Charles E. Reed

Greater frequency of viral respiratory infections in asthmatic children as compared with their nonasthmatic siblings

A longitudinal clinical and microbiologic surveillance was conducted from October to May, 1971–1972, on 16 children with infectious asthma and 15 of their nonasthmatic siblings. Asthmaticchildren experienced a significantly greater frequency of viral respiratory infections than did nonasthmatic ones (5.1 vs. 3.8 per subject). This increased incidence appeared to be largely the result of a greater number of rhinovirus infections. While respiratory infections of identical etiology that occurred concurrently in an asthmatic and his sibling were equivalent in severity, illnesses were longer (but not significantly so) in asthmatic children.

α1-Antitrypsin Deficiency: A Variant with No Detectable α1-Antitrypsin

No α1-antitrypsin could be detected in the serum of a 24-year-old man with advanced pulmonary emphysema by agarose electrophoresis, immnuno-electrophoresis, double diffusion in agarose gel, or α1-antitrypsin genetic typing by a combination of starch-gel electrophoresis and crossed antigen-antibody electrophoresis. A circulating α1-antitrypsin inactivator could not be demonstrated. Evidence was obtained in family members of genetic transmission of this new α1-antitrypsin variant.

Where is the allergic reaction in ragweed asthma?: II. Demonstration of ragweed antigen in airborne particles smaller than pollen☆

Abstract Asthma from ragweed pollen presents a paradox. The pollen grains are too large to penetrate the lower airway, but amounts of pollen sufficient to cause asthma when inhaled through the mouth do not do so when applied directly to the nasal mucosa. This paradox could be resolved if ragweed antigen existed in particles 5μ and smaller. An Andersen sampler was operated continuously from mid-August to mid-September to collect airborne particles of various sizes. Rayweed pollen was found only on the first two stages, but each stage was found to have ragweed antigen when tested by the passive transfer antigen neutralization technique. The results demonstrated airborne particles, less than 5μ in diameter, capable of neutralizing ragweed reagin. These particles could penetrate to lower airways and initiate an allergic reaction there.

Where is the allergic reaction in ragweed asthma

Abstract As ragweed pollen grains are 20 μ in diameter and too large to penetrate into the bronchi, it is conceivable that an allergic reaction in the nose might cause asthma through reflex or other mechanisms. Eight patients with ragweed asthma were challenged by direct application to the nasal mucosa of solutions of increasing concentrations of histamine and, on another day, of increasing amounts of dry ragweed pollen. One to 20 mg. of histamine was required to produce sneezing, rhinorrhea, and nasal stuffiness, but a drop in FEV 1 was not observed in any subject. Pollen grains applied directly to the nasal mucosa provoked severe hay fever, but doses up to 1,500 grains did not cause a drop in FEV 1 . On the other hand, inhalation of 100 to 500 grains through the mouth on a different day did provoke coughing and a 20 per cent drop in FEV 1 . Up to 5,000 grains placed on the posterior third of the tongue provoked drop in FEV 1 in 2 of the 8 patients. We conclude that ragweed asthma is not initiated by an allergic reaction in the nose. If obstruction of small airways arises through reflex mechanisms, the sensory arc of this reflex originates below the oropharynx.

Comparison of some metabolic responses in normal and asthmatic subjects to epinephrine and glucagon

Abstract Nine asymptomatic asthmatic men and 9 normal men were given an intravenous infusion of epinephrine 0.1 μg per kilogram per minute for 10 minutes. Blood samples were taken every 10 minutes for an hour and analyzed for glucose, free fatty acids, and glycerol. Initial values of these metabolites were similar in both groups, but the rise in glucose was smaller in the asthmatic group. There was no difference in the rise in free fatty acid and glycerol. Six asthmatic men and 9 normal men were given 7 μg per kilogram glucagon intravenously. The blood glucose response was smaller in the asthmatic group, but the difference was not statistically significant. The diminished hyperglycemic response to epinephrine in patients with asthma who were not receiving sympathomimetics or corticosteroid drugs and who were asymptomatic at the time of the study indicates that asthma itself is associated with a diminished glycemic response to epinephrine.

