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PubMed1989

Effect of breathing pattern during inhalation challenge on the shape and position of the dose-response curve.

To examine the effect of breathing pattern on the dose-response curve, 4 mild asthmatic and 9 normal subjects inhaled increasing concentrations of methacholine (0.03-256 mg/ml) using a quiet tidal breathing pattern or tidal breathing with a forced expiratory phase. The provocative concentration of methacholine causing a 20% decrease in the forced expired volume in 1 s (PC20FEV1) or a 200% increase in pulmonary resistance (PC 200RL) was determined. In addition, the maximal change in FEV1 and RL and the slopes of the dose-response curves were measured. The forced expiratory pattern caused an increase in the central/peripheral deposition ratio of a [99m]technetium-labeled aerosol (n = 3). There were no differences in mean tidal volume, minute ventilation, inspiratory flow rates, or baseline FEV1 or RL between the quiet breathing or forced expiration studies, although mean expiratory flows were increased in the latter (p less than 0.001). PC20FEV1 and PC200 RL decreased (p less than 0.001) but the maximal change in FEV1 and RL was unchanged in the forced expiration studies. Forced expiration during inhalation challenge did not alter the slope of FEV1 or RL dose-response curves. These results suggest that the sensitivity (PC20, PC200) and maximal response of in vivo dose-response curves may be affected independently by factors such as aerosol deposition.

Adult↗
PubMed1988

A computer-based method for on-line acquisition and analysis of bronchial challenge test.

We developed a computer program for the optimization and management of data collection in order to compute the change of forced expiratory volume in the first second (delta FEV1), provocative doses and to plot the dose-response curve for bronchial challenge test. Doses of methacholine are entered via the keyboard and forced vital capacity (FVC) with the highest FEV1 value obtained in each step is selected. When the imposed threshold of response has been reached, doses of administered methacholine and corresponding spirometric parameters are displayed and printed. Dose-response relationships are analysed: the increase of delta FEV1 for each unit of metacholine is computed in the interval between the two doses where delta FEV1 reached one of the imposed values (i.e. 15% or 20% or 30%). Finally spirometric values, dose-response curve and provocative doses are shown in a print-out. Computer values of provocative doses are higher than those obtained manually. This difference may be ascribed to the incorrect manual linear extrapolation. In conclusion the computer program is able to reduce consistently the time spent to analyze data from bronchial challenge test and allows a more precise determination of provocative doses by avoiding also inter-intra individual errors.

Asthma↗
PubMed1985

Comparison of metaproterenol, isoetharine and salbutamol in the relief of methacholine-induced bronchospasm in dogs.

We evaluated cardiovascular effects and effectiveness of isoetharine, metaproterenol and salbutamol, when administered intratracheally to relieve methacholine-induced bronchospasm in dogs anaesthetized with 50 per cent nitrous oxide, oxygen, halothane and mechanically ventilated. Methacholine 2 micrograms X kg-1 X hour-1 was administrated first followed by halothane (1 MAC) for 30 minutes (control), then metaproterenol, isoetharine or salbutamol. Metaproterenol (15 mg) significantly decreased transpulmonary pressure to 20.1 +/- 0.5 (SE) from 22.5 +/- 1.15 cmH2O (p less than 0.025) after three min and to 15 +/- 0.5 cmH2O (p less than 0.005) after 90 min. Isoetharine (2.5 mg) decreased transpulmonary pressure after five min to 22.1 +/- 1 from 24.5 +/- 1.5 cmH2O (p less than 0.05), and to 21.75 +/- 0.55 mmH2O after 90 min. Salbutamol 25 micrograms X kg-1 decreased transpulmonary pressure to 20.7 +/- 0.75 from 24.25 +/- 1.28 after three min and to 16 +/- .5 after 90 min. The peak effects on airway pressure occurred at 15 min for metaproterenol, 25 min for salbutamol and 20 min for isoetharine. Pulmonary vascular resistance was not significantly changed during halothane anaesthesia alone but decreased significantly after metaproterenol and isoetharine infusion. Heart rate increased ten per cent after metaproterenol, three per cent after isoetharine, and five per cent after salbutamol. No arrhythmias occurred in any group. Cardiac output increased significantly to 3.25 +/- 0.2 from 1.5 +/- 0.17 L X min-1 (p less than 0.025) after metaproterenol to 3.2 +/- .025 from 1.45 +/- .009 after salbutamol and was unchanged after isoetharine. Metaproterenol and salbutamol in the presence of 1 MAC halothane anaesthesia relieved methacholine-induced bronchospasm more rapidly than did isoetharine. The onset of effect was 3 +/- 0.05 min for metaproterenol and salbutamol and 5 +/- 0.01 min for isoetharine. The effect lasted 210 +/- 10.5 min for metaproterenol, 170 +/- 12.5 min for salbutamol and 90 +/- 4.75 min for isoetharine.

