In vitro studies showed that relaxations induced after vagal stimulation of the guinea pig stomach are mediated via nitric oxide (NO). The role of NO in canine gastric relaxation in response to vagal stimulation has as yet not been studied. The present study examined the influence of NG-nitro-L-arginine (L-NNA) on gastric relaxations after vagal nerve stimulation in the anesthetized dog. In beagle dogs (n = 7), the ventral and dorsal abdominal vagal nerves were connected to a pair of platinum electrodes. Gastric tone was measured by means of a barostat. Changes in gastric motility were measured with force transducers sutured on the fundus and the antrum. The cervical vagi were sectioned, and dogs were given atropine (0.2 mg/kg i.v.) and guanethidine (5 mg/kg i.v.). Electrical stimulation of the vagal trunks (19 V, 1-ms duration, for 15 s every 2 min, 1-30 Hz) induced frequency-dependent increases in volume. On the fundus, frequency-dependent relaxations could be observed (maximal effect at 5 mmHg and at 10 Hz). During electrical stimulation, the spontaneous antral contractions were completely blocked. After cessation of the stimulus, "rebound" contractions could be observed. L-NNA (5 mg/kg i.v.) completely blocked the increases in gastric volume and the relaxations on the fundus. On the antrum, however, contractions were observed during the electrical stimulation. L-Arginine (250 mg/kg i.v.) gradually restored the relaxations on electrical stimulation. This study demonstrates that NO mediates short-lasting vagally induced gastric relaxations in the anesthetized dog.
The effects of domperidone, cisapride, metoclopramide and bethanechol were determined on antroduodenal coordination, in vitro in the gastroduodenal preparation of the guinea pig and in vivo in conscious Beagle dogs implanted with strain gauge force transducers. In vitro dopamine inhibited and the dopamine antagonist domperidone stimulated antroduodenal coordination. The effect of domperidone was blocked by atropine or tetrodotoxin, but not by hexamethonium. Propranolol, prazosin, and yohimbine did not enhance antroduodenal coordination. Only at one of the concentrations tested did bethanechol moderately enhance antroduodenal coordination. Cisapride stimulated antroduodenal coordination in a dose-dependent manner. This effect could also be blocked by atropine or tetrodotoxin. Metoclopramide (at higher concentrations) also enhanced antroduodenal coordination. The order of potency (expressed in terms of EC50-values) was domperidone mediated via cholinergic nerves in the myenteric plexus and the moderate effects of metoclopramide may be mediated via both mechanisms.
Simultaneously acquired BEG and BOLD (Blood Oxygenation level dependent contrast) MRI allowed to study on line the neurophysiological changes in rat brain during epileptic seizures. MRI aiid EEG data were acquired with a specially designed high quality MR RF-antenna with incorporated non-invasive carbon EEG electrodes. The problem of severe pollution of the BEG data due to MR gradient switching during simultaneous EEGIMRI acquisitions was solved by a specially designed automated effective filtering algorithm. We measured continuously EEG data, and T2 -weighted coronal MRI sections of rat brain before and after the injection of penteirazol (43mg1(kg body weight) PTZ; convulsive dose 97%), an epilepsy inductor. In this way, we could correlate the abnormalities in the EEG traces, with changes in the MRJ BOLD signal intensities. Immediately after PTZ induction and before epileptic discharges were observed on the EEG traces, the cortex displayed an increase in BOLD signal intensity (increase in blood flow). Much later and correlated with epileptic discharges on the EEG traces, the ventromedial hypothalamic nuclei showed an increased BOLD signal while the BOLD signal intensity dropped in the entire brain, except for the hypothalamus. The decreased BOLD signal reflected general hypoxia and subsequent ischemia as a consequence ofthe sustained depolarization of neurons during the seizure.
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