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Biomedical subjects

H O COLLIER

Publications and source records attributed to H O COLLIER.

At least 19 recordsLinked to original sources
PubMed1964

BRONCHOCONSTRICTOR ACTION AND ANTAGONISM OF A SLOW-REACTING SUBSTANCE FROM ANAPHYLAXIS OF GUINEA-PIG ISOLATED LUNG.

Slow-reacting substance produced in anaphylaxis (SRS-A) increased resistance of the lungs to inflation in the guinea-pig in vivo and caused isolated preparations of its tracheobronchial muscle to contract. SRS-A also contracted human isolated bronchial muscle and some but not all preparations of rabbit trachea. Nonsteroid anti-inflammatory drugs, which antagonize bronchoconstriction induced by kinins, but not that by histamine, acetylcholine, 5-hydroxytryptamine, substance P, angiotensin or lung prostaglandin, also antagonized the bronchoconstrictor action of SRS-A. This antagonism resembled that of kinins in being surmounted by higher doses of agonist, in the potencies of active drugs and in the types of drugs which were inactive. However, receptors in guinea-pig tracheobronchial muscle for SRS-A seem to be distinct from those for bradykinin, since preparations of this muscle could become unresponsive to either agent in vivo and in vitro, while remaining responsive to the other.

Acetylcholine↗
PubMed1963

Antagonism by mefenamic and flufenamic acids of the bronchoconstrictor action of kinins in the guinea-pig.

In the guinea-pig, N-(2,3-xylyl)anthranilic acid (mefenamic acid) and N-(alpha,alpha,alpha-trifluoro-m-tolyl)anthranilic acid (flufenamic acid), two new anti-inflammatory agents, antagonize bronchoconstriction, but not hypotension, produced by kinins. They do not reduce bronchoconstrictor responses to acetylcholine, histamine or 5-hydroxytryptamine. The antibradykinin potencies of mefenamic and flufenamic acids approximately equal that of acetylsalicylic acid when given intravenously and of phenylbutazone when given into the duodenum. After administration of mefenamic and flufenamic acids, the bronchoconstrictor response can be restored by higher doses of bradykinin. The quantitative relationship between the intravenous dose of sodium mefenamate or flufenamate and the dose of bradykinin needed to surmount either antagonist in bronchial muscle fulfils the requirements for competitive antagonism. Antagonism by calcium acetylsalicylate can also be surmounted with higher doses of bradykinin, but in this instance the relationship of antagonist to agonist fulfils requirements for competitive antagonism only at the lower part of the dose range.

Acetylcholine↗
PubMed1963

NOCICEPTIVE RESPONSES OF GUINEA-PIGS TO INTRADERMAL INJECTIONS OF BRADYKININ AND KALLIDIN-10.

Nine behavioural responses were observed to follow with reasonable frequency intradermal injection into guinea-pigs of strongly anisotonic solutions, which are known to cause pain in human skin. These responses were recorded on a form, and a procedure was devised for obtaining a nociceptive score from the records. Intradermal injection of bradykinin or kallidin-10 gave a response pattern indistinguishable from that to a strongly anisotonic solution. Each kinin raised the nociceptive score in response to the control solutions, as also did acetylcholine and histamine; but 5-hydroxytryptamine and pH changes within the range of 3.1 to 10.3 did not significantly raise the control score. The effect of bradykinin was depressed by subcutaneous injection of morphine or codeine, but was unaffected by amidopyrine, calcium acetylsalicylate, chlorpromazine or phenylbutazone.

Acetylcholine↗
PubMed1963

ASPIRIN.

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Aspirin↗
PubMed1962

Kinins.

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Humans↗
PubMed1962

Actions of some peptides on bronchial muscle.

The decapeptide kallidin-10, substance P and angiotensin increased the resistance of guinea-pig lungs to inflation; lysine- or arginine-vasopressin and oxytocin were inactive. Acetylsalicylate antagonized this action of kallidin-10, as it does that of bradykinin, but it failed to antagonize substance P or angiotensin. Bradykinin also increased resistance to inflation of rabbit lungs and, to a lesser extent, rat lungs. It caused a relatively slow contraction of guinea-pig tracheal and bronchial muscle in vitro, but it did not contract isolated rabbit, dog or human bronchus. The relative potencies of different substances on different bronchial test preparations, and also in different species, were not parallel.

