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

The action of morphine on the superior cervical ganglion and on the nictitating membrane of the cat.

The intravenous injection of 0.05 to 2.5 mg. of morphine reduced the response of the nictitating membrane in the cat to pre- and post-ganglionic stimulation. This inhibitory action of morphine was due neither to inhibition of ganglionic transmission nor to a depressant action on the smooth muscle of the nictitating membrane. It is suggested that morphine inhibits the release of the sympathetic transmitter from the postganglionic nerve endings.Small amounts of morphine (5 to 20 mug.) injected intravenously reduced or abolished the contraction of the nictitating membrane due to the injection of histamine, pilocarpine and 5-HT into the arterial blood supply of the superior cervical ganglion. This inhibitory action of morphine was due to an action on the ganglion cells, since such small amounts of morphine did not reduce the response of the nictitating membrane to postganglionic stimulation. Similar amounts of morphine did not abolish the stimulation of the ganglion by nicotine, tetramethylammonium and potassium chloride.The results provide further evidence for the view that histamine, pilocarpine, and 5-hydroxytryptamine have no "nicotine-like" properties but act on receptors of the ganglion cells different from the acetylcholine receptors.

Animals↗
PubMed1957

Inhibition by morphine of the release of acetylcholine from the intestine of the guinea-pig.

In experiments on the isolated small intestine of the guinea-pig, morphine inhibited the release of acetylcholine (ACh) into the bath fluid. Experimental evidence is presented which suggests that the reduced release of ACh could not be explained by an inhibition of the synthesis of ACh, nor by stabilization of the bound form of ACh in the tissue. Apparently morphine reduces the excitability of postganglionic structures and thereby the liberation of ACh from nerve endings during the process of excitation.

Acetylcholine↗
PubMed1957

The action of morphine and related substances on contraction and on acetylcholine output of coaxially stimulated guinea-pig ileum.

Morphine depresses the twitch and tetanus of stimulated guinea-pig ileum by reducing acetylcholine released from cholinergic nerve endings. Acetylcholine output per shock falls to roughly the same residual amount at varying stimulation rates. Since normal output per shock declines with increasing stimulus frequency, the proportionate effect of morphine diminishes as stimulus frequency rises. Acute "tolerance" to morphine and a state of "morphinedependence" can be produced. Phenadoxone, dihydromorphinone, metopon, methadone, and heroin are more active, codeine and pethidine less active, than morphine. Nalorphine also depresses the twitch and can desensitize the gut both to itself and to morphine.

Acetylcholine↗
PubMed1958

The inhibitory action of morphine on the contraction of the longitudinal muscle coat of the isolated guinea-pig ileum.

Morphine (0.05 to 0.1 mug./ml.) markedly inhibited the contractions of the isolated guinea-pig ileum caused by nicotine, barium, and 5-hydroxytryptamine while the actions of acetylcholine, carbachol, and histamine were affected only a little. Atropine (0.025 to 0.05 mug./ml.) had a similar effect, in addition to its known effects on acetylcholine and carbachol contractions. Morphine had no additional effect on the inhibitory action of atropine, while in the presence of morphine, atropine had a significant additional inhibitory action only on the contraction caused by nicotine.The action of barium was complex. It caused contractions of a rhythmic type alternating with relaxations, a pattern which is similar to that produced by the emptying phase of the peristaltic reflex; these oscillations were inhibited by hexamethonium. On the other hand, that part of the sustained barium contraction which was inhibited by morphine may be explained by an action on the nerve cells innervating the muscle fibres (motor neurones). Similarly, the morphinesensitive component of the 5-hydroxytryptamine (5-HT) contraction was probably also due to an action on the motor neurones. The morphine-insensitive contractions of barium, 5-HT, and nicotine were believed to be caused by a direct action on the muscle fibres.The morphine inhibitors, nalorphine and levallorphan, had different effects with the different agonists. Their morphine-like action was particularly pronounced on the effect of 5-HT, which they antagonized, while their morphine-protecting action was most strongly present on the effect of nicotine.

Acetylcholine↗
PubMed1959

The effect of morphine on vagal inhibition of the heart.

The action of morphine (0.1 to 100 mg./kg.) on the cardiac slowing produced by stimulation of the right vagus nerve varied in the four species investigated. In the guinea-pig, morphine had no inhibitory effect and in the cat the effect was small, but in the rat and the rabbit stimulation of the vagus slowed the heart much less after administration of morphine than before. Further, in the last two species morphine delayed the onset of cardiac slowing. Nalorphine, which given alone had a slight morphine-like action, partly reversed the effect of morphine.

Animals↗