SEARCH · Search PubMed

Results for “DIBENAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

PubMed1961

Studies on the pathogenesis of staphylococcal infection. IV. The effect of bacterial endotoxin.

Intracutaneous and intravenous injection of pyrogenic, non-lethal doses of bacterial endotoxin were found to increase the infectivity of pathogenic but not non-pathogenic staphylococci in rabbit skin. The increased infectivity of the microorganism was characterized by accelerated multiplication at the site of inoculation and by the production of necrosis and hemorrhage locally. Histologically, the infection of skin in endotoxin-prepared animals was characterized by necrosis, masses of bacteria, but absence of leukocytic infiltration into the area of bacterial growth. The infectivity of staphylococci in skin of endotoxin-prepared rabbits could be controlled by antibody to the alpha hemolysin of the microorganism. The effect of endotoxin upon staphylococcal infection was demonstrable only within 4 hours after injection of the endotoxin. It could not be prevented with chlorpromazine or dibenamine and was closely related to the effect of endotoxin upon leukocytes. It was suggested that the effect of endotoxin upon leukocytes was probably responsible for its influence upon staphylococcal infection. The implications of these findings in the pathogenesis of staphylococcal infection are discussed.

Animals↗

PubMed1977

Adrenergic mechanisms in infection. III. alpha-and beta-receptor blocking agents in treatment.

Raised epinephrine concentrations concentrations developed in the blood of mice near death after an intraperitoneal challenge with 10(9) Staphylococcus aureus or Escherichia coli. Both epinephrine levels were elevated in the urine near death. These challenges were infections and not intoxications, as they could be successfully treated with antibiotics. Using the same model infections, we studied the effect of alpha-and beta-receptor blocking agents and other adrenergically active compounds. The compounds alone were not toxic in the doses used. alpha-Blockers, such as phenoxybenzamine, dibenamine, and ergotamine and beta-blockers, such as butoxamine, timolol, and practolol, were ineffective. Phentolamine alone or propranolol alone showed some evidence of an ability to prolong life in S. aureus infections. Together they lengthened life significantly in S. aureus-challenged mice. In E. coli infections this beneficial effect was not noted. Mice pretreated with reserpine (7 mg/kg) and challenged with S. aureus lived 55% longer than saline-treated controls. Less benefit was noted in E. coli infections. Serontonin treatment was helpful in S. aureus infections and deleterious in E. coli infections.

Adrenergic alpha-Antagonists↗

PubMed1986

Separate neural systems mediate the steroid-dependent and steroid-independent suppression of tonic luteinizing hormone secretion in the anestrous ewe.

In the ewe, two types of seasonal fluctuations in secretion of tonic luteinizing hormone (LH) have been described: a steroid-dependent change whereby estradiol gains the capacity to suppress LH pulse frequency in anestrus, and a steroid-independent decrease in pulse frequency in ovariectomized animals during anestrus. We have proposed that the former reflects activation, in anestrus, of estradiol-sensitive catecholaminergic neurons that inhibit gonadotropin-releasing hormone (GnRH). Three results reported here support this hypothesis: dopaminergic (pimozide) and alpha-adrenergic (phenoxybenzamine) antagonists increased LH in intact anestrous ewes without altering pituitary responses to GnRH; other dopaminergic (fluphenazine) and alpha-adrenergic (dibenamine) antagonists also increased LH in anestrus; agonists for dopaminergic (apomorphine) and alpha-adrenergic (clonidine) receptors suppressed LH secretion in both seasons, suggesting that the appropriate receptors are present in breeding-season ewes. In contrast, catecholamines do not appear to mediate the steroid-independent suppression of pulse frequency; neither pimozide nor phenoxybenzamine increased LH pulse frequency in ovariectomized ewes during anestrus. When antagonists for 6 other neurotransmitter receptors (muscarinic and nicotinic cholinergic, GABAnergic, serotonergic, opioid, and beta-adrenergic) were tested in anestrus, only cyproheptadine, the serotonergic antagonist, increased pulse frequency in ovariectomized ewes. Cyproheptadine had no effect on frequency during the breeding season. On the basis of these results, we propose that the steroid-dependent and -independent actions of anestrous photoperiod occur via catecholaminergic and serotonergic neurons, respectively.

