Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Methacholine Chloride”

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.

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

At least 343 records · Page 19Linked to original sources
PubMed1987

Airway responses to nitrogen dioxide in asthmatic subjects.

Nitrogen dioxide is a common indoor air pollutant. In order to characterize the respiratory responses to this gas, 10 asthmatics (mean age +/- SD = 30 +/- 8 yrs) were exposed to air and 0.5 ppm NO2 gas for 1 h in a 30-m3 environmental chamber on different days in a double-blind randomized fashion. The forced vital capacity, (VC), functional residual capacity, forced expiratory volume in 1 s, partial expiratory flow at 40% VC (Vp 40), and specific airway conductance were measured before and after exposure. Airway reactivity to methacholine inhalation was determined after each exposure. The dose of methacholine in milligrams per milliliter to cause a 40% decrease in Vp 40 was measured. None of the subjects reported any significant symptoms after exposure. Significant potentiation of airway reactivity was noted after NO2 exposure in asthmatic subjects as a group [PD40(AIR) = 9.2 +/- SD 15.0 versus PD40(NO2) = 4.6 +/- SD 8.2 mg/ml, p = 0.042]. No significant changes were noted in other lung functions after NO2 exposure. These findings indicate that asthmatics exposed to 0.5 ppm NO2 develop heightened airway reactivity.

Adult↗
PubMed1990

Dose-response relationship of ozone-induced airway hyperresponsiveness in unanesthetized guinea pigs.

The effect of ozone dose (the product of ozone concentration and exposure time) on airway responsiveness was examined in unanesthetized, spontaneously breathing guinea pigs. Airway responsiveness was assessed by measuring specific airway resistance (sRaw) as a function of increasing concentration of inhaled methacholine (Mch) aerosol (the concentration of Mch required in order to double the baseline sRaw: PC200Mch). The airway responsiveness was measured before and at 5 min, 5 h, and 24 h after exposure. A 30-min exposure to 1 ppm ozone (dose 30 ppm.min) did not change PC200Mch at any time after exposure. Both a 90-min exposure to 1 ppm ozone and a 30-min exposure to 3 ppm ozone, which are identical in terms of ozone dose (90 ppm.min), decreased PC200Mch to a similar degree. A 120-min exposure to 3 ppm ozone (360 ppm.min) produced a much greater decrease of PC200Mch at 5 min and 5 h after exposure, compared with low-dose exposure. There was a significant correlation between ozone dose and the change in airway responsiveness. In all groups, the baseline sRaw was increased by approximately 50% at 5 min after exposure, but there was no correlation between the changes in PC200Mch and the baseline sRaw. This study suggests that ozone-induced airway hyperresponsiveness in guinea pigs is closely related to ozone dose.

Aerosols↗
PubMed1984

Sulfur dioxide and ammonium sulfate effects on pulmonary function and bronchial reactivity in human subjects.

The effect of exposures to 1 ppm sulfur dioxide (SO2) and 500 micrograms/m3 respirable ammonium sulfate [(NH4)2SO4] was studied in 20 nonsmoking subjects to determine if a response can be measured at these atmospheric levels and if the response is additive or synergistic. Four-hour separate and combined exposures were employed. Each subject acted as his or her own control and performed two light-to-moderate exercise stints (612 kg-m/min) for 15 minutes on each day's confinement in the environmental chamber. Pulmonary function tests (body plethysmography and spirometry) and bronchial reactivity to methacholine were performed to assess the response of these exposures. No significant changes in pulmonary function or bronchial reactivity were observed in the individual exposures [(NH4)2SO4 or SO2], the combined exposure [(NH4)2SO4 and SO2], or 24 hours post-exposure. This study design and the observed results did not demonstrate any readily apparent risk to healthy subjects with these exposures. Since no significant changes were measured, it was not possible to conclude if these two pollutants in combination produce an additive or synergistic response.

Adult↗
PubMed1988

Systemic blood pressure and intraocular pressure relationship.

The relationship between intraocular pressure (IOP) and arterial blood pressure (BP) was analyzed in response to two pressor agents (norepinephrine and angiotensin II) and two depressor agents (methacholine and isoproterenol) in pentobarbital anesthetized cats. Both IOP and BP were measured manometrically in the same animals. Intravenous norepinephrine and angiotensin II produced dose-dependent increases, whereas intravenous methacholine and isoproterenol produced dose-dependent decreases of both BP and IOP. The IOP response to methacholine was biphasic, with an initial decrease followed by an increase above the pre-drug level. In some experiments a cannula loop was inserted into a carotid artery in order to separate the direct ocular effect of drugs on IOP from that contributed by the changes in systemic BP. Intravenous administration of norepinephrine and angiotensin II produced a larger increase in IOP on the side where drugs were delayed by the loop. Conversely, methacholine produced a larger fall in IOP on the cannulated side while the effect of isoproterenol was essentially unchanged. In other experiments injections were made directly into the ocular arterial blood supply. Norepinephrine and angiotensin II produced a decrease in IOP, methacholine produced a rise of IOP and isoproterenol was not active by this route. The present findings indicate that IOP is largely influenced by arterial BP changes in the acute phase and that the IOP response to drugs is the algebraic sum of effects on systemic BP and their direct ocular effects.

