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Biomedical subjects

A S Banner

Publications and source records attributed to A S Banner.

At least 19 recordsLinked to original sources
PubMed1994

Mechanism of respiratory arrest in an animal model of acute fatal bronchoconstriction.

The cause of respiratory arrest in acute asthma is not known. By its nature, respiratory arrest is difficult to study clinically. The possible causes of respiratory arrest include cardiovascular dysfunction, respiratory muscle fatigue, and central respiratory failure. We used a dog model of respiratory arrest in acute bronchoconstriction that examined the effects of hypoxemia and intrinsic loading in an attempt to establish the mechanism. Our hypothesis was that, in a setting of hypoxemia and intrinsic loading similar to human fatal asthma, respiratory arrest is caused by a central respiratory failure, more specifically, failure of the central rhythm generator. We studied 18 dogs divided into 1) an intrinsically loaded group, 2) a hypoxemic group, and 3) both a loaded and a hypoxemic group. Intrinsic loading was induced with methacholine combined with selective beta 2-blockade, and the hypoxemia was controlled by varying inspired O2 fraction. Respiratory arrest occurred only in animals with both hypoxemia and intrinsic loading. We found no evidence of hemodynamic instability or respiratory muscle fatigue. Instead, there was an abrupt cessation of ventilation while the intensity of the central neural output was maintained. Our results are consistent with a failure of the central rhythm generator as the causal agent in respiratory arrest.

Acute Disease↗
PubMed1991

Acute respiratory failure caused by pulmonary vasculitis after L-tryptophan ingestion.

This report describes two women who presented with severe respiratory failure and diffuse pulmonary infiltrates in the fall of 1989. Both required prolonged assisted ventilation because of severe shunt physiology. Open lung biopsies on admission revealed a small vessel vasculitis as the sole morphologic abnormality in both patients. Both responded to high dose corticosteroids. Neither patient exhibited evidence of systemic vasculitis, and neither had serologic evidence of an immune disorder. Common to both patients was ingestion of L-tryptophan. One patient exhibited several features of the eosinophilia-myalgia syndrome. The other patient did not appear to have the syndrome, but the temporal relationship between the onset of symptoms and initiation of L-tryptophan treatment was striking. The presentation of these patients alters our notions concerning the spectrum of clinical manifestations caused by this agent, and the response to methylprednisolone supports its efficacy in the treatment of this disorder.

Acute Disease↗
PubMed1988

Relationship between cough due to hypotonic aerosol and the ventilatory response to CO2 in normal subjects.

This study tests the hypothesis that susceptibility to the tussive effect of hypotonic aerosol is related to the ventilatory response to CO2. The threshold concentration of saline required to elicit cough and the ventilatory response to CO2 were determined in 18 normal subjects. Twelve subjects coughed with hypotonic aerosol (responders), and six did not (nonresponders). The CO2 ventilatory responses, which were normalized for vital capacity, were greater in the responders than in the nonresponders (0.64 +/- 0.16 and 0.43 +/- 0.12 L/min/mm Hg/L, respectively, p less than 0.02). The differences in the ventilatory responses to CO2 were consequent to a lesser increase in respiratory frequency in the nonresponders as compared to the responders (0.35 +/- 0.33 and 0.77 +/- 0.32 breaths/min/mm Hg, respectively, p less than 0.02). There were no differences in vital capacity-normalized tidal volume responses between the 2 groups (0.02 +/- 0.01 and 0.02 +/- 0.01 L/mm Hg/L). These findings suggest that susceptibility to the tussive effect of hypotonic aerosol and CO2 ventilatory response may be determined by a common neural mechanism. Differences in the respiratory patterns assumed by the responders and nonresponders during CO2 rebreathing suggest that the blunted CO2 response in the nonresponders may be related to a decrease in gain of volume-related vagal feedback. It is suggested that hypotonic cough threshold and CO2 ventilatory responses may be mediated by similar airway receptors.

Adult↗
PubMed1985

The tussive effect of hyperpnea with cold air.

The tussive and bronchoconstrictive effects of hyperpnea with cold air (HCA) are described in 3 patients with exercise-induced cough, 7 volunteers with exercise-induced cough, and 7 asymptomatic volunteers. Cough associated with HCA exceeded baseline cough in each of the patients and volunteers with exercise-induced cough and in all but one of the asymptomatic volunteers. The time course of cough was similar in each group. Maximal cough frequency occurred during the first 5 min after HCA and persisted to a much lesser degree during the ensuing 26 min. The time course of bronchoconstriction was similar to that of cough, with maximal decrements in specific airway conductance measured 5 min after HCA. Pretreatment with albuterol blocked HCA-induced bronchoconstriction but had no effect on HCA-induced cough. No subject in any of the 3 groups was hyperreactive to methacholine aerosols. In subjects who are nonhyperreactive to methacholine aerosols, HCA has a characteristic, reproducible, and predictable tussive effect. Thus, HCA may be a useful tool for investigating the mechanism of cough and for evaluation of antitussive drugs.

Adult↗
PubMed1985

Homeostatic regulation of bronchomotor tone by sympathetic activation during bronchoconstriction in normal and asthmatic humans.