Abnormal autonomic mechanisms in asthma

Excessircb irritability of the airways is thr hallmark of asthma. It is conspicuous in patients with asthma of allergic origin as well as in patients in whom allergic causes cannot bc found. ?tI,v purpose is to review the mechanism of this excessive irritability, focusing cspc~c’ially up011 t,hc autonomic nervous system control of the airways. This paper is not int,cnclcd as an rxhaustivtl review of the sub.ject, but rathctr a summary oi’ present informut,ion and an indication of possible directions oE futurrb advances. Evidence has been accumulated that t.his mechanism could bc an ;~bnol*malit~ in each of thr major branches ot’ the autonomic nervous system, or, pcrhal)s more likclg, in the intcgratioii of 1111, control of bronchial smooth musc&lc, blood \-csscls, mu(aous glands, and othm target cells by cholinergic and adrcncqic neurons.

Correlation between increased bronchial response to acetylcholine and diminished metabolic and eosinopenic responses to epinephrine in asthma

Abstract The threshold amount of inhaled acetylcholine required to induce bronchoconstriction was determined in each of 21 patients with asthma of varying severity. On another day each was given an intravenous infusion of epinephrine, 0.1 μg per kilogram per minute, for 10 minutes. Blood samples were taken before and 5, 20, and 30 minutes after epinephrine and analyzed for glucose, free fatty acids, lactic acid, and insulin. Blood pressure and pulse rate were also measured. Eosinophils were counted before and 3 hours after epinephrine. The threshold amount of acetylcholine required to induce bronchoconstriction showed low but statistically significant correlations with the degree of hyperglycemia, hyperlactacidemia, and eosinopenia but not with the other responses to epinephrine. The patients with asthma had no gross abnormality in either the basal insulin levels or the insulin response to epinephrine. These correlations indicate that increased bronchial response to acetylcholine and decreased metabolic and eosinopenic responses to epinephrine may arise from a common defect, such as beta-adrenergic blockade, but the experimental design does not permit us to conclude that they necessarily do so.

Reduced effect of epinephrine on circulating eosinophils in asthma and after beta-adrenergic blockade or Bordetella pertussis vaccine: With a note on eosinopenia after methacholine☆

Abstract These experiments were undertaken to clarify the role of adrenergic and cholinergic influences on the level of circulating eosinophils and to determine if the eosinophilia of pertussis sensitization and bronchial asthma might be relatively resistant to epinephrine. In rats, the beta-adrenergic blocker, propranolol, inhibited epinephrine-induced eosinopenia, but the alpha-adrenergic blocker, dibenamine, did not. Methacholine, like epinephrine, had an eosinopenic effect which was dependent on the adrenal gland and probably mediated by epinephrine and glucocorticoids. The eosinopenic effect of epinephrine was greatly reduced following injection of pertussis vaccine, the reduction being maximal 7 days after the vaccine. In man, the mean eosinopenic response of 9 asymptomatic asthmatic subjects was less than that of 9 normal persons.

The effect of partial beta adrenergic blockade on the bronchial response of hay fever subjects to ragweed aerosol

Abstract One hypothesis of the cause of asthma proposes that it is the result of impaired autonomic homeostasis manifested by a partial blockade of the adrenergic beta receptors of cells. This study was undertaken to determine whether a pharmacologically induced beta blockade would increase the bronchial obstruction produced by ragweed aerosol challenge in subjects with hay fever. Ten volunteers with ragweed hay fever were studied before the ragweed season. Each subject was his own control. On each of two separate days the subject was challenged with progressively increased doses of an aerosol of ragweed extract. Before the second challenge, 5 mg. of propranolol, a potent beta adrenergic blocking agent, was given intravenously. A year later, these 5 subjects were again studied with the order of the propranolol and control tests reversed. The response to the aerosol was determined by comparing the volumes of the first second of a forced expiration (FEV 1 ) before and 15 minutes after the aerosol. The mean change in FEV 1 was −13 per cent with the control and −22 per cent with the propranolol. When the order of challenge with propranolol and the control was reversed, these values were much the same, −6 and −19. Partial beta blockade increased the bronchial response to inhaled allergen, a result consistent with the stated hypothesis.

Farmer's lung.

Excerpt We have previously described the clincal features of an acute granulomatous interstitial pneumonitis that occurred in 39 agricultural workers after exposure to moldy organic farm dusts (1)....