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At least 55 records · Page 3Linked to original sources
PubMed1957

Prolongation of chloral hydrate sleeping time by 5-hydroxytryptamine and by certain other drugs.

Various drugs have been tested for a capacity to prolong the hypnotic effect of chloral hydrate in mice. Amongst the compounds which, when injected subcutaneously in substantial amount shortly before the chloral hydrate (250 mg./kg. intraperitoneally), increased sleeping time significantly were adrenaline, noradrenaline, phenylephrine, methoxamine, 5-hydroxytryptamine (serotonin), histamine, ergotamine, yohimbine, and atropine. The ability of these drugs to prolong chloral hydrate sleeping time could not be related to any common circulatory property, but most of the active drugs are known to lower body temperature under comparable conditions. It was found that mice which have been pre-treated with 5-hydroxytryptamine or adrenaline suffer a much greater fall of body temperature when chloral hydrate is given subsequently than do mice which have been given chloral hydrate alone. It is suggested that some, at least, of the drugs which prolong the effects of hypnotics do so by virtue of a hypothermic action.

Animals↗
PubMed1957

The effect of lysergic acid diethylamide, 5-hydroxytryptamine, and related compounds on the liver fluke, Fasciola hepatica.

The rhythmical activity of the liver fluke, Fasciola hepatica, was stimulated by 5-hydroxytryptamine and by lysergic acid diethylamide at very low concentrations. The effect was peripheral and was not mediated through the central ganglion. Other amines also stimulated rhythmical activity, the most potent being the indolamines.Bromolysergic acid diethylamide, and other analogues such as yohimbine, harmine, and dopamine depressed rhythmical movement and antagonized the stimulant action of 5-hydroxytryptamine and lysergic acid diethylamide. Evidence which suggests the presence of tryptamine receptors in the trematode is discussed.

Animals↗
PubMed1957

The action of 5-hydroxytryptamine and some of its antagonists on the umbilical vessels of the human placenta.

The vasoconstrictor action of 5-hydroxytryptamine (5-HT) in the human placental preparation is about 10 times stronger than that of adrenaline and is antagonized by anti-adrenaline compounds like phentolamine. Both 5-HT and adrenaline are antagonized by yohimbine and chlorpromazine. Specific and strong anti-5-HT action is demonstrated for lysergic acid diethylamide (LSD) and tryptamine. Both LSD and tryptamine in larger doses have a vasoconstrictor action. Mescaline has no certain modifying effect on the action of 5-HT, but itself causes vasoconstriction in large doses. The antihistamine drug phenbenzamine in histamine blocking doses abolishes the action of 5-HT in half the preparations tested. The ganglionic blocking agent trimetaphan in large doses antagonizes the action of 5-HT added subsequently, and also, to a lesser degree, the effect of adrenaline. Hexamethonium and tetraethylammonium bromides are ineffective in this preparation. No certain modifying action of reserpine on subsequently added 5-HT could be demonstrated, and the same was true for heparin even in very high concentrations.

Antihypertensive Agents↗
PubMed1957

The antidiuretic action of 5-hydroxytryptamine in cats in relation to the production of certain chemoreflexes.

In cats lightly anaesthetized with cnloralose, small (5 to 50 mug./kg.) intravenous doses of 5-hydroxytryptamine temporarily reduced the flow of urine into the bladder in addition to causing reflex falls of blood pressure and heart rate and temporary arrest of breathing. Doses of phenyl diguanide and other aryl diguanides, the reflex effects of which on blood pressure and respiratory movement approximately matched those of 5-hydroxytryptamine, had comparatively little antidiuretic effect. Phenyl diguanide, unlike 5-hydroxytryptamine (tested previously under similar conditions), did not have an antidiuretic effect in hydrated mice in doses of 0.05, 1, and 2.5 mg./kg. subcutaneously. It is concluded that the reflex depressor action of 5-hydroxytryptamine plays little part in reducing urinary output.

Animals↗
PubMed1957

The antagonism of the vascular effects of 5-hydroxytryptamine by BOL 148 and sodium salicylate in the human subject.

2-Bromo-(+)-lysergic acid diethylamide (BOL 148) is a specific antagonist of the constrictor response of the forearm and hand blood vessels to intra-arterial infusions of 5-hydroxytryptamine. This has been shown to be a direct action in the tissue concerned, since the antagonism was as effective when the drug was given by local arterial injection as when given intravenously. Sodium salicylate is also a specific antagonist of 5-hydroxytryptamine, but its action is indirect, occurring only when the general serum level was raised above 10 or 20 mg.%; local limb concentrations of 30 to 40 mg.% had no antagonistic effect. The mechanism of the antagonistic effect of salicylate is not known. It is not related to the associated hyperventilation but is possibly due to the secondary release of, or synergism with, some other substance, probably a hormone.

Blood Vessels↗
PubMed1958

Observations concerning the action of 5-hydroxytryptamine on the peristaltic reflex.

In isolated guinea-pig intestine 5-hydroxytryptamine increased the longitudinal muscle contractions in response to acetylcholine while the ganglionic action of nicotine was first facilitated and then blocked. Phenyldiguanide, veratrine, veratridine and protoveratrine, like 5-hydroxytryptamine, depressed the response to nicotine, leaving that to acetylcholine unaffected.The sensory stimulants, like 5-hydroxytryptamine, facilitated the peristaltic reflex when applied to the mucosa, and abolished it when applied to the serosa. Preceding the block, the initial effect of low concentrations of 5-hydroxytryptamine applied to the serosa was a short stimulation of peristalsis.Concentrations of 5-hydroxytryptamine which had an approximately equal stimulant action (mucosal 1 to 4 x 10(-6), serosal 2 to 8 x 10(-8)) were tested when various parts of the reflex arc were blocked. During block by procaine introduced into the lumen, mucosal application of 5-hydroxytryptamine re-established peristalsis, but serosal application of 5-hydroxytryptamine had no effect. During block by hexamethonium or atropine present in the bath, 5-hydroxytryptamine restored peristalsis more effectively by serosal application than by mucosal application. During block by serosal application of 5-hydroxytryptamine, morphine, phenoxybenzamine or dihydroergotamine, mucosal application of 5-hydroxytryptamine restored the peristaltic reflex while serosal application had no effect. During block by 2-bromo-lysergic acid diethylamide or lysergic acid diethylamide acting from the serosal surface, 5-hydroxytryptamine had no effect whether acting on the mucosal or on the serosal surface.It is concluded that 5-hydroxytryptamine facilitates the peristaltic reflex at two sites: when introduced into the lumen it stimulates mucosal sensory receptors; when acting from the serosal surface it sensitizes the muscle to the transmitter acetylcholine. There is also a transient stimulant action on the ganglia which is soon followed by inhibition; this indicates that 5-hydroxytryptamine applied to the serosa abolishes peristalsis by ganglion block.

Acetylcholine↗