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At least 19 recordsLinked to original sources
PubMed1979

Effect of methacholine chloride on rheology and transport of canine tracheal mucus.

The effect of methacholine chloride (M) on tracheal mucus was investigated in three conscious tracheostomized dogs. Aerosols of M in concentrations of 2--32 mg/ml were delivered intratracheally for 1 min. Mucus was sampled with a cytology brush at 2 min postchallenge and at irregular intervals thereafter. The mechanical properties of each sample were determined in the magnetic microrheometer, and correlated with mucociliary transportability as assayed by the frog palate technique. With high doses of M, there was an increase in volume of secretion collected per unit time. The elastic modulus (G') at 2 min postchallenge went up (to 1.5 x 2.3 x control for 16 and 32 mg/ml, respectively) then fell below control before returning to base line after 30 or 45 min. With low doses of M (2--8 mg/ml) the secretion rate was also above control, but only a decrease in G' (to 0.54 x control) was observed. The decrease in G' at low doses did not significantly alter the frog palate transport rate; however, the increase at higher doses did impede mucociliary transport.

Animals↗
PubMed1987

Proteins are secreted from heterogeneous prestored sources in the exocrine pancreas.

Recent studies demonstrating nonparallel regulated secretion of prestored digestive enzymes in tightly linked groups consistent with the exocytosis mechanism led us to predict that digestive enzymes would be found to be secreted from heterogeneous sources within the exocrine pancreas (J. W. Adelson, and P.E. Miller, Science Wash. DC 228: 993-996, 1985). We explored whether the gland was heterogeneous with respect to its sources of prestored secretory proteins with a double isotopic label method not dependent on activity of secreted digestive enzymes. Rabbit pancreatic proteins were double labeled in vivo by injection of each animal with chemically identical but isotopically distinct mixtures of 3H- and 14C-labeled amino acids, which were administered separately or together on consecutive days after partial depletion of prestored proteins by administration of cholecystokinin (CCK), methacholine chloride, or saline in a protocol in which order of both isotope and secretagogue administration was varied. Three days after labeling, proteins were recovered by collection from cannulated pancreatic ducts of anesthetized animals after stimulation with alternating increasing doses of CCK and methacholine chloride. Pooled secretory data were analyzed to determine whether secretagogue pretreatment resulted in specific and heterogeneous sequestration of proteins after synthesis; data after final secretory stimulation with methacholine chloride and CCK were individually analyzed to determine whether presequestered proteins were mobilized from heterogeneous compartments during secretion. Correlation and regression analysis of isotopic outputs and variance analysis of specific radioactivities of secreted proteins showed sequestration into and secretion from heterogeneous pools of secretory proteins, directly confirming out hypothesis. These results provide a cell biological mechanism explaining regulated nonparallel secretion of digestive enzymes.

Animals↗
PubMed1975

Chronic cholinergic stimulation of canine respiratory tissue. Its effect on the activities of glycosyltransferases and release of macromolecules.

The influence of cholingergic stimulation on the incorporation of D-[6-3H]glucosamine into macromolecules released by canine trachea in vitro, and the capacity of subcellular fraction of this tissue to catalyze the transfer of various sugars to specific glycoproteins were measured. Canine trachea was incubated with radiohexosamine for 18 hours in the presence of methacholine chloride. The [3H]macromolecules subsequently released were fractionated on columns of 1 per cent agarose. Those macromolecules eluted from the columns with a mobility identical to that of large molecular weight, mucin-type glycoproteins of canine tracheal pouch secretions collected in vivo were increased. The tissue then did not respond to further challenges with acetylcholine chloride, at least as regards the release of radiomacromolecular. In addition, in vitro challenges of methacholine chloride failed to alter the specific activities of the tracheobronchial tissue glycosyltransferases. The specific activities of 2 galactosyltransferases, a sialytransferase, and an N-acetylgalactosaminyltransferase were elevated after 1 month and after 2 months of daily subcutaneous injections of methacholine chloride. No further increases were seen during the third month of injections; throughout the 3 months, the specific activity of fucosyltransferase failed to change.

Acetylcholine↗
PubMed1987

Parasympathetic denervation hypersensitivity of the iris in ocular hypertension.

