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PubMed1976

Prinzmetal's variant angina. Coronary arteriogram and left ventriculogram during angina attack induced by methacholine.

Recently, in Prinzmetal's variant angina, many cases with normal coronary arteries have been reported. The anginal attacks frequently relapse after aortocoronary bypass grafting. It is frequently possible to induce an anginal attack by parasympathomimetic agents such as methacholine and pilocarpine. In this study, methacholine (0.13 mg per kilogram) was injected subcutaneously in three cases of this disease to induce an angina attack, and coronary arteriograms and left ventriculograms were recorded. In all cases a coronary arterial spasm corresponding to the site of the ST-segment elevation in the electrocardiogram was observed. Complete occlusion due to the spasm was observed even in the normal coronary artery. Asynergy was seen in the left ventricular wall corresponding to the site of the ST-segment elevation in the electrocardiogram.

Angina Pectoris↗
PubMed1979

Chronic cough as the sole presenting manifestation of bronchial asthma.

Six patients with chronic cough, without history of dyspnea or wheezing, had normal base-line spirometry but hyper-reactive airways, as demonstrated with methacholine. Maintenance therapy with bronchodilators promptly eliminated the cough in all patients. Three to 12 months later therapy was discontinued for three days, cough returned, and detailed pulmonary-function studies were carried out. Again, base-line values were normal, but after methacholine one-second forced expiratory volume decreased an average of 40 per cent in the patients as compared to 30 per cent in normal controls (P less than 0.001). The point of identical flow was increased by methacholine to 43.5 per cent of vital capacity in the patients, as compared to 6 per cent in normal controls (P less than 0.001), and the alveolar plateau was 4.8 deltaN2 per liter, as compared to 1.4 in normal controls (P less than 0.01). Specific airway conductance was lowered in patients and controls, but the post-methacholine value was significantly lower in the patients. On the basis of their persistently hyper-reactive airways, inducible diffuse airway bronchoconstriction and excellent response to bronchodilator therapy, these patients appear to have a variant form of asthma in which the only presenting symptom is cough.

Adolescent↗
PubMed1984

Changes in T-lymphocyte subpopulations after antigenic bronchial provocation in asthmatics.

To determine whether inhaled agents can alter T-cell subsets in the peripheral blood of patients with bronchial asthma, we tested six asymptomatic asthmatics who were sensitive to mixed grass (positive skin test) with mixed grass extract, methacholine, and an antigen to which they were not sensitized (negative skin test). Levels of OKT4 cells (helper T lymphocytes) were reduced in the peripheral blood immediately after the challenge with mixed grass extract, and remained low for at least 72 hours. Levels of Ia-positive (activated) T cells were increased 48 hours after the challenge. No changes were observed in any of these T-cell subpopulations after challenge with methacholine or after the inhalation of an equal amount of an antigen to which the subjects were not sensitized. These results suggest that the selective loss of circulating helper T cells and an increase in activated T cells after an asthmatic attack induced by antigenic inhalation may serve as an indicator of immune-mediated bronchoconstriction.

Adult↗
PubMed1984

Leukocyte activation in allergen-induced late-phase asthmatic reactions.

Some patients with allergen-induced asthma have both an early and late reaction to allergen (dual asthmatic reactions). To investigate the role of leukocyte activation in dual asthmatic reactions, we measured neutrophil chemotactic activity, percentages of neutrophil and monocyte complement rosettes, and one-second forced expiratory volume (FEV1) in 11 patients with allergen-induced dual asthmatic reactions after a challenge with allergen. To control for the effects of bronchoconstriction, the same studies were done after a challenge with methacholine. In all subjects there was a biphasic increase in neutrophil chemotactic activity and the percentages of neutrophil and monocyte complement rosettes, accompanied by a reduction in the FEV1. After methacholine, there were no significant changes in neutrophil chemotactic activity or percentages of complement rosettes, despite bronchoconstriction. Six patients with single-phase allergen-induced asthma had similar responses, but they were monophasic. We conclude that allergen-induced early and late asthmatic reactions are accompanied by activation of leukocytes and that these alterations probably reflect the release of mediators from mast cells rather than an effect of bronchoconstriction.

