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Biomedical subjects

O H Osman

Publications and source records attributed to O H Osman.

At least 19 recordsLinked to original sources
PubMed1987

Effects of disopyramide on the isolated rabbit aorta and pulmonary artery.

1. Disopyramide (8 X 10(-5)-4 X 10(-4) M) contracted the rabbit aortic strips and this could be prevented by verapamil or by omitting Ca2+ from Krebs solution. 2. Disopyramide (1.5-6 X 10(-5) M) significantly potentiated the contractile response of the rabbit aortic strips to noradrenaline, clonidine and methoxamine but not that of potassium chloride. 3. Disopyramide (2-6 X 10(-5) M) attenuated the contractile response of the rabbit pulmonary artery to transmural electrical stimulation but potentiated response to noradrenaline. Similar results were observed with the portal vein. 4. The relaxant effect of acetylcholine, on the rabbit aortic ring precontracted with noradrenaline, was blocked by disopyramide while the relaxant effect of adenosine-5'-triphosphate (ATP) was not blocked.

Animals↗
PubMed1986

Evidence for the presence of histamine in Gaboon viper (Bitis gabonica) venom.

Venom from B. gabonica produced a dose-dependent contraction of both isolated guinea-pig ileum and rabbit aortic strip preparations. The venom-induced contraction was not antagonised by pretreatment with atropine, phentolamine, methysergide or indomethacin, however, it was blocked by the prior addition of chlorpheniramine or cyproheptadine. Upon exhaustive dialysis of the venom, the dialysate contracted both preparations, while the dialysed venom had no effect. Paper and thin-layer chromatography of the venom showed a spot with an Rf value corresponding to authentic histamine. Biological assay of the crude venom on the guinea-pig ileum showed that it contained the equivalent of 2-10 micrograms of histamine per mg dry weight of crude venom. pA2 values for chlorpheniramine using either the venom or histamine as agonists were not significantly different.

Animals↗
PubMed1986

Effects of Naja haje (Egyptian cobra), Naja naja (hooded cobra), Naja nigricollis (spitting cobra) and Naja mossambica mossambica (Mozambique spitting cobra) venoms on the isolated guinea-pig tracheal muscle.

Venoms from N. haje, N. naja, N. nigricollis and N. mossambica were tested on the isolated guinea-pig trachea. The four venoms (1-30 micrograms/ml) contracted the tracheal smooth muscle after a delay of 40-60 sec. A second challenge with the venoms caused either no or a much reduced contraction or a relaxant effect. The contraction could be prevented by pretreatment with antihistaminics, but not by atropine, methysergide or indomethacin, indicating that it is due to histamine release by the venoms. This release requires extracellular Ca2+, as it could be prevented by pretreatment with verapamil. Under conditions which prevented histamine release or its effect, each of the four venoms resulted in a reproducible relaxant effect which was not blocked by propranolol. It is concluded that the venoms have one or more component(s) causing histamine release which masks the relaxation caused by another component(s) of the venoms.

Animals↗
PubMed1986

Effect of venom from Bitis nasicornis (rhinoceros horned viper) on isolated rabbit aortic strips.

Venom from B. nasicornis, but not from Bitis arietans, Echis carinatus or Cerastes cerastes, produced an irreversible contraction of the isolated aortic strip that was slow in onset, increased with time, and reached maximum in about 10-15 min. The contraction was not inhibited by pretreatment with atropine, yohimbine, phentolamine, cyproheptadine or indomethacin, however, it was blocked by incubation in a Ca2+-free solution and was partially blocked by incubation with the Ca2+ channel blockers verapamil and nifedipine. It is concluded that B. nasicornis venom may act by increasing the Ca2+ influx into smooth cells, thus causing an increase in intracellular Ca2+ concentration and hence a contraction of the aortic strip.

Animals↗
PubMed1979

Experimental alterations of endorphin levels in rat pituitary.

Endorphin (END) levels in rat pituitary were assessed with the opiate receptor binding assay. Procedures reported to alter hormone secretion from END-rich intermediate or anterior lobes were examined for their effect on END content. Lesions of the paraventricular nucleus (PVN) had no significant effect on END content. Ingestion of 2% NaCl reduced END levels in a significant majority of the animals. Suckling, a natural physiological stimulus, significantly elevated neurointermediate lobe END. Footshock and immobilization each evoked 40--50% reductions in anterior lobe END content. Pituitary ENDs are thus affected by many of the same stimuli that also promote release of a number of peptide hormones derived from the same biosynthetic precursor. However, separate mechanisms likely exist for control of secretion of these peptides from anterior and neurointermediate lobe.

