A method is described for recording the coronary flow and the rate and the amplitude of contraction of an isolated heart maintained at constant temperature. Both histamine and noradrenaline increased the contractility of the guinea-pig heart. Pronethalol antagonized noradrenaline but not histamine. Mepyramine, 10-(2-pyrrolidin-l'-ylethyl)phenothiazine hydrochloride (pyrathiazine) and diphenhydramine reduced the contractility of the guinea-pig heart but did not antagonize the action of histamine. The influence of histamine and noradrenaline on coronary flow was variable but when the contractility of the heart increased there was a concomitant increase in coronary flow. Histamine decreased the contractility of the rat heart and the domestic fowl heart.In 1910, Dale & Laidlaw showed that histamine increased the contractility of the isolated heart of the cat and the rabbit. A similar effect has been shown on the heart of the guinea-pig (Went & Lissak, 1935), the frog (Tiffeneau, 1941) and the rat (Went, Varga, SzUcs & Feh6r, 1952).Went, Varga, SzUcs & Feh6r (1952 have described experiments in which histamine released an adrenaline-like substance from the heart of the rat, the rabbit, the cat and the guinea-pig, which they considered to be sympathin. However, according to Mannaioni (1960), histamine combines with receptors in the myocardium which are specific for this compound, since in experiments with guinea-pig isolated auricles diphenhydramine antagonized histamine but not noradrenaline, and dichlorisoprenaline antagonized noradrenaline but not histamine. In contrast, Trendelenburg (1960) found that the antihistamine drugs, mepyramine and tripelennamine, did not specifically antagonize histamine acting on isolated auricles. He was also unable to detect any change in the action of histamine when the tests were made with auricles depleted of catechol amines and obtained from animals treated with reserpine.The experiments described in the present paper show that, although histamine increased the contractility of the guinea-pig heart, it depressed the heart of the rat and of the domestic fowl. The action of histamine was not sympathomimetic since it was dissimilar to the action of noradrenaline on the rat heart and the domestic fowl heart, and pronethalol discriminated between the action of histamine and that of noradrenaline on the guinea-pig heart. The antihistamine compounds, mepyramine maleate, 10-(2-pyrrolidin-1'-ylethyl)phenothiazine hydrochloride (pyrathiazine hydrochloride) and diphenhydramine hydrochloride did not antagonize histamine acting on the guinea-pig heart.
The longitudinal muscle of an isolated Remak nerve-rectum preparation from the chicken responded to nerve stimulation with a contraction or, when the tone of the preparation was raised by acetyl-fi-methylcholine (11 0 mM), with a contraction followed by a relaxation. The relaxation of the preparation was unaffected by hexamethonium, antagonized by bretylium, blocked by a combination of propranolol and phentolamine at specific concentrations and was absent or diminished in reserpinised preparations. The contraction was abolished by hexamethonium or tubocurarine and was partially antagonized by hyoscine.Remak's nerve consists of fibres of coeliac and sacral origin [Nolf, 1934]. The effect of autonomic blocking drugs on responses of the chicken isolated rectum to stimulation of Remak's nerve has been investigated to ascertain whether a hyoscine-resistant contraction, as observed in the chicken isolated oesophagus [Hassan, 1969], occurs in an aboral part of the alimentary tract of the domestic fowl. METHODSDrugs. Acetyl-f-methylcholine chloride, bretylium tosylate, hexamethonium bromide, (-) hyoscine hydrobromide, (-) noradrenaline bitartrate, phentolamine mesylate, (+) propranolol hydrochloride, reserpine and (+) tubocurarine hydrochloride were used. Reserpine was dissolved in 20 per cent (w/v) aqueous ascorbic acid and used on the same day. Concentrations of drugs in the text and figures refer to final concentrations in the organ-bath.Chick Remak nerve-rectum preparation. Chicks (Brown Leghorn) aged 1 to 3 weeks were decapitated and bled. The whole rectum together with the Remak nerve and adjoining blood vessels (Fig. 1) was removed and its contents washed out with Krebs solution [Krebs and Henseleit, 1932]. The Remak nerve and caudal mesenteric vein were tied with cotton and freed along 0 5 to 1.0 cm of their length from the caecal end ofthe rectum. The Remak nerve-rectum preparation with open ends was mounted in a 40 ml. organ-bath filled with Krebs solution at 350C and gassed with 5 per cent carbon dioxide in oxygen, responses of the longitudinal muscle being recorded isotonically with a load of 1 to 2 g on the lever. The nerve was stimulated through platinum electrodes with square wave pulses (1 msec, 20 Hz, 5 to 10 V), the stimuli being applied for periods of 15 to 60 sec at 5-15 min intervals. In experiments where relaxations of the longitudinal muscle were recorded the bathing solution contained acetyl-6-methylcholine (11.0 mM) to raise the tone. Preparations were rested for at least 30 min before commencement of an experiment.Guinea-pig hypogastric nerve-vas deferens and vagw.3 nerve-oesophaguw preparations.