Adult↗
PubMed1986

Airway responsiveness to leukotrienes C4 and D4 and to methacholine in patients with asthma and normal controls.

Leukotrienes C4 and D4 may serve as chemical mediators in asthma. Although patients with asthma are known to be hyperresponsive to the bronchoconstrictive effects of histamine and methacholine, whether the same is true for the leukotrienes is controversial. We compared the airway responses to methacholine and to leukotrienes C4 and D4 in 12 asthmatic patients and 6 controls. We found that the patients were more responsive to the leukotrienes than the controls, and we observed a linear correlation between airway response to methacholine and that to leukotriene C4 (r = 0.68, P less than 0.01) and D4 (r = 0.79, P less than 0.001). However, relative to the airway response to methacholine, the response to the leukotrienes was much greater in the controls than in the patients. Furthermore, the asthmatic subjects who were most responsive to methacholine had the lowest relative airway response to both leukotrienes. Thus, the patients with the greatest airway responsiveness to methacholine paradoxically showed the lowest relative airway response to the leukotrienes. In contrast, this difference in relative airway responses has not been observed between methacholine and other bronchoconstrictor mediators, such as histamine. Although no adequate explanation for these observations has yet emerged, our data suggest that leukotrienes C4 and D4 are unique bronchoconstrictors with a possible role in the pathogenesis of asthma.

Adult↗
PubMed1989

Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function.

To elucidate the pathogenesis of bronchospasm in congestive heart failure, we studied 23 patients with chronic impairment of left ventricular function due to coronary artery disease or dilated cardiomyopathy. In 21 of them we found marked bronchial hyperresponsiveness to methacholine. The mean dose (+/- SD) of methacholine that elicited a 20 percent decrease in the forced expiratory volume in one second (FEV1) was 421 +/- 298 micrograms, nearly the same as in patients with symptomatic asthma. In contrast, there was no bronchial response to methacholine in 9 of 10 patients who had coronary artery disease but normal left ventricular function. Administration of the bronchodilator albuterol led to a partial (43 percent) reversal of the methacholine-induced bronchial obstruction. In 12 patients, pretreatment with the alpha-adrenergic agonist methoxamine (10 mg by inhalation), a potent vasoconstrictor, fully prevented the methacholine-induced decrease in FEV1. The protective effect of methoxamine was blocked by the alpha-adrenergic antagonist phentolamine in all six patients who received this agent. We conclude that bronchial hyperresponsiveness to cholinergic agonists is frequent in patients with impaired left ventricular function and may contribute to the wheezy dyspnea commonly observed in such patients. The bronchoconstriction may be mediated at least in part by dilatation of the bronchial vessels.

Adult↗
PubMed1989

Protective effect of inhaled furosemide on allergen-induced early and late asthmatic reactions.

The movement of ions and water across the membranes of bronchial cells is part of the control of the bronchial obstructive response to physical stimuli. In a double-blind, randomized, crossover study, we compared the effect of an aerosol of the loop diuretic furosemide with that of a placebo on the early (within 60 minutes) and late (4 to 12 hours) asthmatic responses to a specific inhaled allergen. We studied 11 subjects with mild allergic asthma, who had both early and late asthmatic responses to a specific inhaled allergen in a preliminary challenge. After placebo administration, the maximal changes (mean +/- SE) from base line in the forced expiratory volume in one second (FEV1) and specific airway resistance were, respectively, a decrease of 35 +/- 4 percent and an increase of 288 +/- 56 percent between 0 and 60 minutes after inhalation of the allergen (early response) and a decrease of 35 +/- 5 percent and an increase of 301 +/- 40 percent between 4 and 12 hours (late response). After furosemide administration (4 ml; 10 mg per milliliter), the early response to inhaled allergen was markedly attenuated in all the subjects, and the late response in all but one. The maximal changes in the FEV1 and specific airway resistance were, respectively, a decrease of 11 +/- 2 percent and an increase of 61 +/- 2 percent between 0 and 60 minutes and a decrease of 20 +/- 4 percent and an increase of 178 +/- 25 percent between 4 and 12 hours (P less than 0.05 for all comparisons). No significant differences were seen in the bronchoconstrictor response to inhaled methacholine after furosemide or placebo administration. We conclude that a furosemide-sensitive mechanism in the airways is involved in the pathogenesis of the reactions of patients with allergic asthma. Whether inhaled furosemide might be useful in the treatment of allergic asthma is uncertain and will require further study.

