bluuebunny/crossref_metadata_2025_split huggingface dataset:
SELECTIVE (+)‐AMPHETAMINE NEUROTOXICITY ON STRIATAL DOPAMINE NERVE TERMINALS IN THE MOUSE
Authors: JONSSON G. , NWANZE E. 
Published: July 2012

Infusion of large doses of (+)‐amphetamine continuously for 7 days by means of osmotic minipumps caused a long‐lasting reduction of endogenous dopamine levels, dopamine nerve terminals demonstrated histochemically and [3H]‐noradrenaline uptake in vitro in the striatum of mice.
The effect was dose‐dependent, fully developed after 4 days and selective for striatal dopamine up to a dose of (+)‐amphetamine of 25 μg/h. Higher doses, which produced increased mortality, also affected dopamine levels in the olfactory tubercle as well as noradrenaline in several regions.
Fluorescence histochemical studies using the Falck‐Hillarp technique disclosed catecholamine accumulations in the striatum after (+)‐amphetamine; a sign of neurotoxic damage. No effects on the dopamine cell bodies were noted. There were also no indications of neurotoxic damage to noradrenaline or 5‐hydroxytryptamine neurones induced by (+)‐amphetamine.
Large doses of (−)‐amphetamine were without effect, demonstrating that the long‐lasting impairment of transmitter uptake‐storage mechanism in striatal dopamine nerve terminals is selective for (+)‐amphetamine.
There was a slow gradual recovery of endogenous dopamine and [3H]‐noradrenaline uptake in the striatum with time, which was almost complete 6 months after the (+)‐amphetamine administration.
The results give further evidence for the view that (+)‐amphetamine in large doses can have a selective neurotoxic action on a vulnerable population of a dopamine nerve terminals in the striatum. The results suggest in addition that there is a slow regrowth and regeneration with time of damaged dopamine nerve terminals.
THE CARDIOVASCULAR EFFECTS OF ICI 118,587: A β1‐ADRENOCEPTOR PARTIAL AGONIST
Authors: NUTTALL A. , SNOW H.M. 
Published: July 2012

In a preparation in which cardiovascular reflexes were prevented from occurring, ICI 118,587 (1‐(p‐hydroxyphenoxy)‐3‐β‐(morpholinocarbonamido) ethylamino‐2‐propranol fumarate) caused dose‐dependent positive chronotropic and inotropic effects upon the dog heart.
The increase in heart rate brought about by ICI 118,587 was about 43% of the maximum increase produced by isoprenaline.
For a given chronotropic effect produced by either ICI 118,587 or isoprenaline, each compound produced a similar inotropic effect as indicated by an increase in LV dp/dt max.
In contrast to the direct stimulant action of ICI 118,587 on the heart no direct effects on vascular smooth muscle were observed.
ICI 118,587 was shown to be a competitive antagonist of the chronotropic and vasodilator effects of isoprenaline on the heart and blood vessels and of the chronotropic effects of noradrenaline on the heart.
It is concluded that ICI 118,587 is a selective β1‐adrenoceptor partial agonist.
THE KINETICS OF UPTAKE OF 5‐FLUOROURACIL BY RAT LIVER
Authors: HSU LORNA S.F. 
Published: July 2012

Slices of rat liver weighing 15–30 mg were incubated at 37°C in 5‐fluorouracil (5‐FU) solution.
The 5‐FU taken up was measured by high pressure liquid chromatography.
Uptake of 5‐FU was found to approximate to Michaelis‐Menton kinetics with the values of Kt and Vmax equal to 15.39 mmol l−1 and 1.96 μmol g−1 min−1 respectively.
Transport of 5‐FU was saturable with the uptake being much greater in the non‐fasting rats.
Intracellular concentration of 5‐FU after 24 min incubation approached but did not significantly exceed that in the extracellular fluid.
Enzymatic destruction of 5‐FU at 2 min was negligible but substantial after a long incubation period.
2,4‐Dinitrophenol was found to inhibit transport of 5‐FU significantly.
Results suggested that the mechanism of uptake of 5‐FU by rat liver is an energy requiring process.
EFFECTS OF ENKEPHALINS AND MORPHINE ON SPONTANEOUS ELECTRICAL ACTIVITY AND ON JUNCTION POTENTIALS ELICITED BY PARASYMPATHETIC NERVE STIMULATION IN CAT AND RABBIT COLON
Authors: BLANQUET FRANCE , BOUVIER MICHEL , GONELLA JEAN 
Published: July 2012