Angiotensin II↗
PubMed1988

An assessment of methacholine inhalation tests in elderly asthmatics.

We have assessed the feasibility and value of measuring nonspecific bronchial responsiveness to methacholine in investigation of asthma in the elderly. Results from duplicated tests in 20 subjects aged 65-82 years were expressed as dose provoking a 20% decrement in 1 second forced expiratory volume (PD20.FEV1) or peak expiratory flow (PD20.PEF). Repeatability for PD20.FEV1 was satisfactory but less good than in younger subjects, 95% confidence limits being 0.39-2.57 and 0.52-1.91, respectively, x initial PD20. For PD20.PEF, confidence limits were wider (0.26-3.91 x initial PD20) but multiple PEF measurements were better tolerated than those of FEV1, which commonly caused fatigue and dizziness. PD20.FEV1 and PD20.PEF correlated closely (r = 0.95, P less than 0.0001) and both predicted bronchodilatation following a 6-week course of inhaled corticosteroid and beta agonist. This was not predicted by the response to a single dose of beta agonist. We conclude that measurement of bronchial responsiveness is feasible and clinically valuable in elderly subjects.

Aged↗
PubMed1982

Methacholine pupillary responses in third nerve palsy and Adie's syndrome.

In order to examine the clinical usefulness of methacholine in assessing the site of ocular parasympathetic lesions, pupillary responses in man were measured in postganglionic (Adie's syndrome) and preganglionic third nerve lesions involving the pupil and in controls. From previous work with methacholine it might have been expected that greater constriction would occur in the postganglionic lesions but similar responses were found in both. Corneal hypoxia due to ptosis appeared unlikely to affect corneal permeability significantly and it is probable that these results reflect an increase responsiveness of the iris at, or distal to, the site of muscarinic acetylcholine receptors. Pupils contralateral to third nerve palsy, when tested on a separate occasion, also constricted by an amount approximately proportional to that of the clinically abnormal pupil. The possibilities that this may result in some way from reduction in total retinal illumination, or from retrograde changes in preganglionic pupilloconstrictor neurons affecting contralateral pupilloconstrictor neurons via central pathways, are discussed. It is concluded that supersensitivity to methacholine, tested carefully in the manner described, is a useful guide to the presence of parasympathetic denervation or decentralization, but that it is not reliable in distinguishing between the two sites.

Adie Syndrome↗
PubMed1986

Effects of adrenergic and muscarinic receptor stimulation on serum potassium concentrations and myocardial electrical stability.

The influence of adrenergic and muscarinic receptor activation on cardiac electrical stability and on serum potassium concentrations was studied in 23 anaesthetised dogs. The ventricular fibrillation threshold was assessed using the single stimulus technique. Adrenaline (1.0 microgram X kg-1 X min-1) caused a brief rise and a subsequent prolonged fall in serum potassium concentration, which was accompanied by a decline in ventricular fibrillation threshold when baroreceptor activation was prevented. After pretreatment with the beta1 adrenoceptor blocking agent metoprolol (0.5 mg X kg-1), adrenaline did not alter vulnerability to ventricular fibrillation but still elicited hypokalaemia. In contrast, selective beta2 adrenoceptor blockade (ICI 118551, 100 micrograms X kg-1) prevented the adrenaline induced lowering of serum potassium concentration but not of ventricular vulnerability. Muscarinic receptor activation by methacholine (3.0 micrograms X kg-1 X min-1) had no effect on serum potassium concentration but increased the ventricular fibrillation threshold by 30%. When methacholine was administered concomitantly with adrenaline the decline in serum potassium concentration persisted, but the increase in ventricular vulnerability was completely prevented. It is concluded that in the normal canine myocardium adrenaline produces an increase in vulnerability that is mediated through beta 1 adrenoceptors and that the beta 2 adrenoceptor mediated hypokalaemia is dissociated from electrophysiological effects of adrenaline. Parasympathetic nervous system activation does not influence serum potassium concentrations but opposes the effects of adrenaline on susceptibility to ventricular fibrillation.

Adrenergic beta-Antagonists↗
PubMed1982

Bronchial reactivity in experimental infections with influenza virus.