Airway Resistance↗
PubMed1993

Respiratory symptoms, lung function tests, airway responsiveness, and bronchoalveolar lymphocyte subsets in B-chronic lymphocytic leukemia.

A respiratory questionnaire was completed and spirometry, tests for lung volumes, diffusion capacity for CO, and methacholine bronchial challenge were performed in 24 outpatients with B-chronic lymphocytic leukemia (B-CLL), aged 44-79, presenting in different stages of their disease. In 10 patients, bronchoalveolar lavage (BAL) fluid was also obtained. Ten of twenty-four patients had symptoms consistent with chronic bronchitis, unrelated both to smoking history and to the clinical stage. Abnormal values (< 2 SD) were found in 4 patients for total lung capacity (TLC), in 9 for vital capacity (VC), 8 for forced expiratory volume in 1 sec (FEV1), 11 for MEF50, 15 for MEF25 and in 7 for diffusing capacity for carbon monoxide. Seven of nineteen patients had PD20FEV1 at less than 1,600 micrograms of methacholine chloride. There was a significantly negative correlation between white blood cell count and VC (r = 0.41, P < 0.05). A positive correlation was found between PD20FEV1 and FEV1/VC (r = 0.61, P < 0.01). The mean and SEM for BAL cells/ml was 463 (71.8) x 10(3). No leukemic cells but a marked increase in T lymphocytes (32.5 +/- 7.8%) were found in BAL fluid. There were significantly negative correlations between the number of BAL CD3+ T lymphocytes and PD20FEV1 (r = 0.61, P < 0.05), and between the number of BAL CD8+ T lymphocytes and PD20FEV1 (r = 0.84, P < 0.01). In conclusion, patients with B-CLL have a high prevalence of respiratory symptoms, small airway dysfunction and CD8 "alveolitis" related to airway responsiveness; despite the well-known lung interstitial lymphocyte infiltration in B-CLL, leukemic cells are not found in BAL fluid.

Adult↗
PubMedDate not supplied

Effects of thyroid function on submaxillary gland sensitivity to autonomic nervous drugs.

The effect of changes in thyroid function on the action of autonomic drugs upon the secretion of saliva by the submaxillary glands was studied in male Wistar rats. Hyperthyroidism was induced by the sc administration every 12 h of 10 micrograms/100 g bw of L-triiodothyronine; hypothyroidism was induced by surgical thyroidectomy 2 weeks before the experiments. The dose-response curves to increasing doses of isoprenaline, norepinephrine or methacholine showed in hyperthyroid animals increased salivary secretion, while in hypothyroid animals the dose-response to the drug was reduced. The threshold dose for isoprenaline was reduced in hyperthyroid animals and increased in hypothyroid ones. The threshold dose for norepinephrine did not change in hyperthyroid or hypothyroid animals while that for metacholine was decreased in hyperthyroid ones. When norepinephrine was given to alpha-blocked animals (with phentolamine) the difference in the dose-response curves between hyperthyroid and control animals was increased. But when norepinephrine was given to beta-blocked animals (with propranolol) the difference between the dose-response curves of hyperthyroid and control animals disappeared. The results above presented show that the sensitivity of the submaxillary salivary glands of rats to some adrenergic and cholinergic drugs was altered by the thyroid hormone. The effect was greater in the responses mediated by beta receptors. The structural changes in these glands may have some role in these effects.