The effects of Leu‐enkephalin, Met‐enkephalin and morphine on excitatory junction potentials (e.j.ps) and inhibitory junction potentials (i.j.ps) elicited by stimulation of efferent parasympathetic nerves were studied in cats and rabbits, anaesthetized and in vitro.
Enkephalins (0.008 mg/kg in vivo and 10−6m in vitro) enhanced e.j.p. amplitude in rabbit proximal colon and decreased it in rabbit distal colon and in cat colon. Enkephalins decreased i.j.p. amplitude in all the three models.
Morphine (0.2 mg/kg in vivo and 10−6m in vitro) had the same effects as enkephalins on e.j.ps. In contrast, morphine decreased i.j.p. amplitude in rabbit proximal and distal colon and increased it in cat colon.
Enkephalins and morphine induced (especially in the cat) spike activity which was potentiated by atropine (0.1 mg/kg in vivo or 10−6m in vitro).
All the effects of enkephalins and morphine were antagonized by naloxone (0.2 mg/kg in vivo or 10−6m in vitro).
These results suggest that the facilitatory effects of enkephalins and morphine on e.j.ps of rabbit proximal colon are due to the absence of opiate receptors on the excitatory nerve pathway and to a removal of inhibition by blockade of the non‐adrenergic, non‐cholinergic inhibitory pathway. Enkephalinergic intramural neurones may modulate the activation of either excitatory or inhibitory pathways in intramural reflexes.
THE EFFECT OF CHLORPROMAZINE ON THE FUNCTION OF COLONIC AND ILEAL MUCOSA IN THE ANAESTHETIZED RAT
Authors: BUNCE K.T. , SPRAGGS C.F. 
Published: July 2012

The effect of chlorpromazine (Cpz) on the net fluxes of water and sodium in the ileum and colon has been studied in the anaesthetized rat.
Under control conditions both the ileum and colon absorbed water and sodium. Cpz (100 μmol/kg, s.c.) had no significant effect on these basal rates of absorption.
Intestinal secretion was stimulated by a combination of intra‐arterial prostaglandin E1 (PGE1; 10 nmol kg−1 min−1) and intraluminal theophylline (25 mm). A marked potentiation occurred between PGE1 and theophylline in the stimulation of colonic and ileal secretion.
In the ileum, a dose‐related inhibition of the PGE1/theophylline‐induced changes in the net fluxes of water and sodium was produced by Cpz (0.1 to 100 μmol/kg, s.c.). Under these conditions the inhibition of the secretagogue‐induced changes was significant using Cpz at 1 μmol/kg (s.c.) and a dose of Cpz of 100 μmol/kg (s.c.) returned the net fluxes of both water and sodium to basal levels.
In the colon, Cpz, at doses of 0.1 and 1 μmol/kg subcutaneously did not inhibit the PGE1/theophylline‐induced changes in the net fluxes of water and sodium, and, in contrast with the ileum, significant changes were only obtained with Cpz at 10 μmol/kg. Increasing the dose of Cpz to 100 μmol/kg further inhibited the net flux of sodium, but not that of water in the colon, and in each case the secretagogue‐induced changes were not returned to basal levels.
EFFECTS OF METHIONYL‐TYROSYL‐LYSINE ON NEURONES IN THE RAT CENTRAL NERVOUS SYSTEM
Authors: NORMANTON J.R. , WEST D.C. , WOLSTENCROFT J.H. 
Published: July 2012

The effects of microiontophoretically applied methionyl‐tyrosyl‐lysine (Met‐Tyr‐Lys) were studied on single neurones in several brain regions of rats anaesthetized with urethane.
Met‐Tyr‐Lys inhibited 13.5%–25% of neurones in the spinal cord, cerebellar cortex, thalamus and hippocampal formation. No significant inhibitory effects were seen in the cerebral cortex.
Additionally, Met‐Tyr‐Lys excited some cells in the Purkinje cell body layer of the cerebellar cortex (11 %) and in the pyramidal cell body layer of the hippocampus and granule cell body layer of the dentate gyrus within the hippocampal formation (17.5%).
Both excitatory and inhibitory effects of Met‐Tyr‐Lys were dose‐dependent, of similar rapid time course and were observed both on spontaneously active cells and cells induced to fire by continuous iontophoretic application of dl‐homocysteic acid.
The possibility that Met‐Tyr‐Lys might be a novel inhibitory neurotransmitter in both spinal and supraspinal regions of the mammalian CNS is discussed.
VASOACTIVE INTESTINAL POLYPEPTIDE IS MORE POTENT THAN PROSTAGLANDIN E2 AS A VASODILATOR AND OEDEMA POTENTIATOR IN RABBIT SKIN
Authors: WILLIAMS T.J. 
Published: July 2012