Seventy-eight ocular hypertensive patients and 47 age-and sex-matched control subjects were assessed for parasympathetic denervation hypersensitivity of the iris using topical application of 2.5% methacholine chloride solution. Constriction of the pupil in response to methacholine stimulation of the sphincter pupillae was significantly greater in the ocular hypertensive patients than the control group (P less than 0.001). The implications are discussed, with particular reference to the association between autonomic neuropathy and the primary glaucomas.

Administration, Topical↗
PubMed1986

Methacholine sensitivity and cAMP protein kinase in tracheal smooth muscle.

We studied regional variation in canine trachealis smooth muscle sensitivity and responsiveness to methacholine as well as basal and methacholine-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) and cAMP-dependent protein kinase activity. The trachea between the cricoid cartilage and the carina was divided into three segments of equal length (designated cervical, middle, and thoracic regions), each consisting of approximately 12-14 cartilage rings. Smooth muscle strips from each of the three regions were exposed to cumulative half-log increments of methacholine chloride. The sensitivity (-log EC50) and responsiveness (force per cross-sectional area and force per milligram protein) of the smooth muscle to methacholine in each region was determined from these data. Smooth muscle strips from cervical and thoracic regions were frozen before and after exposure to cumulative half-log increments of methacholine up to each region's previously determined EC50. Frozen samples were assayed for cAMP content or cAMP-dependent protein kinase activity. The relationship between resting tension and methacholine sensitivity and responsiveness were studied. For the size strips we used, 4 g resting tension set the average cervical and thoracic strips at 96 and 101% of their optimal length, respectively. The methacholine EC50 was not affected by a variation in resting tension. Sensitivity to methacholine was 7.1, 6.8, and 6.5 for cervical, middle, and thoracic regions, respectively. The responsiveness of the cervical and thoracic smooth muscle to methacholine was 16.4 and 16.3 g force/mm2, respectively, at an EC50 methacholine. Basal cAMP was lower in cervical smooth muscle than in thoracic. cAMP-dependent protein kinase activity ratios under both basal and EC50 methacholine-stimulated conditions were lower in cervical smooth muscle than in thoracic. We have observed in trachealis smooth muscle an inverse relationship between methacholine sensitivity and either cAMP or cAMP-dependent protein kinase activity. We suggest that cAMP and cAMP-dependent protein kinase play a role in the regulation of airway smooth muscle sensitivity to cholinergic agonists.

Animals↗
PubMed1989

Assessing clamp-related vascular injuries by measurement of associated vascular dysfunction.

The development of vascular clamps requires a reliable method to quantitate clamp-related vascular injuries. The degree of vessel damage usually is estimated subjectively from photomicrographs made with scanning electron microscopy. In order to test whether the use of vascular rings to assess residual vascular function may be a better method, rabbit thoracic aortas were occluded by five types of clamps: a Fogarty softjaw bulldog, a Fogarty Hydragrip, a 6-inch Satinsky clamp, an Edslab bulldog, and a silicone vessel band. Each area of clamp injury was sectioned into a vascular ring and suspended in a tissue bath. Residual vascular function was determined by contraction in response to phenylephrine and by relaxation in response to methacholine chloride and sodium nitroprusside. Morphologic studies with use of Evans blue dye and scanning electron microscopy complemented the vascular-function studies. The Fogarty bulldog clamp was the best at preserving vascular contraction and relaxation; the more crushing Satinsky clamp was the worst. The testing of vascular rings for residual function appears to be a useful technique for objectively quantitating vascular clamp-related vascular damage.

Animals↗
PubMed1986

Methacholine-induced airway reactivity of inbred rats.

Dose-response curves to inhaled aerosolized methacholine chloride (MCh) were obtained in anesthetized spontaneously breathing rats. Thirty rats (10/strain), randomly selected from highly inbred ACI, Lewis (L), and Brown Norway (BN) strains and 40 rats (20/strain) from similarly inbred Wistar-Furth (WF) and Buffalo (Buf) strains were studied. Airway responses were quantitated from changes in pulmonary resistance (RL) and airway reactivity was calculated as the dose of MCh required to increase RL to 150% (ED150RL) and 200% (ED200RL) of base line. There were no statistically significant differences in ED150RL and ED200RL among the five rat strains. Large interindividual variability was present as evidenced by 128-fold differences in ED150RL and ED200RL between the least and most sensitive animal of the same strain. In contrast, seven animals studied repeatedly on different days had values of ED150RL that differed by an average of only 2.9-fold (range 1.6-5.3). Thirteen rats that were studied on two occasions separated by an interval of 3 mo showed no systematic changes in airway reactivity. We conclude that airway reactivity to inhaled methacholine in anesthetized nose-breathing rats is not strain related, and despite animals of a given strain being genetically identical, the variability in airway reactivity within strains suggests that environmental rather than genetic factors are the major determinants of that reactivity.