Animals↗
PubMed2002

Endothelial vasodilatory function is predicted by circulating apolipoprotein B and HDL in healthy humans.

Endothelium-dependent vasodilation (EDV), LDL particle size, and antibodies against oxidized LDL (oxLDLab) have been shown to be related to the development of atherosclerosis and cardiovascular disease. In this study, we investigated whether LDL particle size, oxLDLab, apolipoproteins, and lipoproteins are related to endothelial vasodilatory function in a population sample of 58 apparently healthy subjects aged 20 to 69 yr. EDV and endothelium-independent vasodilation (EIDV) were studied in the forearm during local administration of methacholine chloride (2 and 4 microg/min) or sodium nitroprusside (5 and 10 microg/min). Forearm blood flow was determined with venous occlusion plethysmography. In multiple stepwise regression analyses, neither oxLDLab nor small LDL particles were significantly predictive of endothelial vasodilatory function. Instead, a high level of apolipoprotein B (apoB) was an independent predictor of both attenuated EDV and EIDV (r = -0.43, P < 0.01, and r = -0.34, P < 0.05, respectively). HDL cholesterol, on the other hand, was the only lipid variable that was significantly related to the EDV to EIDV ratio, an index of endothelial vasodilatory function (r = 0.35, P < 0.01). The inverse associations between apoB and both EDV and EIDV indicate that apoB might be an early marker of structural vascular changes in healthy subjects, whereas HDL seems to be more specifically related to endothelial vasodilatory function.

Adult↗
PubMed1987

Role of calcium in endothelium-dependent relaxation of arterial smooth muscle.

Endothelium-dependent relaxation was studied in rings of rabbit thoracic aorta. Relaxation responses were induced with methacholine, the calcium ionophore A23187 and maitotoxin before and after removal of Ca++ from the external medium; in the presence of calcium-channel entry blockers (verapamil and nifedipine); or with trifluoperazine. Deletion of Ca++ greatly impaired responses to all 3 agonists while trifluoperazine only blocked cholinergic-induced relaxation. The calcium-channel blockers had effects that were concentration- and time-dependent, but their action included blockade of A23187. Cytosolic-free Ca++ concentrations were measured in cultured endothelial cells after incubation of the cells with 10 microM Fura-2/AM or 50 microM Quin 2/AM. Bradykinin (1 X 10(-10) to 1 X 10(-7) M) and melittin (0.5 to 5 micrograms/ml) caused dose-dependent increases in intracellular Ca++ with maximal responses at 3 X 10(-8) M and 3 micrograms/ml, respectively. Both agents were able to induce an increase in cytosolic-free Ca++ in the presence of EGTA (1.5 X 10(-3) M) or verapamil (1 X 10(-5) M). The plateau phase of the Ca++ transient appeared to be modified slightly by verapamil, while the peak responses and plateau were attenuated by '0' Ca++/EGTA. To assess a function of the endothelium, production of endothelium-derived relaxing factor (EDRF) was studied in cells grown on microcarrier beads superfused in a column, and the column effluent was bioassayed on aortic rings.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Hyperventilation syndrome and asthma.

Hyperventilation syndrome is a common and often disabling condition. Traditional treatment consists of reassurance and anxiolytic drugs. Hyperventilation is known to precipitate an asthmatic reaction. A retrospective review of patients with hyperventilation syndrome was performed to ascertain the frequency of asthma as well as the response to bronchodilator medication. Forty-seven patients were seen. Thirty-eight were tested, and asthma was proved in 36. Two additional patients had positive clinical responses with bronchodilators. Thus, asthma was identified in 38 of 47 consecutive patients seen for hyperventilation syndrome (80 percent), and asthma was proved in 36 of 38 of patients tested (95 percent). Hyperventilation syndrome was eliminated in 29 of 35 patients (90 percent) treated with a combination of explanation and bronchodilator treatment.

