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Biomedical subjects

N Chand

Publications and source records attributed to N Chand.

At least 91 records · Page 5Linked to original sources
PubMed1979

Reactivity of isolated canine bronchus and pulmonary blood vessels to autonomic, autacoid agents and antigen.

Adult dogs were sensitized to horse plasma. Reactivity of isolated bronchus and pulmonary blood vessels to antigen and some selected autonomic and autacoid agents were studied. Pulmonary veins contracted to bradykinin, 5-HT, PGF2alpha, PGE2, histamine, carbachol and antigen (Schultz-Dale reaction). Pulmonary arterial strips contracted to 5-HT and histamine, but only weakly to horse plasma. Bronchial strips contracted to carbachol, 5-HT, histamine and horse plasma, relaxed to isoprenaline, PGE1 and PGE2. Subsequent antigen challenge produced 'desensitization'. Allowing the tissues to 'rest' for 1 and 2 h resulted in partial 'recovery' of the anaphylactic response. This investigation suggests that the contractions of sensitized pulmonary vein and bronchus to specific antigen may contribute to the patho-physiology of pulmonary hypersensitivity in dogs.

Anaphylaxis↗
PubMed1979

Coronary anaphylaxis in vitro.

1 The reactivity of isolated coronary arteries and cardiac veins of the calf to selected chemical mediators of anaphylaxis and to sensitizing antigen (horse plasma) was studied. 2 Both the coronary arteries and cardiac veins contracted to bradykinin, 5-hydroxytryptamine (5-HT), prostaglandin E2 (PGE2), PGF2 alpha, histamine and carbachol. 3 Isoprenaline and PGE1 relaxed vessels which had been partially contracted by PGF2 alpha, PGE2, histamine, 5-HT, bradykinin, carbachol or antigen. 4 Horse plasma (antigen) contracted coronary vessels obtained from sensitized calves, but not from control calves. Subsequent antigen 'challenge' produced 'densensitization' (tachphylaxis). After 1 or 2 h of rest, the anaphylactic response partially recovered although there was no change in tissue reactivity to the exogenous agonists. 5 Specific doses of atropine, mepyramine (H1-blocker) and methysergide (5-HT antagonist) did not modify the anaphylactic reaction in coronary arteries, suggesting a negligible role for these biogenic amines. 6 Compound PRD-92-EA (a new anti-allergic agent) exhibited non-specific receptor blocking activity towards histamine, 5-HT and carbachol and inhibited the coronary anaphylactic reaction.

Anaphylaxis↗
PubMed1979

Relaxant response of goat trachea to 5-hydroxy-tryptamine mediated by D-tryptamine receptors.

1 Goat isolated trachea contracted in response to carbachol, histamine and 2-pyridylethylamine (an H(1)-receptor agonist) and relaxed after application of isoprenaline. 5-hydroxytryptamine (5-HT) and phenylephrine.2 Mepyramine, a selective H(1)-receptor antagonist, blocked histamine- and 2-pyridylethylamine-induced contractions. In high doses it also exhibited some nonspecific antagonism to carbachol. After H(1)-receptor blockade, 4-methylhistamine and dimaprit (specific H(2)-agonists) relaxed the carbachol-contracted trachea.3 Propranolol, a beta-adrenoceptor blocker, antagonized relaxation in response to isoprenaline and phenylephrine. In high doses, it produced a reversal of the phenylephrine response.4 Indomethacin enhanced contractions in response to carbachol and histamine.5 Relaxation to 5-HT was not affected by propranolol, indomethacin, metiamide or cimetidine (H(2)-blockers). These findings appear to exclude the involvement of adrenergic, prostaglandinergic and H(2)-histaminergic mechanisms in the mediation of this response.6 Atropine potentiated 5-HT-induced relaxations. This suggests the participation of a ;masked' excitatory cholinergic mechanism.7 Methysergide, dibenamine and dibenzyline selectively antagonized or reversed 5-HT-induced relaxation. Dibenamine and dibenzyline enhanced relaxations to isoprenaline.8 This investigation showed (i) a relaxant response of goat trachea to 5-HT, mediated via D-muscular tryptamine receptors; (ii) a small population of excitatory M-neuronal tryptamine and alpha-adrenoceptors; and (iii) predominance of H(1)-histamine receptors in the goat trachea.