Anestrus↗

PubMed1996

Actions of galanin and some of its analogues on rat isolated gastric fundus.

The study was undertaken to characterize the effects of porcine galanin (pGal) and some of its analogues on rat gastric fundus muscle strips. pGal, galantide (M15) and pGal(1-14)-[Abu8]SCY-I evoked reproducible concentration-dependent contractions in concentrations of 1-300, 3-1,000 and 100-3,000 nM, respectively, with EC50 values of 13, 70 and 187 nM. Hill's coefficient for pGal is 1.03, indicating an interaction of one pGal molecule with one receptor, fulfilling criteria of classical receptor theory. For M15 and pGal(1-14)-[Abu8]SCY-I, Hill's coefficients are significantly different from 1, namely 0.73 and 1.56, so that one drug molecule may not interact with one receptor. The stimulatory effects of pGal were not modified by dibenamine 10 microM or glybenclamide 1 or 10 microM. Diltiazem 0.1, 1 and 10 microM, papaverine 0.1, 10 microM or dibutyryl cAMP (dib cAMP) 100 and 300 microM, blocked the contraction to pGal in a concentration-dependent manner, indicating an important role for the influx of extracellular calcium ions and regulation by cAMP the pGal-evoked contraction. Diltiazem, dibutyryl cAMP and papaverine were not competitive antagonists of pGal in the stomach smooth muscle.

Analysis of Variance↗

PubMed1957

The ethyleneiminium ion as the active species in 2-haloalkylamine compounds.

Certain 2-haloethylamine compounds which exert antagonism to adrenaline and noradrenaline of the type shown by dibenamine have been examined. The compounds were N-ethyl-N-chlorobenzyl-2-chloroethylamine hydrochlorides in which the Cl is in the p-, o-, and m- positions of the benzene ring, and the three related ethyleneiminium picrylsulphonates. In addition the Cl- and Br- compounds of the N-ethyl-N-9-fluorenyl-2-haloethylamine hydrohalide series were examined. For the haloethylamines, a curve was provided which showed the relation between probable production and decay of ethyleneiminium ion in neutralized solution with time. A correlation was established between the shape of this curve and the curve relating anti-adrenaline and anti-noradrenaline activity of samples of solutions of these compounds treated in an identical way. The relation to antagonism of histamine and 5-hydroxytryptamine was not so exact and varied with species.The ethyleneiminium ions of the three chlorobenzyl compounds exerted a typical long-lasting non-competitive antagonism to the pressor actions of adrenaline and noradrenaline. They also antagonized the effect of 5-hydroxytryptamine and histamine on blood pressure. The ED50 of the ion when administered as ethyleneiminium picrylsulphonate was always less than the ED50 of the same ion when administered in the form of 2-haloethylamine. There was, therefore, a variable loss of effective ion during transformation in vivo. The observations throw some light on the importance of the substituent groups on the nitrogen atom for effectiveness. It is concluded from these results and a discussion of other work that 2-haloethylamine compounds form an ethyleneiminium ion in neutral solution, which is the pharmacologically active species in effective compounds. It is a necessary but not a sufficient condition that a molecule should be an alkylating agent for this type of antagonism to be present, but the importance of the substituent groups on the N atom is equally great because not all ethyleneiminium ions are effective antagonists.

Amines↗

PubMed1958

The pressor effect of peptone in the rat.

Peptone normally causes a rise of blood pressure in rats. Since the pressor response was not abolished or even diminished by adrenalectomy, it could not have been caused by a release of pressor substances from the adrenal glands. The group of drugs (dibenamine, dihydroergotamine, ergotamine, tolazoline, nicotine and hexamethonium) which antagonize or block the peptone-induced pressor action suggests that the pressor effect may be secondary to a release of sympathin by the stimulation of sympathetic ganglia. Since it was not possible to duplicate the pressor response to peptone by either 48/80 or histamine, the hypothesis that peptone acts by liberating histamine can be ruled out.