Adult↗
PubMed1987

Comparison of pseudoachalasia and achalasia.

Malignancies involving the gastric cardia or distal esophagus can result in a clinical syndrome termed pseudoachalasisa that mimics idiopathic achalasia. If not promptly recognized, pseudoachalasia can result in inappropriate pneumatic dilatation of the lower esophageal sphincter segment and delay appropriate treatment of the underlying malignancy. During the past 14 years, six patients with pseudoachalasia and 161 patients with primary idiopathic achalasia were encountered. Pseudoachalasia occurred mainly in the elderly and represented about 9 percent of these patients over 60 years of age with suspected achalasia. Five of the six pseudoachalasia cases were secondary to adenocarcinoma that originated in the gastric fundus, and one was caused by a squamous cell carcinoma of the distal esophagus. Conventional esophageal manometry did not discriminate achalasia from pseudoachalasia. On the other hand, esophagogastroscopy with biopsy resulted in a diagnosis of pseudoachalasia in five of these cases and in 24 of 32 cases reported previously. Ominous endoscopic findings are mucosal ulceration or nodularity, reduced compliance of the esophagogastric junction, or an inability to pass the endoscope into the stomach. Radiographic evaluation, particularly in conjunction with amyl nitrite inhalation, was also useful in discriminating pseudoachalasia from primary achalasia. It is concluded that pseudoachalasia generally mimics idiopathic achalasia imperfectly and can usually be diagnosed prior to surgery by fastidious endoscopic and radiographic examination.

Adult↗
PubMed1983

Intraspecies variation in methacholine-stimulated esterase release from mouse submandibular gland.

Esterase release was investigated in male and female submandibular glands of 5 strains of mice (ICR/BR, ND/4BR, SW/BR, DDS/Cox and C57BL/6BR) using dispersed cells prepared by treatment with collagenase and hyaluronidase. The muscarinic-cholinergic agonist methacholine stimulated esterase release in C57BL/6BR, DDS/Cox and SW/BR females and DDS/Cox males in a dose-dependent manner, but did not stimulate esterase release in ICR/BR and ND/4BR strains of both sexes. The percentage release of esterase over control in response to methacholine in females was of the descending order: C57BL/6BR, DDS/Cox, SW/BR, ND/4BR, ICR/BR. There was a close relationship between the percentage release of esterase by methacholine and the esterase activity in homogenate of submandibular gland. The lower the esterase content in the homogenate of mouse submandibular gland, the higher the percentage release of esterase by methacholine stimulation in the dispersed cells.

Animals↗
PubMed1984

Methacholine-stimulated release of benzoyl-arginine-ethylester esterase from mouse submandibular gland cells.

The possible existence of cholinoceptor for inducing benzoyl-arginine-ethylester (BAEe) esterase release in the mouse submandibular gland was investigated using dispersed-cell preparations from normal male and female, castrated male and testosterone-treated female mice. Methacholine (a cholinoceptive agonist) induced esterase release only in normal female and castrated male mice, both of which had low esterase activity in the submandibular glands, whereas norepinephrine (an alpha-adrenoceptor agonist) induced esterase release in all of the mice. Methacholine-induced esterase release was completely inhibited by atropine, a cholinoceptive antagonist, but not by phenoxybenzamine, an alpha-adrenoceptor antagonist. The effects of metacholine and norepinephrine on esterase release were additive. The results suggest the coexistence of cholinoceptor and alpha-adrenoceptors for esterase release in the mouse submandibular gland. Calcium was essential for esterase release induced by either methacholine or norepinephrine.

