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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 60 (1987), S. 394-396 
    ISSN: 1432-0738
    Keywords: Barbiturate poisoning ; Pentobarbitone ; Phenobarbitone ; Gastric emptying ; Gastrointestinal transit ; Peristaltic reflex ; Rat ; Guinea-pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Anaesthetic doses of pentobarbitone (50 mg/kg) were found to inhibit gastric emptying and gastrointestinal transit in the rat. Gastric emptying was more profoundly suppressed than gastrointestinal transit. Phenobarbitone (150 mg/kg) had a similar effect. Since pentobarbitone and phenobarbitone also blocked the peristaltic reflex in the isolated small intestine of the guinea-pig, it would appear that the inhibitory effect of anaesthetic doses of barbiturates on gastrointestinal motility is mainly due to a direct action on the digestive tract. Together with the observation that considerable amounts of phenobarbitone were found in the stomach of an intoxicated patient 3 days after drug intake, these results might indicate that gastric lavage should also be considered in the treatment of protracted barbiturate poisoning.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 307 (1979), S. 257-264 
    ISSN: 1432-1912
    Keywords: Peristaltic reflex ; Guinea-pig ileum ; Neuropeptides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. A peristaltic reflex preparation of the isolated guinea-pig ileum was developed which had an intact vascular supply and into which drugs were infused intraarterially. Intraluminal pressure and intraluminal volume propelled per time were recorded. Peristalsis was triggered by raising the intraluminal pressure at constant time intervals. 2. Caerulein (〉0.2 pmoles min−1), substance P (〉5 pmoles min−1), 5-hydroxytryptamine (〉90 pmoles min−1), and bethanechol (〉900 pmoles min−1) initiated peristalsis when intraluminal pressure was not raised. 3. Under conditions of isotonic longitudinal contraction pressure-induced peristalsis was reduced by substance P and bethanechol, but not affected by caerulein and 5-hydroxytryptamine. 4. Under conditions of isometric longitudinal contraction, caerulein (0.5 pmoles min−1), substance P (2.4 pmoles min−1), 5-hydroxytryptamine (180 pmoles min−1), and bethanechol (355 pmoles min−1) increased the efficiency of the peristaltic reflex. 5. d-Ala2-d-met5-enkephalin (〉27 pmoles min−1) and d-ala2-mephe4-met-(O)5-ol-enkephalin (FK 33-824, 〉11 pmoles min−1) inhibited the peristaltic reflex, thus exceeding the potency of morphine, atropine, noradrenaline, hexamethonium, and isoprenaline 100–1000-fold. 6. ATP, 13-nle-motilin, somatostatin, and vasoactive intestinal polypeptide had no influence on the peristaltic reflex. 7. Since substance P and enkephalin are the most potent compounds of mammalian origin in affecting peristalsis it is concluded that they are involved in the nervous mechanisms of the peristaltic reflex.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Peristaltic reflex ; Atropine-resistant peristalsis ; Guinea-pig ileum ; Substance P ; Cholecystokinin octapeptide ; Bombesin ; Neurotensin ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Slow peristalsis (less than one peristaltic wave/min) was induced by continuous elevation of intraluminal pressure in vascularly perfused segments of the guinea-pig isolated ileum. The intraluminal pressure at the aboral side of the segment and the volume of fluid propelled by each peristaltic wave were recorded. 2. Intraarterial infusion of substance P (11.5–115 pmoles min−1), cholecystokinin octapeptide (CCK-8; 1.5–15 pmoles min−1), bombesin (1–10 pmoles min−1), and neurotensin (3.6–36 pmoles min−1) dose-dependently stimulated peristalsis, the degree of stimulation being largest with CCK-8. Histamine, a drug contracting the smooth muscle directly, did not stimulate peristalsis. 3. Atropine (1 μM in the bath and perfusion solution) caused a transient inhibition or blockade of the peristaltic reflex, followed by a partial recovery of peristalsis (“atropine-resistant peristalsis”). Atropine-resistant peristalsis was greatly stimulated by CCK-8 (6–15 pmoles min−1), only slightly stimulated by bombesin (4 pmoles min−1), and first stimulated and then inhibited by neurotensin (36 pmoles min−1). 4. Substance P (11.5–1,000 pmoles min−1) inhibited or abolished atropine-resistant peristalsis, which was probably due to desensitization of intestinal smooth muscle and/or neurones against the peptide. [d-Pro2, d-Trp7,9] substance P, an analogue of substance P with antagonistic properties (40 nmoles min−1), also inhibited atropine-resistant peristalsis. 5. Naloxone (4.6 nmoles min−1) stimulated peristalsis both in the absence and in the presence of atropine; this indicates that endogenous opioids modulate peristaltic motility. 6. It is concluded that neuropeptides stimulate peristalsis by exciting intramural cholinergic and non-cholinergic neurones. The inhibitory actions of substance P desensitization and of the substance P antagonist in the presence of atropine indicate that substance P neurones play a role in the mechanism af the atropine-resistant peristalsis.
    Type of Medium: Electronic Resource
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