Angiotensin Amide↗
PubMed1961

Multiple toe-pinch method for testing analgesic drugs.

In guinea-pigs and rats, an immediate squeak was one of the most consistent and readily observed responses to application of a light artery clip to the base of a toe. Morphine and related drugs suppressed this response. Squeak-responses from each toe of an experimental animal formed the basis of a technique for measuring activity of analgesic drugs. A statistical method was developed to analyse the correlated quantal observations obtained. It provided an estimate of the increase of information from several toes compared with one. Testing all toes of each animal yielded a substantial increase of information, because the correlation between responses of different toes was low. Among drugs having an analgesic action in man, 1-(beta-diethyl-aminoethyl)-2-(p-ethoxybenzyl)-5-nitrobenzimidazole, methadone, morphine, pethidine and codeine (in descending order of potency) were active in this test in guinea-pigs. Acetylsalicylic acid, amidopyrine, amphetamine, chlorpromazine, 4-hydroxyisophthalic acid, lysergic acid diethylamide, mephenesin, nalorphine, pentetrazole, phenobarbitone, phencyclidine, phenytoin, salicylamide, strychnine and troxidone showed little or no activity. The time-courses of active drugs were estimated, and morphine had the longest action.

Aminopyrine↗
PubMed1960

Analgesic antipyretic drugs as antagonists of bradykinin.

The antagonism between analgesic antipyretic drugs and bradykinin was examined quantitatively, using the bronchoconstrictor response of guinea-pigs in vivo. The dose of bradykinin required to overcome antagonism by calcium acetylsalicylate increased with the dose of acetylsalicylate given, the ratio being roughly constant. Fifty times the quantity of acetylsalicylate which just antagonized bradykinin did not modify bronchoconstriction due to small doses of histamine, 5-hydroxytryptamine, or acetylcholine. A method of measuring the potency of this anti-bradykinin action was developed. Acetylsalicylic acid, phenylbutazone, amidopyrine, and phenazone had a high potency; paracetamol, cinchophen, sodium salicylate, and acetanilide had a moderate potency; and phenacetin, salicylamide, and 4-hydroxyisophthalic acid had little or none. Cortisone, hydrocortisone, aldosterone, amodiaquine, and morphine were ineffective or their action was non-specific. In sensitized guinea-pigs, an injection of antigen caused bronchospasm. This response was greatly lessened by pretreatment with mepyramine, but was not affected by calcium acetylsalicylate, lysergic acid diethylamide, or atropine. Acetylsalicylic acid, phenylbutazone, and amidopyrine did not specifically antagonize the action of bradykinin on the capillaries of guinea-pig skin in vivo, on guinea-pig ileum in vitro or on rat duodenum in vitro.

Acetaminophen↗
PubMed1960

The bronchoconstrictor action of bradykinin in the guinea-pig.

Bradykinin was found to be a potent bronchoconstrictor agent in the guinea-pig anaesthetized with urethane. This action was not affected by vagotomy, or by treatment of the animal with mepyramine, atropine, lysergic acid diethylamide, or cortisone. Adrenaline and isoprenaline suppressed the bronchoconstrictor responses to bradykinin and histamine. Small doses of acetylsalicylic acid, however, suppressed only that to bradykinin. Bradykinin also produced bronchoconstriction in the isolated perfused lungs of the guinea-pig. The closely related peptide, wasp kinin, was also a potent bronchoconstrictor.

Animals↗
PubMed1960

Potentiation of sulphadimidine by 2,4-diaminopteridines and other 6,7-disubstituted 2,4-diaminopteridines against Eimeria infections of chicks.

Six 2,4-diaminopteridines substituted in the 6 and 7 positions were tested as potentiators of sulphadimidine against Eimeria tenella. 2,4-Diamino-6,7-di-isopropylpteridine and 2,4-diamino-1'-propylindolo(2',3':6,7)pteridine were selected for further study. Both potentiated sulphadimidine against E. tenella and the di-isopropylpteridine potentiated it against E. necatrix. A 10% mixture of the di-isopropylpteridine with sulphadimidine (or other sulphonamides) appears to offer advantages in the treatment of E. tenella and still more of E. necatrix.

Animals↗