Adrenal Glands↗

PubMed1959

The action of antisympathomimetic drugs on the urinary excretion of adrenaline and noradrenaline.

In cats anaesthetized with pentobarbitone sodium, phenoxybenzamine, dibenamine, phentolamine, and piperoxane reduced the blood pressure and increased the urinary excretion of noradrenaline. When the fall of blood pressure after phenoxybenzamine was prevented by repeated injections of vasopressin, the urinary excretion of noradrenaline did not rise. Hydergine and hydrallazine reduced the blood pressure without raising the urinary excretion of noradrenaline. In dogs, the infusion of small amounts of noradrenaline led to a significantly higher urinary recovery of the amine after phenoxybenzamine than before. It is concluded that antisympathomimetic drugs interfere with the destruction in the body of noradrenaline, whether released reflexly in hypotension or injected.

Animals↗

PubMed1959

The pharmacology of a molluscan smooth muscle.

The effects of a number of pharmacologically active substances on contraction and on membrane polarization of the anterior byssal retractor muscle of Mytilus edulis, L., have been studied. Tetramethylammonium bromide, trimethyl(4-oxopentyl)ammonium chloride and nicotine, like acetylcholine, produced depolarization and sustained contraction. Nicotine, on repeated application, lost acetylcholine-like activity and effectively blocked acetylcholine. In order of decreasing potency, methanthelinium, tubocurarine, benzoquinonium, tetraethylammonium, atropine, pentamethonium, and decamethonium blocked acetylcholine action. These agents did not show initial acetylcholine-like action and did not relax sustained contractions. Adrenaline, noradrenaline, tyramine, dibenamine, phentolamine, and lysergic acid diethylamide relaxed sustained contractions without reducing initial depolarization and tension development in response to acetylcholine or electrical stimuli. Adrenaline and noradrenaline often caused depolarization and contraction when first applied, and displayed relaxing action on subsequent application.

Acetylcholine↗

PubMed1959

Nicotine and the effect of antisympathomimetic agents on the aorta of the rabbit.

The responses of strips of rabbit aorta to almost maximal doses of nicotine were less readily antagonized by five antisympathomimetic agents than were comparable responses to noradrenaline. The effect was most marked with dibenamine, ergotamine, and tolazoline: approximately twice the dose of noradrenaline was required to match the test dose of nicotine after treatment with the antagonists. Dose/response curves for nicotine before and after phentolamine 10(-7) indicate that the phenomenon may be reversed with low doses of nicotine and that the release of noradrenaline by nicotine within the tissues is probably a graded response. The pattern of nicotine/phentolamine antagonism in this preparation is consistent with the view that nicotine acts indirectly by releasing a noradrenaline-like substance, and the difficulty found in antagonizing responses to nicotine with antisympathomimetic agents is probably similar to that responsible for failure of atropine to block some parasympathomimetic responses to nicotine.

Animals↗

PubMed1961

The effect of reserpine on the pressor response to injection of 2-halogenoethylamines.

Dibenamine-like compounds sometimes caused an increase in blood pressure when injected intravenously in mammals. This response varied with species, with the preparation, and with the structure of the compound. The response became smaller after repeated injections. In spinal atropinized rats injected with hexamethonium 5 mg/kg this pressor effect produced by injection of the adrenaline antagonist, compound AT3 [ethylfluoren-9-yl(2-iodoethyl)amine hydriodide], was reduced by prior treatment for five days with 1 mg/kg reserpine. Acute adrenalectomy also reduced this effect of the adrenaline antagonist; reserpine plus adrenalectomy abolished it. Subsequent injection of adrenaline and noradrenaline restored it.

Adrenalectomy↗

PubMed1961

The formation of an isoprenaline-like substance from adrenaline.