Adolescent↗
PubMed2000

Induced sputum: comparison of postinfectious cough with allergic asthma in children.

BACKGROUND: Cough persisting after a respiratory infection is common in children and is often managed as asthma. However, little is known about the pathophysiologic mechanisms of such cough and how it compares with asthma. OBJECTIVE: We used the technique of induced sputum to examine the inflammatory index values associated with persistent cough or allergic asthma in children. We hypothesized that the sputum from children with persistent postinfectious cough would differ from that of children with allergic asthma in that the former would lack eosinophils compared with the latter. STUDY DESIGN: Sputum production was induced with hypertonic saline solution in 34 children: 12 with cough persisting for 1 month or more after an apparent respiratory tract infection, not treated with corticosteroid; 11 with untreated atopic asthma, not using inhaled corticosteroid; and 11 with treated atopic asthma using inhaled corticosteroid. RESULTS: The percentage of eosinophils in the sputum of children with cough was significantly lower than in the sputum of children with untreated allergic asthma (median 0.5% vs 14.5%, P <.0001). Similarly, the percentage of eosinophils in the sputum of children with asthma treated with inhaled steroids was significantly lower compared with untreated asthmatic children (1.5% vs 14.5%, P <.0001). The peripheral blood eosinophils, serum eosinophil cationic protein, and nasal percent eosinophils of the patients with cough were also significantly lower than those from patients with untreated asthma. Methacholine challenge in 6 of the 11 cough patients tested showed mild-to-moderate hyperresponsiveness, whereas the other 5 had a negative methacholine challenge. CONCLUSIONS: Children with persistent postinfectious cough do not have airway eosinophilia typical of untreated asthma. Despite the absence of eosinophilic inflammation, some of the patients with chronic cough had reactive airways. These results suggest that postinfectious cough in children has different pathophysiologic features than allergic asthma and probably represents a different disease.

Asthma↗
PubMed1989

Endothelial injury and vascular dysfunction associated with the Fogarty balloon catheter.

Endothelial-derived relaxing factor is an important modulator of vascular relaxation, and its production is very sensitive to endothelial injury. The abdominal aortas of five groups of rabbits were subjected to Fogarty balloon catheterization via the femoral artery. Some rabbits were killed immediately (time 0), and others were killed at weekly intervals. At time 0, isolated vascular rings sectioned from the abdominal aortas and suspended in tissue baths failed to exhibit any endothelial-derived relaxing factor dependent vascular relaxation. Vascular relaxation progressively returned but was not normal until 4 weeks after the initial injury. Morphologic changes studied by means of Evans blue dye and by scanning electron microscopy with silver staining corresponded well with these functional changes. At time 0, the delicate endothelium was completely denuded, but it progressively regenerated over the subsequent 4 weeks. This severe injury to the vascular endothelium and the resultant vascular dysfunction may result in an increased risk of early postoperative spasm and thrombosis after the use of a Fogarty balloon catheter.

Animals↗
PubMed1973

The importance of calcium ions for the regulation of guanosine 3':5'-cyclic monophosphage levels.

