Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to test whether fluid and electrolyte secretion evoked in the small intestine by the dihydroxy bile salt sodium deoxycholate could be due to activation of a nervous reflex mechanism. The effect of the bile salt on small intestinal motility was also investigated, and an analysis was made of factors involved in passive and active transport mechanisms relevant to bile salt-induced secretion. Luminal perfusion with sodium deoxycholate changed net fluid transport from absorption to secretion. Hexamethonium, a ganglionic receptor blocker, lidocaine, a local anaesthetic and tetrodotoxin, a sodium channel blocker, inhibited the induced fluid secretion. The inhibitory effect increased in proportion to the rate of secretion. Elimination of the bile salt from the perfusate also inhibited the secretion. A minor part of the induced change in net fluid transport was resistant to nerve blockade or to bile salt elimination. The change of net fluid transport was paralleled by a change of sodium and chloride transport from absorption to secretion. The change of net sodium transport was due to both a reduced uptake and increased losses. Villus tissue hyperosmolality was reduced by the bile salt. Hexamethonium inhibited the electrolyte secretion. The bile salt caused epithelial lesions in the upper parts of the villi. The lesions persisted also after the bile salt-induced secretion had been inhibited by nerve blockade or by bile salt elimination. Lesions also appeared in intestines which failed to develop net fluid secretion. The bile salt also induced characteristic intestinal contractions which showed a good correlation with the rate of net fluid secretion. The motility was also inhibited by nerve blockade or bile salt elimination. Atropine abolished the induced motility but did not influence the secretion. Indomethacin, a prostaglandin synthesis inhibitor, or pyrilamine, a histamine 1-receptor antagonist, did not inhibit either motility or secretion. The bile salt caused a mucosal vasodilatation, total blood flow increasing about 50%. Capillary filtration coefficient remained unchanged. Lymph flow did not increase. No correlation was found between the change of intestinal blood flow and the change of net fluid transport. Hexamethonium and tetrodotoxin inhibited the induced secretion without influencing blood flow. It is concluded that sodium deoxycholate evokes intestinal secretion and motility via an enteric nervous reflex arch consisting of a presynaptic cholinergic neuron and two postganglionic neurons, one cholinergic innervating the intestinal smooth muscle cell and the other non-cholinergic, non-adrenergic influencing intestinal flu
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PMID:Mechanisms in bile salt-induced secretion in the small intestine. An experimental study in rats and cats. 346 Mar 9

A major aim of the present study was to investigate whether exposing the jejunal mucosa to a noxious stimulus induces a net fluid secretion by activating the enteric nervous system (ENS) and, if so, to what extent an axon reflex was involved. Net fluid transport was measured in vivo with a gravimetric method. The intestinal mucosa was exposed to an isotonic solution with an unphysiologically low pH (1.0). This evoked a fluid secretion, which was markedly attenuated by giving hexamethonium (nicotinic receptor antagonist) i.v. or exposing the intestinal serosa to lidocaine (local anaesthetic). Atropine (muscarinic receptor antagonist) had no effect. Luminal acid evoked a fluid secretion of the same magnitude in acutely denervated segments and in segments denervated about 3 weeks prior to the experiments. Luminal capsaicin (1.6-16 mM) did not influence jejunal net fluid transport. A second aim of the study is to investigate the effect of nifedipine (Ca channel blocker of L-type) on the acid-induced fluid secretion. Nifedipine markedly attenuated acid-induced fluid secretion. In contrast to cholera toxin-evoked secretion, the nifedipine effect was not mediated via 5 hydroxytryptamine (5-HT) as judged by measurements of 5-HT release into the intestinal lumen and the lack of effect of granisetron (5-HT3 receptor antagonist). It is concluded that the net fluid secretion evoked by hydrochloric acid in the small intestine is mainly mediated via an intramural reflex in the ENS. No experimental evidence was obtained for the involvement of an axon reflex. The site of action of the calcium channel blocker is tentatively discussed.
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PMID:The effects on net fluid transport of noxious stimulation of jejunal mucosa in anaesthetized rats. 1037 79

1. The depressant drugs which have been studied in this series of experiments were found to resemble morphine and heroine in that they depressed expiration more than inspiration, but they acted only in narcotic doses and always depressed inspiration at the same time. Ether caused a sharp expiratory rhythm, persisting until narcosis was very deep, probably a result of irritation of the air passages. Chloroform sometimes caused dyspnea, even in very deep narcosis, probably because of circulatory depression. Hydrated chloral made respiration more rapid, but shallower. Urethane usually made expiration active, often with inspiratory pauses, such as may follow vagotomy. Magnesium seemed to produce the most uniform, uncomplicated depression of all the depressants tried. Luminal resembled morphine and heroine more closely than any of the general depressants, making expiration passive without depressing inspiration, but it acted only in narcotic doses, unlike morphine and heroine. 2. Caffeine and strychnine, whenever they caused acceleration after morphine, brought back active expiration. Atropine never stimulated, and commonly acted as a synergist to morphine. 3. It is suggested that the results outlined in this and the preceding paper point to the existence of a separate central mechanism for the control of each of the phases of respiration, and that, while each responds to the same chemical stimuli, the threshold of the expiratory is higher than that of the inspiratory. Evidence is presented to indicate that if expiration remains passive a marked increase in depth of breathing may slow the rate, and a respiratory mechanism that lacks active expiration may be so inefficient that a CO(2) concentration which stimulated when expiration was active may depress when it is passive.
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PMID:THE ACTION OF DRUGS ON RESPIRATION : II. ETHER, CHLOROFORM, CHLORAL, URETHANE, LUMINAL, MAGNESIUM, CAFFEINE, STRYCHNINE, AND ATROPINE. 1986 14