Animals↗
PubMed1977

Hyperpyrexic interaction between debrisoquine and pethidine in rabbits.

Pethidine injection into rabbits treated with debrisoquine either acutely or chronically resulted in severe interaction and fatal hyperpyrexia. Pretreatment of rabbits with p-chlorophenylalanine, chlorpromazine, or crypoheptadine protected them against the interaction, while alpha-methyl-p-tyrosine was ineffective. In addition the administration of debrisoquine into 5-HTP pretreated rabbits produced a severe interaction and hyperpyrexia. The hepatic N-demethylation of pethidine was significantly inhibited by debrisoquine pretreatment both in vivo and in vitro. The debrisoquine-pethidine interaction could be due to 5-HT potentiation or prevention of uptake. Alternatively it could be due to inhibition of biotransformation of pethidine by debrisoquine. However, neither mechanism by itself alone could be held responsible as the sole explanation of the interaction.

Animals↗
PubMed1975

Furazolidone-pethidine interaction in rabbits.

1 The intravenous injection of pethidine in rabbits pretreated with furazolidone administered orally but not systemically resulted in severe interaction and fatal hyperpyrexia. 2 Treatment with rho-chlorophenylalanine, chloropromazine of cyproheptadine protected the rabbits against the furazolidone-pethidine interaction, while alpha-methyl-rho-tyrosine was ineffective. 3 5-Hydroxytryptophan produced a fatal hyperpyrexia in furazolidone pretreated rabbits. 4 Pretreatment of rabbits with 1,1,1-trichloro-2, 2-bis(rho-chlorophenyl)ethane (DDT) accelerated and enhanced the furazolidone-pethidine interaction, while oxytetracycline pretreatment completely prevented the interaction. 5 It is concluded that furazolidone-pethidine interaction might depend mainly on potentiation of the effects of 5-hydroxytryptamine in the CNS and that the transformation of furazolidone into an active monoamine oxidase inhibitor metabolite might occur mainly in the gut microflora in the gut lumen.

5-Hydroxytryptophan↗
PubMed1975

Hypothermic effect of cocaine in rats.

Cocaine injected intraperitoneally into rats resulted in a dose-dependent hypothermia. Intracerebral injection of smaller doses also produced a fall in body temperature. In rabbits and guinea-pigs, cocaine produced hyperthermia, in mice and chicks it produced hypothermia while inconsistent changes were produced in goats. Pre-treatment of rats with 6-hydroxydopamine, alpha-methyl-m-tyrosine or haloperidol significantly antagonized the cocaine hypothermia. Pre-treatment of the rats with either hyoscine or methscopolamine resulted in some but non-significant attenuation of the cocaineinduced hypothermia. Pre-treatment with p-chlorophenylalanine, however, did not modify the cocaine hypothermia. Pargyline pre-treatment significantly antagonized the hypothermic action of cocaine. It is suggested that cocaine may cause the release of noradrenaline centrally or it may potentiate its action by interfering with the uptake mechanism. It is also possible that cocaine may have a direct effect on the heat regulating centre in the hypothalamus.

Animals↗
PubMed1975

The interaction of cyproheptadine with agents affecting neuromuscular transmission.

Using the rat phrenic nerve diaphragm, cyproheptadine at concentrations of 1 to 8 mug/ml did not affect or slightly augmented indirect muscle twitches, but potentiated blockade by tubocurarine, decamethonium and succinylcholine, and antagonized the augmentation of twitches by neostigmine. Ketamine, choline and tetraethylammonium at concentrations causing no blockade produced, when given after cyproheptadine (6 mug/ml), a high degree of blockade. At concentrations of 9 to 20 mug/ml, cyproheptadine induced neuromuscular blockade which was slow in onset, more apparent at higher rate of stimulation and was not reversed by neostigmine, choline or tetraethylammonium. In the cat tibialis anterior muscle, it potentiated blockade by tubocurarine, decamethonium and succinylcholine, and blocked acetylcholine twitches. In the chick biventer cervicis muscle, the durg was more effective in blocking indirect twitches than responses to carbachol.

Animals↗