Animals↗
PubMed1979

Pharmacology of Schultz-Dale reaction in canine lung strip in vitro: possible model for allergic asthma.

1 Isolated lung parenchymal strips of the dog contracted in response to histamine > carbachol > prostaglandin F(2alpha) (PGF(2alpha)) > bradykinin (Bk) > 5-hydroxytryptamine (5-HT). The order of the relative activity of these agents on the tracheobronchial smooth muscles (TBSM) was carbachol > 5-HT > histamine; PGF(2alpha) and Bk were inactive. Thus there are marked differences in the responsiveness of the smooth muscle of central (trachea and bronchus) and peripheral (lung strip) airways to autonomic and autacoid agents.2 Lung strips and TBSM partially contracted by carbachol, histamine or horse plasma, were relaxed by isoprenaline, PGE(1) and PGE(2).3 Lung strips from dogs sensitized to horse-plasma contracted in response to antigen (Schultz-Dale anaphylactic reaction). Tachyphylaxis or desensitization to subsequent antigen challenge was invariably observed; it was followed after 1 to 2 h of rest by partial recovery of the anaphylactic response.4 Mepyramine selectively antagonized responses to histamine without altering responses to carbachol and antigen.5 Metiamide, an H(2)-receptor antagonist, did not influence responses to histamine, carbachol or horse plasma.6 Indomethacin was found to be ineffective as an inhibitor of the Schultz-Dale anaphylactic reaction.7 The results showed the presence of H(1)-histamine receptors mediating constriction in the peripheral airways of the dog. Histamine and PGF(2alpha) appear to have no important role in the anaphylactic reaction in this tissue. The involvement of slow reacting substance of anaphylaxis (SRS-A) and endoperoxides (thromboxanes) in allergic reactions of canine lung is strongly suggested.

Anaphylaxis↗
PubMed1979

Dual histamine receptor mechanism in guinea-pig lung.

Isolated guinea-pig lung parenchymal strips (GPLS) relaxed in response to the selective histamine H2-receptor agonists, dimaprit and 4-methylhistamine (4-MeH), and to low doses of histamine (10(-9) to 10(-7) mol/l) and contracted in response to several spasmogens. The order of the relative activity of the spasmogens was 2-methylhistamine (2-MeH) greater than histamine greater than carbachol greater than 2-pyridylethylamine (2-PE). Dimaprit and 4-MeH also relaxed GPLS which were contracted by 2-MeH, 2-PE or carbachol. Metiamide (a selective H2-antagonist: 5 x 10(-5) mol/l inhibited or reversed relaxations to histamine, dimaprit and 4-MeH, and significantly enhanced contractile responses to histamine without altering responses to carbachol. Mepyramine (a selective H1-receptor antagonist: 10(-8) to 10(-6) mol/l antagonized histamine-induced contractions. This investigation shows: (1) histamine is more active than carbachol in GPLS and (2) the occurrence of histamine H1-receptors mediating contraction and H2-receptors mediating relaxation in guinea-pig lung.

Animals↗
PubMed1979

Evidence for the existence of alpha-adrenoceptors in the rat lung.

Isolated rat lung parenchymal strips responded to carbachol, 5-HT and phenylephrine (PE) with contractions. Bradykinin (BK), histamine, PGF2 alpha, PGE1, PGE2 and dimaprit were either inactive or produced weak relaxations. Isoproterenol, noradrenaline (NA) and epinephrine (E) relaxed lung strips. The further increase in their concentrations produced contractions of varying magnitudes. The lung strips contracted to 5-HT or carbachol, responded to isoproterenol and E and NA with relaxations. Metiamide and cimetidine (selective histamine H2-receptor antagonists) did not alter responses to histamine and carbachol. Propranolol (a beta-adrenoceptor blocker) antagnoized or reversed relaxations to E and isoproterenol, and markedly enhanced contractions to NA, PE and E. Atropine and phentolamine or dibenzyline antagonized contractions to carbachol and sympathomimetic agents, respectively. From study it may be concluded that there are alpha- and beta-adrenergic receptors mediating contractions and relaxations in the peripheral airways of rat.