1 The addition of furazolidone to the feed at the therapeutic level (0.04% w/w, 10 days) inhibited monoamine oxidase (MAO) activity by 47 to 72% in chicken duodenal mucosa, heart and brain, but in the liver the enzyme activity was unaffected by the treatment. 2 Furazolidone (200 mg/kg) administered by crop tube inhibited MAO activities in duodenal mucosa, liver, heart and brain. 3 Furazolidone (200 mg/kg) injected intramuscularly did not inhibit MAO activity in the chicken. 4 Pretreatment of the chickens with intramuscular neomycin did not antagonize the inhibition of MAO activity produced by furazolidone (200 mg/kg, crop tube). 5 Pretreatment with neomycin by crop tube to suppress the alimentary flora significantly reduced the effect of furazolidone on MAO activity, suggesting that the drug was transformed by the alimentary flora to an active metabolite which subsequently inhibited MAO activity in other organs. 6 Furazolidone in the feed (0.04% w/w, 10 days) or administered by crop tube (200 mg/kg) had no effect on the activity of aminopyrine demethylase in chicken liver. 7 The activity of aspartate transaminase in plasma was unaffected by the addition of furazolidone to the feed (0.04% w/w, 10 days).
1 Histamine (0.02-0.1 Mg/ml) contracted the chicken rectum preparation. This effect was antagonized by mepyramine (0.01 ,ug/ml) but not by hyoscine (0.02 ,ug/ml). 2 5-Hydroxytryptamine (0.05-0.25 Mg/ml) relaxed the rectum preparation and at higher concentration produced a biphasic response. These responses were not antagonized by methysergide (0.01 Mg/ml), and the relaxation was not antagonized by tetrodotoxin (0.1 Mg/ml) or a combination of propranolol (0.05 ,ug/ml) and phentolamine (0.1 ,ug/ml).3 Neither mepyramine (0.1 g/ml) nor methysergide (0.01 g/ml) antagonized the contractions produced by nerve stimulation in vagus nerve/oesophagus and Remak nerve/rectum preparations.4 5-Hydroxytryptamine (2 Mg/ml) in the presence of methysergide (0.01 Mug/ml), inhibited the contractions produced by nerve stimulation in Remak nerve/rectum and vagus nerve/oesophagus preparations. 5 Adenosine, adenosine 5'-phosphate (AMP), adenosine 5'-diphosphate (ADP) and adenosine 5'-triphosphate (ATP), in order of decreasing potency, produced slow contractions in most oesophagus preparations. The action of ATP in this preparation was antagonized by tetrodotoxin (0.1 Mg/ml), hyoscine (0.1 ,ug/ml) and strychnine (5 ,ug/ml). 6 Desensitization of the vagus nerve/oesophagus preparation to ATP did not produce any antagonism of the contractions to nerve stimulation. 7 Adenosine and AMP produced relaxations and ADP and ATP contractions in the rectum preparation. ATP was about 100 times as potent as ADP in producing fast contractions which were not antagonized by tetrodotoxin, hyoscine or strychnine. 8 Desensitization of the Remak nerve/rectum preparation to ATP resulted in the contractions to nerve stimulation and acetylcholine being inhibited to the same extent. 9 Prostaglandin E2 produced slow contractions in the oesophagus and rectum preparations which were not antagonized by tetrodotoxin (0.1 pg/ml). Polyphloretin phosphate (10 Mg/ml) antagonized spontaneous movements and responses to prostaglandin E2 in the rectum but not the oesophagus.10 Neither polyphloretin phosphate (60 ,g/ml) nor indomethacin (20-100 Mg/mi) antagonized the contractions produced by nerve stimulation in vagus nerve/oesophagus (with hyoscine in the bathing solution) and Remak nerve/rectum preparations.11 These experiments seem to exclude histamine, 5-hydroxytryptamine, adenosine and its nucleotides and prostaglandin E2 as possible motor transmitters in synapses and neuromuscular junctions in the chicken vagus nerve/oesophagus and Remak nerve/rectum preparations.
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