The 28 amino acid polypeptide, vasoactive intestinal polypeptide (VIP) induced increased local blood flow when injected intradermally in the rabbit.
VIP was found to be even more potent than prostaglandin E2 (PGE2) in increasing blood flow; VIP induced a significant effect at a 1 pmol dose.
VIP was shown to be poor in increasing microvascular permeability but very potent in enchancing local oedema induced by two substances which increase permeability, bradykinin and C5a des Arg. VIP was more potent than PGE2 as an oedema potentiator.
Indomethacin had no effect on oedema potentiation induced by VIP, suggesting that a release of endogenous prostaglandins was not involved.
These results support our hypothesis for the regulation of oedema formation by arteriolar vasodilators, although the observations do not exclude the possibility of additional regulation by agonist interaction in the region of the venule.
VIP may be involved in the physiological control of normal blood flow and in hyperaemia in some types of inflammatory reactions.
THE EFFECTS OF AMFONELIC ACID AND SOME OTHER CENTRAL STIMULANTS ON MOUSE STRIATAL TYRAMINE, DOPAMINE AND HOMOVANILLIC ACID
Authors: JUORIO A.V. 
Published: July 2012

The concentrations of p‐ and m‐tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous administration of amfonelic acid, (+)‐amphetamine or nomifensine.
The administration of 2.5 −25 mg/kg of amfonelic acid produced a reduction in p‐tyramine that lasted at least 8 h. m‐Tyramine was significantly increased and this was observed between 2 and 24 h after drug treatment. The levels of homovanillic acid were increased within 4 h after amfonelic acid administration.
(+)‐Amphetamine treatment (5 mg/kg) produced a reduction in p‐tyramine observed up to 4 h after its administration and no significant changes in m‐tyramine.
The administration of 10 mg/kg of nomifensine produced no significant changes in p‐tyramine, m‐tyramine or homovanillic acid. By increasing the dose to 20 mg/kg, nomifensine produced an increase in p‐tyramine and homovanillic acid.
The present results support the view that amfonelic acid and (+)‐amphetamine would respectively release granular or newly synthesized dopamine, both actions being accompanied by an increase in tyrosine hydroxylase activity and dopamine turnover which in turn reduces p‐tyramine but produces no change or an increase in m‐tyramine.
The effects of nomifensine were observed after the administration of a relatively high dose (20 mg/kg), that was lethal to some mice (about 20%, at 2 h), and more likely to possess unspecific actions.
VOLTAGE‐ AND TIME‐DEPENDENT DEPRESSION OF MAXIMUM RATE OF DEPOLARIZATION OF GUINEA‐PIG VENTRICULAR ACTION POTENTIALS BY TWO STEROIDAL ANTIARRHYTHMIC DRUGS, CCI 22277 AND ORG 6001
Authors: CAMPBELL TERENCE J. 
Published: July 2012

The voltage‐ and time‐dependence of the depression of the maximum rate of depolarization (V̇max) by two steroidal anti‐arrhythmic drugs, CCI 22277 and Org 6001 were studied in guinea‐pig ventricle.
At normal resting potentials CCI 22277 (2 μm and 4 μm) produced very little depression of V̇max at very low driving rates (resting block) but trains of stimuli at interstimulus intervals (ISI) of less than 10,000 ms led to an exponential decline in V̇max to a new plateau over 100–200 beats.
This ‘rate‐dependent block’ (RDB) increased with rate over the range ISI = 4800 to ISI = 200 ms.
Org 6001 30 μm and 60 μm produced a similar degree of RDB over the same range of frequencies but the new plateau level of V̇max was reached much more rapidly (20–30 beats) and there was a moderate degree of depression of V̇max in the resting tissue.
Recovery from RDB in the presence of both drugs was an exponential process with time constants (τre) of 80.4 ± 7.4 s for CCI 22277 and 4.6 ± 0.5 s for Org 6001.
Both drugs shifted the steady‐state inactivation curve, relating V̇max to resting membrane potential, in the hyperpolarizing direction, implying selective depression of depolarized cells.
PINANE THROMBOXANE A2 ANALOGUES ARE NON‐SELECTIVE PROSTANOID ANTAGONISTS IN RAT AND HUMAN STOMACH MUSCLE
Authors: BENNETT ALAN , SANGER GARETH J. 
Published: July 2012