Guanosine 3':5'-cyclic monosphosphate (cyclic GMP) levels in the ductus deferens of the rat were increased 2- to 3-fold by acetylcholine (10-1000 muM) or by 125 mM KCl, while adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels were not changed. After incubation for 30 min in the absence of Ca(++), cyclic GMP control levels were decreased by 85% and were not affected by acetylcholine or KCl. The readdition of Ca(++) (1.8 mM) for 3 min to Ca(++)-deprived tissue partially restored basal cyclic GMP levels and the effects of acetylcholine and KCl. The addition of Sr(++) (3.6 mM) or of Ba(++) (1.8 or 10 mM) also caused an increase in basal cyclic GMP in Ca(++)-deprived tissue. Cyclic AMP levels were not significantly changed under any of these conditions. The addition of the phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine (0.1 mM), to ductus deferentes increased the amount of cyclic AMP about 50% and that of cyclic GMP about 2-fold. The later effect also depended on the presence of Ca(++). 1-Methyl-3-isobutylxanthine (0.1 mM) increased cyclic GMP and cyclic AMP levels in slices of rat submaxillary glands. Methacholine increased cyclic GMP if added in the presence of methyl isobutylxanthine. Cyclic GMP control levels and the effect of methyl isobutylxanthine were unchanged by Ca(++) omission, but the effect of methacholine was abolished.These findings indicate that calcium ions are important for the control of cyclic GMP levels in these tissues.

Acetylcholine↗
PubMed1974

Muscarinic cholinergic binding in rat brain.

Binding sites with high affinity and specificity for [(3)H]quinuclidinyl benzilate (QNB) are present in homogenates of rat brain. The characteristics of the binding sites resemble those of muscarinic cholinergic receptors. Specific binding is saturable with respect to [(3)H]QNB and tissue concentration and is time-, temperature-, and pH-dependent. The bimolecular rate of association (2.0 x 10(8) M(-1) min(-1)) and dissociation (1.2 x 10(-2) min(-1)) at 35 degrees indicate a dissociation constant of 60 pM and a density of 65 pmol/g of brain. Muscarinic antagonists and agonists displace specific [(3)H]QNB binding, while nicotinic and non-cholinergic drugs possess little affinity for [(3)H]QNB-binding sites.

Acetylcholine↗
PubMed1978

Opposing effects of estradiol and progesterone on oxytocin receptors in rabbit uterus.

Estradiol-17beta administration to young (10- to 12-week-old) rabbits to produce the "estrogen-dominated" uterus increased the uterine contractile response to both oxytocin and methacholine in vitro. In "progesterone-dominated" uteri, obtained from rabbits that received progesterone for 4 days after estrogen pretreatment, the contractile response to oxytocin in vitro was selectively abolished; the response to methacholine was unaffected. Parallel changes were observed in the concentration (but not affinity) of specific sites in uterine microsomal membranes that bind [(3)H]oxytocin with selectivity features expected for oxytocin receptors. Thus, estrogen-dominated uteri have an increased number of specific [(3)H]oxytocin binding sites per mg of membrane protein relative to untreated controls, whereas specific oxytocin binding sites are reduced to barely detectable levels in the progesterone-dominated uterus. Similar results are obtained when binding sites are measured in membranes from the myometrium of estrogen- or progesterone-dominated uteri. Short-term (24-hr) progesterone administration to estrogen-pretreated rabbits decreased, but did not abolish, specific [(3)H]oxytocin binding; the concentration of specific [(3)H]oxytocin binding sites was reduced without influence on the affinity of these sites. A sublethal dose of actinomycin D, administered over a 24-hr period to rabbits pretreated with estradiol for 4 days, likewise reduced specific oxytocin binding; additive effects were not observed when progesterone and actinomycin D were administered together. These results suggest that the regulatory effects of estrogens and progesterone upon the rabbit uterine contractile response to oxytocin are achieved, at least in part, by the opposing actions of these steroids in regulating the number of oxytocin receptors in smooth muscle cells. Estradiol increased the concentration of uterine oxytocin receptors; the maintenance of high receptor levels appears to depend upon the continuous de novo synthesis of oxytocin receptors. In contrast, progesterone, like actinomycin D, appears to act at the nuclear locus to repress synthesis of oxytocin receptors.

Animals↗