In an attempt to develop an objective, quantitative test to assess the reactogenicity of candidates for attenuated influenza virus vaccines, the clinical responses and bronchial reactivity to methacholine were assessed in 36 normal volunteers lacking antibody to both hemagglutinin and neuraminidase (doubly seronegative) who were inoculated with either wild-type or temperature-sensitive attenuated influenza A (H1N1) virus by intranasal droplets. Five of six volunteers infected with wild-type virus developed systemic and/or febrile illness that lasted for a mean of five days. Nineteen of 30 persons who received attenuated virus developed infection without febrile or systemic illness. In the six recipients of wild-type virus, bronchial reactivity appeared to increase after inoculation and persist for four weeks. This trend was not observed in infected or noninfected vaccinees. Analysis of variance provided suggestive (but not significant) evidence that the different trends in bronchial reactivity manifested by the wild-type virus and vaccine groups were distinct (P = 0.075).

Airway Resistance↗
PubMed1987

Enhanced cAMP accumulation after termination of cholinergic action in the heart.

Cholinergic agents decrease myocardial contractility in part by inhibiting adenylate cyclase (EC 4.6.1.1) activity. We have found that after a prolonged preincubation period (greater than 6 h), washout of cholinergic agents from embryonic chick hearts or cultured heart cells results in a persistent increase in their basal and catecholamine-stimulated cAMP content. Membranes prepared from pretreated cells have elevated basal, forskolin-, and catecholamine-stimulated adenylate cyclase activities. This myocardial adaptation to cholinergic agents is analogous to changes in nerve cells and other cell types after prolonged exposures to narcotics or other inhibitors of adenylate cyclase, respectively. A rapid (less than 5 min) adaptation response to cholinergic agents can also be demonstrated in heart cells by quickly blocking agonist action with atropine. Atropine alone has no effect, but after a brief preincubation period with agonists (methacholine or oxotremorine), the addition of atropine transiently enhances catecholamine-stimulated cAMP accumulation by 2.5-fold. These responses are absent in heart cells pretreated with pertussis toxin. The data indicate that the response is not mediated by the phosphoinositide pathway, which has been demonstrated to be insensitive to pertussis toxin in chick heart. Enhanced cAMP accumulation after termination of muscarinic agonist action may provide an explanation for the observation that acetylcholine sometimes produces biphasic contractile responses.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Pulmonary reactivity to methacholine during beta-adrenergic blockade: propranolol versus esmolol.

Pulmonary reactivity to methacholine after equipotent beta-blocking doses of propranolol and esmolol was compared in seven basenji-greyhound dogs during thiopental-fentanyl anesthesia. Equipotent doses of esmolol and propranolol were determined by both heart rate effects and by isoproterenol response curves. Propranolol (2 mg/kg) was administered intravenously as a bolus dose and esmolol (0.4-0.5 mg.kg-1.min-1) was administered by continuous infusion. Both esmolol and propranolol significantly decreased heart rate and mean arterial pressure (P less than 0.001). Baseline pulmonary resistance and dynamic compliance did not change after the administration of either propranolol or esmolol. However, propranolol significantly shifted the methacholine dose-response curve to the left so that methacholine (0.3 mg/ml) increased pulmonary resistance by 7.9 +/- 0.97 cmH2O.l-1.s-1 (mean +/- SEM of seven dogs) after pretreatment with propranolol but only 4.4 +/- 0.89 cmH2O.l-1.s-1 (P less than 0.05) without propranolol pretreatment (control). Esmolol, however, did not significantly shift the methacholine dose-response curve. Methacholine (0.3 mg/ml) increased resistance 4.0 +/- 0.89 cmH2O.l-1.s-1 during esmolol administration. This study shows that at equipotent beta 1-blocking doses, propranolol, but not esmolol, produces significant increases in pulmonary reactivity to methacholine.

Adrenergic beta-Antagonists↗
PubMed1988

Cardiopulmonary effect of various inspiratory flow profiles during controlled mechanical ventilation in a porcine lung model.

We studied the influence of inspiratory flow (VI) patterns on gas exchange and hemodynamics after metacholine inhalation challenge (MIC) in seven swine mechanically ventilated with a constant, sinusoidal, accelerating, and decelerating flow pattern. Blood gas and expired CO2 tensions, pulmonary mechanics, and hemodynamics were measured during each pattern. Flow pattern sequence was randomized and MIC was repeated at 30 to 45-min intervals. MIC reliably reduced PaO2, and increased PaCO2 and peak tracheal pressure (PT). There was no significant difference in gas exchange or hemodynamics between various VI curves. Insufflation with an accelerated VI manifested a significantly higher PT than any other pattern. We conclude that no VI contour studied offers a unique advantage for gas exchange after MIC in swine. However, since accelerated gas flow generates significantly higher PT values, it is not recommended in the presence of significant airway resistance.