Pinane thromboxane A2 (PTxA2) and its epi‐OH isomer were studied on rat and human stomach longitudinal muscle.
PTxA2 (0.5 μg/ml) usually caused a slight contraction of rat gastric fundus. Contractions to PGE2, PGF2α, PGI2 and expoxymethano analogues of PGH2 (U‐46619 and U‐44069) were substantially inhibited, whereas those to PGD2 and acetylcholine were only slightly reduced.
In human stomach, PTxA2 0.5 μg/ml rarely stimulated the muscle. Contractions to PGE2, PGF2α and U‐46619 were antagonized, with little effect on those to acetylcholine.
epi‐PTxA2 (0.5 μg/ml) did not affect rat gastric tone. It was moderately potent against PGI2 on rat gastric fundus, but was less effective than PTxA2 against U‐44069.
RELEASE OF PURINES AND NORADRENALINE BY OUABAIN AND POTASSIUM CHLORIDE FROM VASCULAR ADRENERGIC NERVES
Authors: KATSURAGI T. , SU C. 
Published: July 2012

Release of [3H]‐noradrenaline and 3H‐purine by ouabain (10−4m) or high KCl (50 mm) was investigated in the superfused rabbit pulmonary arterial segment preincubated with [3H]‐noradrenaline or [3H]‐adenosine.
Ouabain elicited a delayed large contraction and a parallel [3H]‐noradrenaline efflux. These were substantially inhibited by Ca2+‐free medium or preincubation with 6‐hydroxydopamine (30 μg/ml, 30 min).
Ouabain caused an 3H‐purine efflux which was slower than the [3H]‐noradrenaline efflux. This was inhibited by 6‐hydroxydopamine and in part by phentolamine (3 × 10−6 m), indicating both neuronal and extraneuronal origins of purines.
In contrast to ouabain, high KCl appeared to induce predominantly purine efflux, which was phentolamine‐insensitive and 6‐hydroxydopamine‐sensitive, indicative of neuronal origin.
It is suggested that the purine efflux evoked by ouabain and high KCl may originate from different neuronal vesicles.
STRUCTURE‐ACTIVITY RELATIONSHIPS OF N‐β‐PHENYLPROPIONYL‐l‐TYROSINE AND ITS DERIVATIVES ON THE INHIBITION OF AN IDENTIFIABLE GIANT NEURONE OF AN AFRICAN GIANT SNAIL
Authors: ARIYOSHI YASUO , TAKEUCHI HIROSHI 
Published: July 2012

Inhibitory effects of N‐β‐phenylpropionyl‐l‐tyrosine, N‐β‐phenylpropionyl‐l‐tryptophan and their derivatives on an identifiable giant neurone, TAN (tonically autoactive neurone) of an African giant snail (Achatina fulica Férussac) were examined in an attempt to elucidate which structural features are necessary to produce the effect.
Of the compounds examined, N‐β‐cyclohexylpropionyl‐l‐tyrosine showed the strongest effect. Its critical concentration (c.c.) was 3 × 10−8‐10−7m, about ten times lower than that of N‐β‐phenylpropionyl‐l‐tyrosine (c.c, 3 × 10−7‐10−6m). N‐β‐cyclohexylpropionyl‐l‐tryptophan (c.c, 10−6m) had an effect almost similar to that of N‐β‐phenylpropionyl‐l‐tryptophan (c.c, 10−6m).
N‐β‐Phenylpropionyl‐N‐methyl‐l‐tyrosine had no effect at a high concentration.
Effects of N‐β‐phenylpropionyl‐l‐tyrosine amide (c.c, 3 × 10−7‐10−6m) and N‐β‐phenylpropionyl‐l‐tryptophan amide (c.c, 10−6m) were very similar to those of N‐β‐phenylpropionyl‐l‐tyrosine and N‐β‐phenylpropionyl‐l‐tryptophan respectively.
N‐β‐Phenylpropionyl‐p‐amino‐l‐phenylalanine (c.c, 3 × 10−5‐10−4m) and N‐β‐phenylpropionyl‐p‐chloro‐l‐phenylalanine (c.c, 10−4m) had only a weak effect.
It is proposed that the structural features producing the effect are as follows: the active compound has a phenyl or a cyclohexyl group (hydrophobic binding group), after a suitable distance a peptide bond (proton donor and proton acceptor), adjacently a carbonyl group (proton acceptor), and a phenolic hydroxyl or an indolyl imino group (proton donor) in the molecule.
WITHDRAWAL OF MAGNESIUM ENHANCES CORONARY ARTERIAL SPASMS PRODUCED BY VASOACTIVE AGENTS
Authors: ALTURA BURTON M. , TURLAPATY PRASAD D.M.V. 
Published: July 2012