Animals↗
PubMed1979

Relaxant action of histamine on rabbit trachea: possible existence of third histamine receptor subtype.

The carbachol contracted rabbit trachea relaxes to isoproterenol, PGE1, E2, histamine and bradykinin. Histamine-induced relaxations were resistant to mepyramine (an H1-antagonist), burimamide, cimetidine, metiamide (H2-antagonists), propranolol (a beta-adrenoceptor blocker), indomethacin (a potent inhibitor of prostaglandin synthesis), trasylol (an inhibitor of kallikreins), aminophylline (a purinergic receptor blocker) and dibenzyline (a "D"-tryptamine receptor antagonist). The evidence achieved with these pharmacological agents appears to suggest that the chemical mediator responsible for the relaxant response to histamine is unlikely to be: catecholamines, prostaglandins, 5-HT, adenosine or ATP or kinins. The existence of H2-(iso or H3) histamine receptor subtype in rabbit trachea is postulated.

Airway Resistance↗
PubMed1979

Pharmacological characterization of the rabbit lung strip.

Isolated rabbit lung parenchymal strips contracted to epinephrine (E), norepinephrine (NE), phenylephrine (PE), histamine, carbachol, PGF2alpha, bradykinin and 5-HT. Lung strips which were maximally contracted to histamine, carbachol and PGF2alpha, relaxed to isoproterenol, salbutamol, terbutaline and PGE1 however, they exhibited superimposed contractions to E, NE and PE. Atropine and mepyramine selectively antagonized contractions to carbachol and histamine respectively, without modifying contractions to the sympathomimetic agents. Phenotolamine antagonized responses to E, NE and PE. The results of this investigation suggest the presence of alpha- and beta-adrenergic and H1-histamine receptors in the rabbit lung strip.

Airway Resistance↗
PubMed1979

The effect of atropine on acetylcholine-induced depressor responses in adult domestic fowl.

In pentobarbital-anaesthetized, spontaneously breathing adult chickens, intravenous administration of acetylcholine, histamine and 5-HT produced a dose-related fall in carotid arterial pressure, rise in central venous pressure and highly variable effects on heart rate. Atropine at low doses (0.1 to 0.2 mg/kg) selectively antagnoized depressor-responses to acetylchline. The blockade persisted for 20 to 30 min. At medium doses (0.5 to 2 mg/kg) atropine strongly antagonized acetylcholine for 50 to 110 min, and also partially antagonized responses to 5-HT and histamine. At higher doses (6 mg/kg), atropine-induced cholinergic blockade persisted for 280 min. It also nonselectively and significantly blocked responses to histamine and 5-HT. Therefore, it is concluded that the effectiveness and persistence of cholinergic blockade in chickens depends upon the dose of atropine used. It seems to rule out the opinion that high doses of atropine are required for cholinergic blockade in chickens.

Acetylcholine↗
PubMed1979

Pharmacological study of bovine airways. Evidence for excitatory and inhibitory effects of histamine.

Bovine airway muscle contracts to carbachol greater than histamine greater than 2-methylhistamine greater than prostaglandin F2 alpha. Trachea of neonatal calves are more sensitive to histamine than those of older cattle. Partially contracted bovine airways relax to prostaglandins E1 and E2 greater than dopamine greater than phenylephrine greater than 4-methylhistamine greater than dimaprit. Histamine-induced airway constriction was incompletely blocked by mepyramine and the mepyramine-resistant component was blocked by atropine. After H1-receptor blockade, histamine-induced tracheobronchial relaxation was incompletely antagonized by metiamide and not blocked by propranolol or indomethacine, suggesting an atypical histamine receptor not associated with catecholamine or prostaglandin production.

Age Factors↗