Role of hydrogen sulfide within the dorsal motor nucleus of the vagus in the control of gastric function in rats.

BACKGROUND: Hydrogen sulfide (H2 S) is a gaseous messenger and serves as an important neuromodulator in the central nervous system. This study aimed to clarify the role of H2 S within the dorsal motor nucleus of the vagus (DMV) in the control of gastric function in rats. METHODS: Cystathionine ß-synthetase (CBS) is an important generator of endogenous H2 S in the brain. We investigated the distribution of CBS in the DMV using immunohistochemical method, and the effects of H2 S on gastric motility and on gastric acid secretion. KEY RESULTS: CBS-immunoreactive (IR) neurons were detected in the rostral, intermediate and caudal DMV, with the highest number of CBS-IR neurons in the caudal DMV, and the lowest in the intermediate DMV. We also found that microinjection of the exogenous H2 S donor NaHS (0.04 and 0.08 mol/L; 0.1 µL; n = 6; p < 0.05) into the DMV significantly inhibited gastric motility with a dose-dependent trend, and promoted gastric acid secretion in Wistar rats. Microinjection of the same volume of physiological saline (PS; 0.1 µL, n = 6, p > 0.05) at the same location did not noticeably change gastric motility and acid secretion. CONCLUSIONS & INFERENCES: The data from these experiments suggest that the CBS that produces H2 S is present in the DMV, and microinjection of NaHS into the DMV inhibited gastric motility and enhanced gastric acid secretion in rats.

Role of nitric oxide in the control of the gastric motility within the nucleus ambiguus of rats.

This study aims to investigate whether exogenous nitric oxide (NO) plays a role in controlling gastric motility within the nucleus ambiguus (NA). Experiments were performed on male Wistar rats anaesthetized with chloral hydrate. A latex balloon, connected to a pressure transducer, was inserted into the pylorus through the fundus for continuous recording of the change of gastric smooth muscle contractile curves. Microinjection of the NO-donor sodium nitroprusside (SNP; 5 nmol) or L-arginine (L-Arg; 5 nmol) into the NA significantly inhibited gastric motility, whereas the treatment of NO-synthase inhibitor N-nitro-L-arginine methylester (L-NAME) increased gastric motility remarkably. The negative effect of SNP or L-Arg on gastric motility was abolished by bilateral subdiaphragmatic vagotomy as well as by intravenous injection of ganglionic blocker, hexamethonium bromide (Hb). These results demonstrated that NO inhibited gastric motility by activating the cholinergic preganglionic neurons in the NA and through the mediation of vagus nerves.

Effects and mediated pathway of electrical stimulation of nucleus ambiguus on gastric motility and mucus secretion in rats.

BACKGROUND: It has been reported that nucleus ambiguus (NA) can regulate gastric motility. However, gastric motility is enhanced or inhibited after NA is excited, and reports have been inconsistent. Does NA affect gastric mucus secretion? This has been unreported up to now. We researched the effects of electrical stimulation of NA on gastric motility and mucus secretion in rats. MATERIAL AND METHODS: The rats were divided into three groups. Group I, right NA was stimulated by four stimulation parameters. Group II, left NA was stimulated by the same parameters. The four stimulation parameters were 30 Hz 0.15 mA, 30 Hz 0.20 mA, 40 Hz 0.15 mA and 40 Hz 0.20 mA, and the width of all stimulation pulses was 0.30 ms. Group III, right NA was stimulated after the vagus nerves beneath the diaphragm were cut. RESULTS: Electrical stimulations of both NAs significantly inhibited gastric motility, the right NA more so than the left. The results for group III show that the inhibitory effect of NA on gastric motility was withdrawn by vagotomy beneath the diaphragm. CONCLUSIONS: NA inhibits gastric motility and the inhibitory degree of right NA is more than that of left NA. The inhibitory effect is mediated by vagus nerves. However, NA has no effect on gastric mucus secretion.

[Studies on the time domain and power spectrum of high frequency ECG in normal mice].

The features of time domain and power spectrum of high frequency electrocardiogram (HF-ECG) were studied in normal Kunming mice using a microprocessor ECG system. The results were as follows (mean +/- SD): (1) P-R interval was 34.9 +/- 4.7 ms (n = 58), about one third of the cardiac cycle. (2) The duration and peak-to-peak amplitude of QRS complex were 9.2 +/- 1.2 ms and 1.456 +/- 0.480 mV (n = 74) respectively. (3) The duration and amplitude of T wave were 10.2 +/- 3.2 ms and 0.336 +/- 0.115 mV, respectively (n = 58). (4) Q-T interval was 19.4 +/- 3.2 ms (n = 58), about one fifth of the cardiac cycle. (5) The total number of notches and slurs of leads II of 73 mice were 3 and 26 respectively. (6) The relative power content of each frequency range was: 0-80 Hz: 45.48 +/- 15.32%; 80-200 Hz: 43.97 +/- 9.95%; 200-300 Hz: 8.89 +/- 7.83%; 300-1000 Hz: 1.66 +/- 2.74%; 80-1000 Hz: 54.52 +/- 15.32%.

[Studies on the mechanism of gastric mucosal injury induced by water-immersion stress in rats].

Changes in the degree of gastric mucosal injury, gastric acid output, secretion of gastric barrier mucus and gastric motility were made in 5 groups of rat: I, Restraint alone plus saline under room temperature; II, Water-immersion plus saline; III, Water-immersion plus atropine (0.5 mg/kg); IV, Water-immersion plus phenoxybenzamine (10 mg/kg); V, Water-immersion plus pentobarbital (30 mg/kg). The results were as follows: (1) Water-immersion stress resulted in severe gastric mucosal lesions, an increase in the gastric acid output, a decrease in the secretion of gastric barrier mucus and an increase in gastric motility. (2) Atropine attenuated gastric mucosal injury significantly, inhibited gastric acid output and gastric motility, while gastric barrier mucus was increased. (3) Sodium pentobarbital also significantly attenuated gastric mucosal injury and inhibited gastric motility, but had no effect on gastric acid output. (4) Phenoxybenzamine failed to affect on gastric mucosal injury, gastric acid output, gastric barrier mucus secretion and gastric motility. These results suggest that the gastric hypercontractility, the reduction of gastric barrier mucus and the increase in gastric acid output participate in varying degrees in the formation of gastric mucosal injury induced by water-immersion stress, but when gastric motility is inhibited and gastric barrier mucus increases, only the existence of gastric acid can not induce severe gastric mucosal injury.