The influence of external magnesium ions ([Mg2+]o) on the sensitivity (i.e. EC50) and contractility (maximum response) of isolated large and small coronary arteries of the dog, obtained from different regions of the myocardium, to vasoactive agents was studied.
Removal of [Mg2+]o from the physiological salt solution enhanced, while elevation in [Mg2+]o to 4.8 mm, lowered the contractile sensitivity to three different agents, 5‐hydroxytryptamine (5‐HT), angiotensin II and KCl.
Contractility, of both large and small coronary arteries, to 5‐HT and angiotensin II was potentiated and depressed, respectively, by withdrawal and elevation of [Mg2+]o; maximum responses to KCl were not altered by 0 or 4.8 mm [Mg2+]o.
Cumulative concentration‐contractile effect curves to CaCl2 were shifted leftward on removal of [Mg2+]o; elevation of [Mg2+]o to 4.8 mm shifted the CaCl2 concentration‐effect curves to the right. Maximal contractile responses to CaCl2 were enhanced by removal of, and reduced by elevation of, [Mg2+]o
The calcium channel blocking agent, verapamil (10−6m), inhibited completely contractile responses to KCl; contractile responses elicited by angiotensin II and 5‐HT were attenuated by verapamil.
A variety of pharmacological antagonists (phentolamine, propranolol, methysergide, atropine, diphenhydramine), as well as use of a prostaglandin cyclo‐oxygenase inhibitor, did not modify the altered contractile responses evoked by angiotensin II or KCl in different concentrations of Mg2+.
These results suggest: (1) [Mg2+]o may exert considerably greater influence on receptor‐operated rather than membrane‐potential sensitive channels involved in Ca2+ transport in coronary arterial smooth muscle; (2) Mg2+ interferes with the affinity (binding) of certain agonists (5‐HT and angiotensin II) for their respective receptors in coronary vascular muscle; and (3) a functional pool of Ca2+ which is resistant to Ca2+‐depletion, but accessible to activation by 5‐HT and angiotensin II is present in canine coronary arterial smooth muscle.
EFFECTS OF CALMODULIN ANTAGONISTS ON TENSION AND CELLULAR CALCIUM CONTENT IN DEPOLARIZED VASCULAR AND INTESTINAL SMOOTH MUSCLES
Authors: KARAKI H. , MURAKAMI K. , NAKAGAWA H. , OZAKI H. , URAKAWA N. 
Published: July 2012

Several putative calmodulin antagonists have been examined for their inhibitory action on muscle tension and cellular Ca content in the K‐depolarized vascular and intestinal smooth muscles.
The 65.4 mm K‐induced sustained contraction in the media‐intimal layer of rabbit aorta and the 45.4 mm K‐induced sustained contraction in guinea‐pig taenia coli were inhibited by the calmodulin antagonists, prenylamine, chlorpromazine, N2‐dansyl‐l‐argiiiine‐4‐t‐butylpiperadine amide (No. 233), and N‐(6‐aminohexyl)‐5‐chloro‐l‐naphthalenesulphonamide (W‐7), and also by the organic Ca antagonists, verapamil and diltiazem.
The cellular Ca content in rabbit aorta and guinea‐pig taenia coli as measured by a modified lanthanum technique increased in the high‐K solutions. The increments were inhibited by these antagonists at concentrations similar to those required to inhibit the K‐induced contractions. However, W‐7 did not change (in aorta) or only slightly decreased (in taenia coli) the K‐induced increase in the cellular Ca content.
A high concentration (2 × 10−4m) of W‐7 increased the resting cellular Ca content without increasing the muscle tension in aorta. The increment was inhibited by verapamil, sodium nitroprus‐side or hypoxia (N2 aeration).
It is suggested that the inhibitory effects of prenylamine, chlorpromazine and No. 233 may be attributed mainly to the Ca antagonistic effect whereas W‐7 may inhibit the process beyond the transmembrane Ca influx.
INHIBITORY ACTION OF γ‐AMINOBUTYRIC ACID ON THE EXCITATORY BUT NOT INHIBITORY INNERVATION OF THE RAT ANOCOCCYGEUS MUSCLE
Authors: HUGHES P.R. , MORGAN P.F. , STONE T.W. 
Published: July 2012