Airway Resistance↗
PubMed1987

Local effect of vasoactive intestinal polypeptide on human sweat-gland function.

Physiological significance of vasoactive intestinal polypeptide (VIP), a putative co-transmitter of the cholinergic neuron innervating sweat glands, was investigated by its local effect on drug-induced sweating. VIP, methacholine chloride (MCH), or VIP plus MCH dissolved in 0.1 ml of 0.9% NaCl solution to a specified concentration was injected intradermally at the center of a forearm test area of 15 cm2 and the sweat rate was recorded continuously by capacitance hygrometry. In a cool environment (Ta, 23 degrees C), VIP failed to cause sweat secretion, but increased the rate of MCH-induced sweating, most markedly at a concentration of 10(-5) g/ml, where the rise in local skin temperature was the greatest. On an area anesthetized by nerve block in a hot environment (Ta, 35 degrees C), the effect was less obvious and less consistent, indicating that the sweat-facilitatory effect of VIP is reduced under the condition of passive cutaneous vasodilation. It may be postulated that VIP plays a role in securing ample oxygen supply to functioning sweat glands, especially with a relatively high cutaneous vasoconstrictor tone.

Adult↗
PubMed1990

Inflation of antishock trousers increases bronchial response to methacholine in healthy subjects.

We studied changes in lung volumes and in bronchial response to methacholine chloride (MC) challenge when antishock trousers (AST) were inflated at venous occlusion pressure in healthy subjects in the standing posture, a maneuver known to shift blood toward lung vessels. On inflation of bladders isolated to lower limbs, lung volumes did not change but bronchial response to MC increased, as evidenced by a greater fall in the forced expiratory volume in 1 s (FEV1) at the highest dose of MC used compared with control without AST inflation (delta FEV1 = 0.94 +/- 0.40 vs. 0.66 +/- 0.46 liter, P less than 0.001). Full inflation of AST, i.e., lower limb and abdominal bladder inflated, significantly reduced vital capacity (P less than 0.001), functional residual capacity (P less than 0.01), and FEV1 (P less than 0.01) and enhanced the bronchial response to MC challenge compared with partial AST inflation (delta FEV1 = 1.28 +/- 0.47 liter, P less than 0.05). Because there was no significant reduction of lung volumes on partial AST inflation, the enhanced bronchial response to MC cannot be explained solely by changes in base-line lung volumes. An alternative explanation might be a congestion and/or edema of the airway wall on AST inflation. Therefore, to investigate further the mechanism of the increased bronchial response to MC, we pretreated the subjects with the inhaled alpha 1-adrenergic agonist methoxamine, which has both direct bronchoconstrictor and bronchial vasoconstrictor effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Comparison of nasal responsiveness to histamine, methacholine and phentolamine in allergic rhinitis patients and controls.

In a selected group of rhinitis patients with an IgE-mediated allergy to house dust mites the nasal response to insufflation of histamine chloride, methacholine and phentolamine was demonstrated to be higher than in a control group. With the methods used histamine chloride was better at discriminating between healthy subjects and patients than methacholine or phentolamine. This discrimination was shown by assessing the severity of reflex-mediated symptoms such as the number of sneezes and the amount of secretion, and not by differences in nasal airway resistance.

Adult↗
PubMed1992

L-arginine improves endothelium-dependent vasodilation in hypercholesterolemic humans.

Endothelium-dependent vasodilation is impaired in hypercholesterolemia, even before the development of atherosclerosis. The purpose of this study was to determine whether infusion of L-arginine, the precursor of the endothelium-derived relaxing factor, nitric oxide, improves endothelium-dependent vasodilation in hypercholesterolemic humans. Vascular reactivity was measured in the forearm resistance vessels of 11 normal subjects (serum LDL cholesterol = 2.76 +/- 0.10 mmol/liter) and 14 age-matched patients with hypercholesterolemia (serum LDL cholesterol = 4.65 +/- 0.36 mmol/liter, P < 0.05). The vasodilative response to the endothelium-dependent vasodilator, methacholine chloride, was depressed in the hypercholesterolemic group, whereas endothelium-independent vasodilation, induced by nitroprusside, was similar in each group. Intravenous administration of L-arginine augmented the forearm blood flow response to methacholine in the hypercholesterolemic individuals, but not in the normal subjects. L-arginine did not alter the effect of nitroprusside in either group. D-arginine had no effect on forearm vascular reactivity in either group. It is concluded that endothelium-dependent vasodilation is impaired in hypercholesterolemic humans. This abnormality can be improved acutely by administration of L-arginine, possibly by increasing the synthesis of endothelium-derived relaxing factor.