Intravenous injections of adrenaline, but not those of noradrenaline, caused the appearance of a substance which resembled isoprenaline in R(F) value and pharmacological activity in blood withdrawn from the lower abdominal aortae of chloralosed cats rested after acute adrenalectomy and induction of lasting block in autonomic ganglia with hexamethonium. The formation of the isoprenaline-like compound was prevented by pretreatment with pyrogallol but not by pretreatment with reserpine, cocaine, phentolamine, dibenamine, harmaline, or iproniazid. The liver proved a main site of the origin of this isoprenaline-like substance.

Animals↗

PubMed1961

The persistence of a depressor response to oxytocin in the fowl after denervation and blocking agents.

The effects of oxytocin and vasopressin on the blood pressure of the fowl have been studied after surgical or chemical interruption of parts of the central and peripheral nervous systems, and after the administration of stilboestrol and progesterone. An augmented and prolonged depressor response to oxytocin was seen after atropine, bretylium, tetraethylammonium or decapitation, but not after decerebration, dihydroergotamine or dibenamine. There was a tendency for the pressor action of vasopressin to disappear after decapitation, decerebration, and all the blocking agents used, except tetraethylammonium. The differences between these results and those which have been obtained in rats are discussed.

Animals↗

PubMed1961

Effect of cocaine and related drugs on the uptake of noradrenaline by heart and spleen.

Noradrenaline uptake by heart and spleen after intravenous infusion of noradrenaline was measured in the pithed rat. Cocaine, given before the infusion, inhibited the noradrenaline uptake in relation (a) to the dose administered and (b) to the amount of noradrenaline infused. There was an association between increase in the pressor response to a test dose of noradrenaline and inhibition of the uptake by the heart. Drugs related chemically to cocaine, such as alpha-cocaine, amethocaine, and atropine, did not alter the noradrenaline uptake or potentiate the blood pressure response to noradrenaline. The noradrenaline uptake by the heart was unchanged after dibenamine, but blocked by the dichloro-analogue of isoprenaline. It was concluded that cocaine specifically prevented the uptake of noradrenaline by tissues, thus increasing the amount of noradrenaline available for combination with adrenergic receptors. The dichloro-analogue of isoprenaline appeared to block both uptake by the heart and the combination with receptors.

Animals↗

PubMed1961

Stress-induced block of milk ejection.

A simple method has been described by which the action of drugs on the stress-induced block in milk ejection can be investigated on lactating guinea-pigs. Reserpine, meprobamate and chlorpromazine when administered to the lactating mother at various periods before suckling reduced the block in milk ejection caused by the stress. Dibenamine and dichloroisoprenaline did not affect in any way the stress-induced block. It is suggested that the stress-induced block in milk ejection is probably a nervous block and not mediated through adrenaline.

Breast Feeding↗

PubMed1970

Adrenoceptors in the cat choledochoduodenal junction studied in situ.

1. The effects of adrenaline, noradrenaline, isoprenaline and terbutaline (PINN), 1-(3,5-dihydroxyphenyl)-2(t-butylamino)-ethanol, on the sphincter of Oddi were studied in anaesthetized cats. Both adrenaline and noradrenaline (1-4 mug/kg) increased resistance to flow through the sphincter. This effect was blocked by dibenamine (0.5-2.5 mg/kg) and by phenoxybenzamine (0.5-1.0 mg/kg).2. Isoprenaline (0.5-5.0 mug/kg) as well as terbutaline (0.5-10.0 mug/kg) inhibited the spontaneous sphincter activity and decreased flow resistance. In these doses, isoprenaline provoked marked tachycardia and relaxation of the duodenum, whereas the cardial and intestinal effects of terbutaline were minimal. The effects were blocked by propranolol (0.5-1.0 mg/kg).3. The results confirm earlier observations of the presence of alpha-adrenoceptors active in contraction of the sphincter musculature and of beta-adrenoceptors active in its relaxation. It is suggested that the beta-adrenoceptors belong to the beta(2) type according to Lands' classification.