Animals↗
PubMedDate not supplied

Effects of pharmacologic agents on induced atrial flutter in dogs with right atrial enlargement.

The effects of selected drugs on the sustained atrial flutter induced in conscious dogs with surgically produced right atrial enlargement (TI dogs) were evaluated. This was done to better understand the electrophysiologic mechanism of the tachyarrhythmias. Agents known to cause a slowing of atrioventricular (AV) nodal conduction--verapamil, methacholine, and phenylephrine--did not significantly decrease the rate of the induced flutter, whereas beta-adrenergic stimulation with an infusion of isoproterenol increased the rate of the flutter in all trials. Propranolol and atropine had little effect on the atrial flutter rate. Agents known to increase atrial refractoriness, such as procainamide, n-acetylprocainamide, bretylium, and clofilium, all increased the cycle length of the induced flutter and, in some cases, terminated the arrhythmia. These results suggest then that the perpetuation of the sustained atrial flutter in the conscious TI dog is not due to a delayed afterdepolarization mechanism but is more likely due to reentrant excitation. Furthermore, it is unlikely that the flutter is due to reentry over a pathway involving the AV node; rather, the arrhythmia seems to be caused by reentrant excitation of the leading circle type.

Acecainide↗
PubMed1986

Approaches to assessing pulmonary dysfunction and susceptibility in workers.

Indices of the maximal forced expiration are the most widely adopted method of screening for occupational lung disease because of their ease of measurement, employee acceptability, and reproducibility. However, these indices may lack sensitivity, specificity, or validity in detecting cases of some occupational lung diseases at asymptomatic stages when intervention may affect outcome. In populations at increased risk for occupational asthma, pneumoconiosis, or hypersensitivity pneumonitis, three other types of screening are being evaluated in field settings: tests for bronchial hyperreactivity, barriers to diffusion, and abnormalities in gas distribution in the lung. The potential methods of screening--cold air challenge, methacholine challenge, peak flow logs, diffusing capacity, and single breath nitrogen tests--await clinical trials in industrial settings to evaluate whether early case finding of susceptible subjects can result in prevention of morbidity.

Cold Temperature↗
PubMed1988

Does seasonal employment in grain elevators increase nonspecific airways responsiveness?

Grain handling and increased airways responsiveness (AR) have been independently associated with an accelerated decline in forced expiratory volume in 1 sec. We performed methacholine inhalation bronchial challenge tests in 45 river port grain handlers during layoff and again during employment to determine whether short-term exposure increased AR. To assess bias, due to seasonal/temporal influences, AR was also measured in 56 nonexposed men of similar age and socioeconomic status. AR, slightly higher among laid-off grain handlers than the comparison group, fell more among grain handlers during employment than among the comparison group during the same time period. Our results do not support the hypothesis that seasonal exposure to grain dust increases AR.

Adult↗
PubMed1984

Sweat production in the isolated eccrine sweat gland of the rat.

A method has been developed to isolate a single rat eccrine sweat gland, together with the attached sweat duct, and to induce sweat secretion directly from the gland in vitro. Sweat production was induced using carbachol (2 X 10(-5) M to 3 X 10(-5) M) and methacholine (2 X 10(-5) M) in isolated plantar sweat glands maintained in a suitable environment (modified Krebs-Ringer bicarbonate at 38 degrees C containing 30% w/v fresh rat serum). The output of sweat was measured every 5 minutes for 85 minutes and the maximal final volume obtained with any one gland was 23 nl. Sweat production ceased on administration of appropriate concentrations of atropine (1 X 10(-5) M to 5 X 10(-5) M), withdrawal of calcium ions from the bathing fluid, and reduction of the medium temperature to 4 degrees C.

Animals↗
PubMed1986

Electrical field stimulation of isolated primate sweat glands.

An in vitro method is described for inducing secretion in isolated monkey eccrine sweat glands by means of electrical field stimulation (EFS). Ultrastructural analyses of these glands revealed unmyelinated nerve fibres surrounding the secretory coils. Numerous small clear vesicles, characteristic of cholinergic nerve terminals, were observed, along with a few which were large and dense-cored. EFS elicited an immediate secretory response which ceased abruptly upon termination of the current. The response was inhibited in a dose-dependent manner by atropine (IC50 1.5 X 10(-9) mol/l). Although most glands were completely inhibited by atropine, a minor atropine insensitive component was operative in some preparations. Physostigmine (10(-6) mol/l) potentiated the response to subthreshold EFS. Lidocaine (3 X 10(-4) mol/l) completely and reversibly blocked EFS but had no effect on methacholine (10(-6) mol/l) induced secretion. These results confirm that eccrine sweat gland activation is predominantly via cholinergic pathways and that EFS of isolated glands may be a useful model to study the control of secretory function in normal and diseased states.

Animals↗