Adult↗
PubMed1991

Muscarinic modulation of the vasodilatory effects of vasoactive intestinal peptide at the rat thyroid gland.

In the thyroid gland, vasoactive intestinal peptide (VIP) and acetylcholine (ACh) are found in nerve fibers associated with secretory cells and blood vessels. We have, therefore, initiated studies to explore the actions of and interactions between cholinergic agents and VIP in the regulation of thyroid vascular conductance (VC). Thyroid and other organ blood flows were measured using radiolabelled (141Ce) microspheres injected directly into the left cardiac ventricle of anesthetized male rats. The mean systemic arterial pressure was monitored and used in the calculation of organ VC (blood flow/arterial pressure). Plasma TSH, T3, and T4 levels before and after infusions were measured by RIA. The acute administration of ACh (3 x 10(-8) mol/100 g BW) over 4 min increased thyroid VC, whereas nicotine (10(-7) mol/100 g BW) had no such effect. Circulating TSH and thyroid-hormone levels following ACh or nicotine were not different from those in vehicle-treated animals at 20 min or 2 h after infusion. This observation suggested that ACh acts through muscarinic receptors at the thyroid gland to increase VC. In order to extend these observations and to evaluate whether VIP might exert any of its thyroidal effects on VC via muscarinic receptors, we assessed the effects of ACh, methacholine chloride (MCC), and VIP in the presence and absence of the muscarinic receptor blocker atropine. Rats were treated intravenously with saline or atropine (3 mg/kg) 20 min before intravenous infusions of vehicle, ACh (3 x 10(-8) mol/100 g BW), MCC (5 x 10(-9) mol/100 g BW), or VIP (10(-11) mol/100 g BW).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

[Local effect of calcitonin gene-related peptide on human sweat gland function].

The effect of local administration of calcitonin gene-related peptide (CGRP) on sweating activity was evaluated on normal human volunteers. CGRP and methacholine chloride (MCH) was dissolved in 0.1 ml of 0.9% NaCl solution to a specified concentration, and was injected intradermally at the center of a 1.3 cm2 forearm test area. The sweat rate was recorded continuously by capacitance hygrometry in a relatively cool environment (Ta, 23 degrees C). CGRP did not elicit any sweat secretion when administrated by alone, but significantly increased the sweat rate when it was administrated with MCH. The maximum enhancement of MCH-induced sweating by CGRP was observed at a concentration of 10(-5) g/ml of CGRP. There was clear dose-dependent relationship between the dose of CGRP and its enhancement. Recently, CGRP-like immunoreactivity is demonstrated to be present in cholinergic nerve terminals around the human sweat glands. These observations have strongly suggested that CGRP enhances the cholinergic sweating activity. Although the underlying mechanism is still obscure, CGRP may enhance the sweating as a consequence of vasodilation which has been known to be a major activity of CGRP. As for the evaluation of human sweat gland function, CGRP-induced peptidergic regulation should be considered as well as cholinergic regulation.

Acetylcholine↗
PubMed1989

A comparative study of gastric secretory stimulants in conscious dogs.

1. In conscious dogs with gastric fistulae, Heidenhain pouches and Thomas duodenal fistulae, pentagastrin was found to be a more potent peak acid and pepsin stimulant in both innervated stomach and vagally denervated pouch than methacholine chloride. 2. Slopes of curves relating response to the logs of molar doses of pentagastrin and methacholine, at peak secretion, did not differ significantly. The maximal pentagastrin stimulated secretion from the pouch was smaller than that for methacholine; from the fistula they did not differ. 3. Ganglionic blockade depressed methacholine stimulated peak acid secretion, but did not affect pentagastrin stimulated acid secretion. Dose-response curves for methacholine-induced acid and pepsin secretion at the perigee did not differ from those obtained with ganglionic blockade. 4. Ganglionic blockade depressed pepsin secretion from the fistula whether stimulated with pentagastrin or methacholine. Pouch pepsin secretion was small and no difference between curves was seen.