Adrenergic alpha-Agonists↗

PubMed1971

Effects of isoxazolium cations on some isolated muscle preparations.

1. The quaternary ammonium compound, N,t-butyl-5-methyl isoxazolium perchlorate (BIP), an anionic group reagent, initially causes contractions of the rat phrenic-nerve diaphragm, guinea-pig ileum and rabbit aortic strip preparations in vitro.2. In addition, the drug produces an irreversible block of indirectly elicited twitch responses in the diaphragm and of contractions induced by acetylcholine, methylfurmethide, dimethyl-phenylpiperazinium, 5-hydroxytryptamine (5-HT), histamine, angiotensin and pilocarpine in the ileum, while direct electrical stimulation of the diaphragm and contractions of the ileum to Ba and K ions are relatively unaffected.3. BIP is also an irreversible inhibitor of acetylcholinesterase but not of butyrylcholinesterase.4. On rabbit aortic strip preparations, responses to histamine, noradrenaline and 5-HT were differentially sensitive to irreversible blockade by BIP.5. Diphenhydramine, used in conditions which gave complete protection of the histamine response to irreversible block by dibenamine, did not protect against the blocking action of BIP but increased the blockade.6. These results suggest that BIP reacts covalently with anionic groups which mediate receptor initiated stimuli. The isoxazolium group may be useful in conferring irreversible properties by its substitution in drug molecules for the pyrrole or pyrrolidine group.

Acetylcholine↗

PubMed1980

Preliminary pharmacological characterization of the bovine isolated bronchial artery strip: a new preparation.

1 This paper describes a preliminary pharmacological study of the isolated helical strip of bovine bronchial artery under isotonic conditions in Krebs-Henseleit solution. 2 The tissue contracted to histamine and 5-hydroxytryptamine (5-HT), actions which were selectively antagonized by mepyramine and methysergide respectively. Histamine was not inhibited by metiamide and 5-HT was not affected by morphine. 3 Slow reacting substance of anaphylaxis (SRS-A), prostaglandin F2 alpha (PGF2 alpha) and PGE2 were spasmogenic, whereas PGE1 caused relaxation. No potential antagonists of these agents were tested. 4 Carbachol, at all concentrations, caused contractions of the bronchial artery which were completely, irreversibly blocked by atropine. 5 The spasmogenic action of phenylephrine was selectively blocked by dibenamine. Vessel strips which were partially contracted to histamine, relaxed to isoprenaline and salbutamol. The action of isoprenaline was inhibited similarly by either propranolol or practolol. The evidence therefore suggests the presence of functional alpha, beta 1 and beta 2-adrenoceptors.

Animals↗

PubMed1980

Study of central neurotransmitters in stress-induced gastric ulceration in albino rats.

1 Restraint when combined with cold (4 degrees C) consistently induces gastric ulceration in rats at 2 h. The cold-restraint ulcer (CRU) technique provides a suitable model for acute studies. 2 The peripheral mechanisms in CRU seem to be increased sympathetic and parasympathetic outflow since CRU was significantly reduced by prior spinal transection or vagotomy or by appropriate blocking agents. Since metiamide significantly reduced CRU, H2-histamine receptors are also involved. 3 Central catecholaminergic as well as cholinergic mechanisms seem to be responsible for the activation of peripheral sympathetic and parasympathetic outflow in CRU, since central administration of dibenamine, propranolol, 6-hydroxydopamine and atropine prevented the CRU. 4 Exogenous administration of putative neurotransmitters (adrenaline, noradrenaline and acetylcholine) into the cerebroventricular system produced gastric ulceration similar to CRU. However, dopamine, histamine and 5-hydroxytryptamine failed to induce gastric ulceration. 5 The results with intracerebroventricular adrenaline and acetylcholine indicate a central cholinergic link distal to adrenergic activation in the ulcerogenesis. 6 Intracerebroventricular adrenaline-induced gastric ulceration appears to be most akin to CRU. However, other central neurotransmitter mechanisms may also be involved.

Adrenalectomy↗