The effects of γ‐aminobutyric acid (GABA), ethylenediamine, 3‐aminopropane sulphonic acid and (±)‐baclofen have been examined on the responses to stimulation of the adrenergic excitatory and non‐adrenergic non‐cholinergic inhibitory innervation of the rat anococcygeus muscle in vitro.
GABA produced a dose‐related depression of the contractile responses to field stimulation. Ethylenediamine and baclofen also depressed the contractile responses, though they were less potent than GABA. 3‐Aminopropane sulphonic acid was almost inactive. The inhibitory action of GABA was not modified by phentolamine, propranolol or bicuculline methylbromide.
GABA did not affect the contractile responses of the anococcygeus muscle to noradrenaline, phenylephrine or carbachol in untreated muscles or those treated with 6‐hydroxydopamine in vitro.
In preparations in which tone was raised by continuous perfusion with carbachol in the presence of phentolamine, field stimulation relaxed the muscle. GABA had no effect on this inhibitory response, and did not itself produce any relaxation.
It is concluded that GABA exerts a presynaptic inhibitory action on the excitatory adrenergic but not on the inhibitory innervation of the anococcygeus muscle, and that the GABA receptor involved exhibits properties of the previously described GABAB site.
THE MECHANISM OF ACTION OF A SUBSTANCE P ANTAGONIST (D‐Pro2, D‐Trp7,9)‐SP
Authors: HÅKANSON R. , HÖRIG J. , LEANDER S. 
Published: July 2012

A newly synthesized substance P (SP) analogue, (d‐Pro2, d‐Trp7,9)‐SP, specifically antagonizes the contractile effects of SP on the guinea‐pig isolated taenia coli. In addition, previous studies had indicated that the SP analogue per se is capable of contracting this preparation. The results of the present study on the guinea‐pig taenia suggest that the smooth muscle contractions produced by the SP analogue are due to histamine release. No contractions were observed following blockade of histamine H1‐receptors by mepyramine or following pretreatment with the histamine liberating agent, compound 48/80.
Analysis of the inhibition of SP‐induced contraction by the analogue suggests that the inhibition is of the competitive type; pA2 was calculated to be 6.1.
We conclude that (d‐Pro2, d‐Trp7,9)‐SP is a competitive SP antagonist with histamine‐releasing properties.
THE EFFECT OF MIXED INHIBITORS OF CYCLO‐OXYGENASE AND LIPOXYGENASE ON THE INDOMETHACIN‐INDUCED HYPER‐REACTIVITY IN THE ISOLATED TRACHEA OF THE PIG
Authors: MITCHELL H.W. 
Published: July 2012

Indomethacin enhances muscle contraction to histamine in the pig isolated trachea. The effect of three cyclo‐oxygenase/lipoxygenase inhibitors on these potentiated histamine‐induced responses was examined.
At the higher concentrations BW755c (113–226 μm), 5, 8, 11, 14‐eicosatetraynoic acid (ETYA, 10–100 μm) and phenidone (5–500 μm) abolished the effect of indomethacin on tracheal contractions to histamine (100 μm).
Each of the three inhibitors also reduced the slope of the histamine concentration‐response curve obtained in the presence of indomethacin. However, the sensitivity (pD2) of the smooth muscle to histamine was not affected by BW 755c, ETYA or phenidone.
The results provide further support for a lipoxygenase‐dependent component of indomethacin‐induced hyper‐reactivity in the pig trachea.