It has been assumed previously that the sympathetic nervous system (SNS) serves to antagonize bronchoconstrictor stimuli. To assess the homeostatic regulatory effect elicited by exogenously induced bronchoconstriction, we studied the effect of inhaled methacholine on the SNS response in 12 normal and 9 asthmatic humans. Exogenous SNS response was assessed as change in plasma epinephrine and norepinephrine concentrations from basal levels during inhalation challenge. A 74 +/- 3% decrease in specific airway conductance (SGaw) (p less than 0.001) was induced in normal subjects and a 78 +/- 7% decrease in asthmatics by methacholine challenge (p less than 0.001). Neither plasma epinephrine nor norepinephrine increased significantly from basal concentrations in normal or asthmatic subjects after maximal challenge (p greater than 0.33). To determine if physiologically achievable epinephrine concentrations potentially could modulate bronchoconstriction, the effect of intravenously infused epinephrine was measured in 11 of these subjects. After the highest dose of methacholine, a 15-min intravenous infusion of epinephrine (0.06 micrograms/kg/min) caused an 85 +/- 7% increase in SGaw in normal subjects (p less than 0.02). In asthmatics, a 319 +/- 68% increase in SGaw (p less than 0.002) was observed with similar changes in plasma epinephrine. Plasma epinephrine concentrations after infusion were comparable to those obtained in 4 normal and 1 asthmatic subject undergoing 60-degree, head-up tilt 1 h after volume depletion with intravenously administered furosemide. We conclude that physiologic concentrations of epinephrine can modulate moderately severe bronchoconstriction. However, the SNS does not regulate bronchomotor tone during mild to moderate bronchoconstriction.

Adolescent↗
PubMed1984

Relation of respiratory water loss to coughing after exercise.

Exercise has been shown to result in bronchoconstriction, the extent of which is related to respiratory heat loss. Some normal subjects report coughing after exercise, and to determine whether this might also be related to respiratory heat loss, we monitored cough frequency after hyperpnea with air of varying temperature and water content in seven such subjects. Hyperpnea with fully saturated air at 37 degrees failed to provoke coughing and was not associated with heat loss or water loss. Hyperpnea with dry air at 37 degrees C resulted in more water loss (P less than 0.0005), less heat loss (P less than 0.01), and more coughing (P less than 0.001) than hyperpnea with subfreezing air. Hyperpnea with ambient air was associated with a similar cough frequency and water loss but with less heat loss (P less than 0.001) than hyperpnea with subfreezing air. There was a direct relation between cough frequency and respiratory water loss but no consistent relation between cough frequency and respiratory heat loss. This study indicates that coughing after hyperpnea with poorly conditioned air is related to the overall rate of respiratory water loss. Since strenuous exercise is associated with marked hyperpnea, coughing after exercise may also result from respiratory water loss.

Adult↗
PubMed1984

Tuberculous main-stem bronchial stenosis treated with sleeve resection.

The unusual complication of bronchial stenosis from scarring due to tuberculosis developed in a 33-year-old woman, despite otherwise effective antibiotic therapy. She then was treated successfully with conservative surgical management by sleeve resection of the involved segment. This unusual sequela and its workup contain important implications for the management of tuberculosis.

Adult↗
PubMed1983

Comparison of the tussive effects of histamine and methacholine in humans.

The tussive and bronchoconstrictive effects of histamine inhalation in 7 normals, 7 asthmatics, and 24 patients with chronic cough (PCC) were measured by counting coughs during a standard histamine inhalation challenge. All PCC had a tussive response. Fifteen PCC exhibited significant linear correlations between cough count and either the change in forced expiratory volume at 1.0 (delta FEV1) or conductance-volume ratio (sGaw) (delta sGaw). Normals and asthmatics had little or no cough. Metaproterenol pretreatment in seven PCC reduced both the FEV1 and cough response to histamine without changing the relationship between cough and delta FEV1. The tussive and bronchoconstrictive effects of methacholine inhalation were also measured in 7 asthmatics and 16 PCC. One asthmatic coughed. Fifteen PCC coughed. There were significant linear correlations between cough count and delta FEV1 or delta sGaw in 10 PCC. At comparable delta FEV1 and delta sGaw, histamine produced more cough than methacholine. These data indicate that during inhalation of histamine or methacholine by PCC cough is related to, and may be caused by, bronchoconstriction. Histamine also causes cough by an additional mechanism not related to bronchoconstriction.

Adult↗
PubMed1980

Rifampin-isoniazid therapy of alcoholic and nonalcoholic tuberculous patients in a U.S. Public Health Service Cooperative Therapy Trial.

A history of alcoholism is often regarded as a relative contraindication to the use of isoniazid and rifampin in patients with tuberculosis. To test the validity of this assumption the outcome of 6 months of rifampin-isoniazid therapy was analyzed for the first 531 eligible patients enrolled in a U.S. Public Health Service Cooperative Trial of Short-Course Chemotherapy of Pulmonary Tuberculosis. In this study, data were available to classify a patient as an alcoholic in the following 2 ways: (1) patient's statement that he was a moderate, heavy, or excessive user of alcohol, or (2) patient's score of 6 or more on a Brief Michigan Alcoholism Screening Test (MAST). Based on their statements, 58% of the patients were classified as alcoholic, whereas only 17.9% were thus classified by their MAST scores. Although alcoholics had more abnormal concentrations of aspartate aminotransferase (AST) before and during therapy, there was no significant difference between the alcoholics and non-alcoholics in the incidence of adverse reactions, including hepatotoxic reactions, including hepatotoxic reactions, attributed to the drugs. We concluded that in the absence of clinically significant and persistent pretreatment abnormalities of hepatic function tests, rifampin and isoniazid are not contraindicated in patients categorized as alcoholic by our 2 commonly used methods.

Alcoholism↗