons were increased during the restraint water-immersion stress in therat (the results from our lab). Therefore it can be surmised that the prefrontal cortex mayberegulate gastric function during the restrain water-immersion stress in rats. In this study, it isplaned to explore the function of the prefrontal cortex from the point of gastric motility andgastric acid secretion.The article was composed of acute experiments and chronic experiments.The acute experiments:1) The left PL and IL were electrically stimulated respectively to monitor the changes ofgastric motility. The parameters of stimulation were square-wave pulses of 30Hz, 0.2mA, 0.5msand the stimulating time lasted 5min. To do this, two groups of experiments were performed:PL group and IL group. Gastric motility curves were recorded with intraluminal balloons andthe Physiological Signal Recording System(BL-420E). The frequency, average duration, total duration, average amplitude, total amplitude, index of motility and contraction fraction of thegastric contraction waves were taken as the indexes to estimate the gastric motility function.The above indexes within 5min before and after stimulation were analyzed. The results showedthere was no significant effect on gastric motility no matter PL or Il was electrically stimulated.It prompted us that PL and IL have no regulation on gastric motility in normal rats underanesthesia.2) PL and IL were electrically stimulated respectively to monitor the changes of gastric acidsecretion, respiratory rate and heart rate. The parameters of stimulation and the groups ofexperiments were the same as 1), but the stimulating time lasted 10min. Gastric acid in whichthe amounts of H+was taken as index was collected with perfusion technique and was detectedby acid-base titration. Gastric juice was collected every 15min for three times before and afterstimulation respectively. The average amounts of H+before stimulation was compared with thedata after stimulation. The results showed that gastric acid secretion had no significant changesbefore and after stimulation. It was supposed that PL and IL have no regulation on gastric acidsecretion in normal rats under anesthesiaThe upper two results showed that there were no relationships between mPFC andgastrointestinal primary center, but anesthesia might obscure the role of the PL and IL under thenormal physiological state.The chronic experiment:1) Electrolytic lesions were placed in PL, and IL. Changes of gastric motility before andduring 4h restraint water-immersion stress were monitored. PL and IL were destroyed with DCcurrent (1.5mA, 4s) two times. Four groups of experiments, including group of control, groupof bilateral PL and IL lesions, group of bilateral PL lesions and group of bilateral IL lesions,were performed. Four days later, the rats were restrained, and were immersed in cold water(21±1℃) for 4h. Gastric motility was recorded at the same time. Statistical indexes were thesame as the acute experiments 1). The results showed that:①Before the restraintwater-immersion stress, there were no significant differences in all gastric motility indexesbetween the control group and the experimental groups under the awake state. It could beconcluded that mPFC did not participate in the regulation of functional activity of the stomach under normal physiological conditions, and anesthesia had no influence.②The gastric motilityof the bilateral PL and IL lesions group was significantly inhibited during the restraintwater-immersion stress, compared no matter with before stress or with the control group.Comparing with the control group, the bilateral IL lesions group had a significant reduction ofthe total amplitude in the fourth hour, but there were no significant changes in the group ofbilateral PL lesions. It was supposed that PL and IL regulate gastric motility under the restraintwater-immersion stress in rats.2) Electrolytic lesions were placed in PL and IL, and changes of gastric acid secretion weremonitored also under the restraint water-immersion stress. The parameters of stimulation werethe same as 1). Two groups of experiments, including group of bilateral PL and IL lesions,group of its control. Pylorus ligation method was used to collect gastric juice, and thesupernatant after centrifugation was got for acid-base titration. Gastric juice volume, amountsof H+and concentration of H+were taken as the statistical indexes. The results showed thatthere were no significant differences between the tow groups. It was supposed that PL and ILhave no regulation on gastric acid secretion under the restraint water-immersion stress.It could be concluded that PL and IL, to some extent, were involved in regulating the gastricmotility during the restraint water-immersion stress, and the function of IL is prior and therewere synergistic effects between PL and IL. PL and IL have no regulatory effect on gastricgland cells. |
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