Animals↗
PubMed1977

Gastric secretory and motility studies in chronic chagasic patients.

In Chagas' disease, the degeneration of the nerve cells of the intramural parasympathetic ganglia of the stomach causes a wide range of motor and secretory disturbances of the organ. To assess and to correlate the alterations of these two gastric functions, electromanometric and secretory studies were performed in 22 chagasic patients and in 12 control individuals. The gastric antrum electromanometric records were carried out in basal conditions and under the stimulation of methacholine chloride (Mecholyl). Gastric secretory studies were carried out in two sessions with a Kay's test: in the first, with the test alone; in the second, associated with bethanechol chloride (Urecholine). The chagasic patients were divided into two groups according to their gastric motor response to methacholine. It was concluded that the parasympathetic denervation in Chagas' disease changes both acid and pepsin secretions in the same direction but that as the disease worsens, the responsiveness of pepsin secretion to cholinergic action tends to disappear earlier than that of acid secretion.

Adult↗
PubMed1987

Calcium uptake into guinea-pig trachealis: the effect of epithelium removal.

Removal of the epithelium from preparations of guinea-pig airways in vitro increases the responsiveness of the smooth muscle of normal and ovalbumin-sensitized animals to a number of contractile agents. To determine if epithelium removal results in an increase in Ca2+ entry into the smooth muscle, the effect of removing the epithelium on Ca2+ uptake into the trachealis smooth muscle was studied using a modified La3+-technique. KCl increased Ca2+ uptake in the presence and absence of the epithelium in control and sensitized animals. Methacholine did not promote Ca2+ uptake, whether or not the epithelium was present, in either control or sensitized animals. Ovalbumin did not stimulate Ca2+ uptake into the trachealis of sensitized animals. These results indicate that the increase in responsiveness of airway smooth muscle seen on epithelium removal is not a consequence of a facilitation of Ca2+ entry into the muscle. The increased responsiveness to methacholine in control animals, and to ovalbumin in preparations in tension studies in epithelium-free tissues from sensitized animals, cannot be explained by an increased availability of extracellular Ca2+ into the muscle, but, rather may reflect some other effect of the epithelium-derived modulatory factor.

Animals↗
PubMed1977

Abnormal vascular reactions in atopic dermatitis.

Vascular reactions to mechanical stroking, topical application of nicotinic acid ester, and methacholine chloride were examined in both the normal and abnormal skin of 100 patients with atopic dermatitis and 20 patients with allergic contact dermatitis. White dermographism, nicotinic acid blanching, and delayed blanch with methacholine consistently occurred in areas of skin with eczematous change of patients with atopic dermatitis and those with allergic contact dermatitis. Normal skin of atopic patients did not show the abnormal vascular reactions. It is suggested that white dermographism, nicotinic acid blanching, and delayed blanch with methacholine seen in atopic dermatitis are secondary phenomena that give no definite information concerning the diagnosis of this disease.

Adult↗
PubMed1988

The combined effects of histamine and methacholine on the maximal degree of airway narrowing in normal humans in vivo.

In normal subjects in vivo the dose-response curve to inhaled nonsensitizing stimuli reaches a plateau at mild degrees of airway narrowing. We investigated whether the limitation of the response is due to non-optimal smooth muscle activation, by administering high doses of histamine and methacholine together. In fifteen normal subjects a complete dose-response curve to methacholine was recorded by a tidal breathing method on three randomized days. On a separate day a complete histamine inhalation test was carried out. Each methacholine test was directly followed by double blind inhalation of the highest dose of either histamine or methacholine, or a dose of saline. The response was measured by flows from partial flow-volume curves (V 40p), and was expressed in % fall from baseline. Twelve subjects reached a maximal response plateau to methacholine which was reproducible. The addition of saline or extra methacholine did not change the response from its methacholine plateau value. Histamine caused a small increase in the response on top of the methacholine plateau (+ 9.0% fall; p less than 0.001). However, the response to the combined histamine and methacholine was not significantly larger than the maximal response to histamine alone. We conclude that there is no interaction between histamine and methacholine on the maximal degree of airway narrowing. This suggests that the plateau of the dose-response curve in normal subjects in vivo is due to other factors than limited smooth muscle activation.

Adult↗