Animals↗
PubMed1985

Amylase in parotid saliva of rats after sympathetic nervous decentralization.

The marked increase in the amylase secretion that occurs in parasympathetic saliva some days after sympathetic ganglionectomy occurred after decentralization also; hence, it results from lack of impulses from the central nervous system. It occurred whether salivation was evoked by activating muscarinic receptors with methacholine, peptidergic receptors with substance P or physalaemin, or alpha-adrenoceptors with phenylephrine. Unilateral operation affected to some degree the contralateral gland also.

Amylases↗
PubMed1989

Secretion of amylase from the rat parotid salivary gland after degeneration of the auriculotemporal nerve.

The output of amylase into saliva secreted after injection of methacholine or substance P was increased after parasympathetic denervation, but the salivary concentration of amylase was unchanged. The increased output corresponded to the increased flow. Isoprenaline injected during the methacholine-induced secretion raised the output, more being secreted from the denervated than from the contralateral gland. Vasoactive intestinal peptide, given while substance P caused salivation, also increased the amylase output, but equally from the two glands.

Amylases↗
PubMed1987

Effect of platelet-activating factor on beta-adrenoceptors in human lung.

We examined the effect of platelet-activating factor (PAF) on beta-adrenoceptors in the membranes of human lung and the functional responses to methacholine, histamine and isoproterenol in human lung parenchyma and tracheal strips. Preincubation of the human lung slices with 0.1 microM PAF decreased the density of beta-adrenoceptors without a change in the affinity. In the functional studies, a subthreshold dose of PAF (0.1 microM) significantly reduced the potency of isoproterenol to reverse methacholine or histamine-induced contraction. BN 52021, a PAF antagonist, protected against these PAF-induced changes. These findings suggest that PAF-induced down-regulation of beta-adrenoceptors could be a mechanism of the non-specific airway hyperreactivity in asthma.

Cell Membrane↗
PubMed1987

A disbalance between beta-adrenergic and muscarinic responses caused by hydrogen peroxide in rat airways in vitro.

The effect of hydrogen peroxide on adrenergic and muscarinic responses of rat airway smooth muscle was studied. The trachea muscle and the lung parenchymal strip were contracted with methacholine and relaxed with (-)-isoprenaline. Recording of three (-)-isoprenaline curves on the trachea muscle and the lung parenchymal strip was followed by treatment for 30 min with hydrogen peroxide (H2O2) (1mM) after which a new dose response curve for (-)-isoprenaline was constructed. Using the trachea muscle this treatment with H2O2 resulted in a decrease of 61% of the maximum contraction by methacholine compared with the control and a complete inhibition of the relaxation by (-)-isoprenaline. In the lung parenchymal strip preparation we found, after the same treatment no reduction of the contraction by methacholine and 61% reduction of the relaxation by (-)-isoprenaline, compared with the control. The results demonstrate that the adrenergic response in rat airways is more susceptible to hydrogen peroxide than the muscarinic response.

Animals↗
PubMed1989

Formation of chloramine derivatives of histamine: role of histamine chloramines in bronchoconstriction.

Hypochlorous acid generated by myeloperoxidase reacts with histamine to produce chloramines. At pH 7, one mole of histamine monochloramine (HisCl) was generated per mole of H2O2 provided as substrate for myeloperoxidase. At pH 5, one mole of histamine dichloramine (HisCl2) was generated per two moles of H2O2. HisCl and HisCl2 had two and four oxidizing equivalents per molecule, respectively. In vitro, 30 microM HisCl and HisCl2 induced mepyramine-sensitive guinea pig lung parenchyma contraction with 89 and 56 percent of the response of an equivalent concentration of histamine. Pretreatment of lung strips with chloramines reduced the subsequent contractile response of the tissues to methacholine. These results suggest that H-1 histamine receptors provide for targeting of histamine chloramines to pulmonary tissue which may facilitate modification of tissue responses.

Animals↗