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Biomedical subjects

A G Driver

Publications and source records attributed to A G Driver.

13 recordsLinked to original sources
PubMed1995

Pericardial fluid adenosine in ischemic and valvular heart disease.

Adenosine released by ischemic myocardial cells stimulates coronary artery vasodilation. Measurement of adenosine concentrations in pericardial fluid in animal models of myocardial ischemia has been used to study the process of adenosine release. To determine whether pericardial fluid adenosine concentrations are increased in human ischemic heart disease, adenosine concentrations were measured in pericardial fluid in 23 subjects undergoing open-heart surgery for coronary artery disease. The results were compared with adenosine concentrations measured in pericardial fluid obtained from 20 subjects undergoing surgery for valvular heart disease. Adenosine concentrations also were measured in pleural fluid obtained during internal mammary artery bypass grafting. Adenosine concentrations were significantly increased in subjects with coronary artery disease compared with fluid obtained from subjects with valvular heart disease (2.47 +/- 0.24 vs 1.36 +/- 0.21 [SEM] microM [p = 0.0013]). Adenosine concentrations were higher in pleural fluid than pericardial fluid from the same individuals. Adenosine concentrations were significantly correlated with pericardial fluid cell counts and lactate dehydrogenase concentrations (r = 0.48; p = 0.0012 and r = 0.77, p = 0.0001, respectively). The results are consistent with myocardial release of adenosine in ischemic heart disease. If adenosine concentrations in pericardial fluid approximate those in myocardial interstitial fluid, sufficient adenosine is present to stimulate adenosine receptor activation in coronary artery smooth muscle.

Adenosine↗
PubMed1993

Adenosine in bronchoalveolar lavage fluid in asthma.

The inhalation of nebulized adenosine causes bronchoconstriction in asthmatics. In order to explore whether endogenously produced adenosine may contribute to the pathophysiologic aspects of asthma, we measured adenosine concentrations in bronchoalveolar lavage (BAL) fluid in seven subjects with asthma, eight asymptomatic cigarette smokers, and eight normal subjects. The mean concentration of adenosine in BAL fluid from the normal subjects was 0.72 +/- 0.16 microM. Subjects with asthma and cigarette smokers had significantly increased concentrations of adenosine in BAL fluid, 2.55 +/- 0.50 and 1.89 +/- 0.50 microM, respectively. Corrected for the dilution that occurs as a result of the lavage procedure, mean epithelial lining fluid adenosine concentrations were 60 +/- 13 microM in normal subjects, 193 +/- 58 microM in asthmatics, and 155 +/- 56 microM in smokers. Adenosine concentrations were positively correlated with the protein content of the lavage fluid (r = 0.79). Inhalation of nebulized adenosine in the subjects with asthma provoked a 20% reduction in lung function at concentrations 4- to 195-fold higher than was present in the epithelial lining fluid of the same individuals. The presence of increased BAL adenosine concentrations in asthmatics and in cigarette smokers suggests that adenosine may be a nonspecific marker for inflammation in the lung. The demonstration of physiologically relevant concentrations of adenosine in airway fluids of subjects with bronchial hyperreactivity to inhaled adenosine provides evidence for a role of endogenous adenosine in provoking bronchoconstriction in asthma.

Adenosine↗
PubMed1991

Bronchial challenge with adenosine causes the release of serum neutrophil chemotactic factor in asthma.

In order to investigate the mechanism of adenosine-induced bronchoconstriction in asthma, serum neutrophil chemotactic activity (NCA) was measured in normal individuals and patients with asthma before and 5 min after bronchoprovocation testing with adenosine. Challenge testing was terminated when the FEV1 fell by 20% or a concentration of 10 mg/ml was reached. Participants were separated into three groups: six asthmatics hyperresponsive to adenosine (Group 1), seven asthmatics hyperresponsive to histamine but not adenosine (Group 2), and six normal subjects (Group 3). The mean percentage increase in NCA was 84% for Group 1 (p less than 0.001), 29% for Group 2 (p less than 0.05), and only 13% for Group 3. No significant increase in NCA was observed after histamine challenge in seven individuals with asthma derived from Groups 1 and 2. Four patients from Group 1 were rechallenged after treatment with therapeutic doses of oral theophylline. Theophylline therapy was associated with a significant attenuation of the increase in NCA at the concentration of adenosine which caused a 20% decrease in FEV1 before treatment (18% versus 84%, p less than 0.01). The concentration of adenosine which caused a 20% drop in FEV1 was increased at least twofold for each of the four patients. Analysis of NCA by gel filtration chromatography demonstrated an increase in a high molecular weight neutrophil chemotactic factor in the serum of two Group 1 patients after adenosine challenge. Release of a high molecular weight neutrophil chemotactic factor is consistent with a mast cell source for inflammatory mediators in adenosine-induced bronchoconstriction. The therapeutic effects of theophylline, a potent adenosine antagonist, in asthma may therefore occur in part through the inhibition of this process.

Adenosine↗
PubMed1990

Intravenous streptomycin.

Streptomycin is an effective drug for the treatment of tuberculosis. It is currently recommended for use only by the intramuscular route. This method of drug delivery is accompanied by considerable pain which is unacceptable to many patients. With the advent of many improvements in intravenous therapy that have occurred in the past 40 years, reevaluation of the intravenous use of this drug is warranted. We describe the short-term use of intravenous streptomycin in four patients with pulmonary tuberculosis.

Adult↗
PubMed1989

Expression of histamine H1 receptors on cultured histiocytic lymphoma cells.

Histamine H1 receptors were identified in U937 human histiocytic lymphoma cells using a radioligand binding technique with [3H]mepyramine. Reversible high-affinity binding with this ligand was obtained, and specificity of binding for selected H1 agonists and antagonists was demonstrated. Competition binding experiments with mepyramine and histamine yielded results consistent with single-site binding for mepyramine and two-site binding for histamine. Dissociation constants for the high- and low-affinity histamine binding states were 6.8 X 10(-6) and 2.4 X 10(-4) M respectively. The high-affinity state for histamine binding was abolished when the membranes were coincubated with 100 microM guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S). Saturation binding studies yielded an average of 66 fmol/mg protein binding sites (6000 receptors per cell) with a [3H]mepyramine KD of 9.6 nM. When differentiation of these cells was induced by phorbol-myristate-acetate, receptor density increased by 73% to 114 fmol/mg protein. This increase in receptor density was inhibited by actinomycin D and cycloheximide. Exposure of native and differentiated U937 cells to 10(-5) and 10(-4) M histamine for 24 hr resulted in a dose-dependent down-regulation in receptor density. The data indicate that U937 cells may provide a model cell line for the study of histamine receptor gene expression.

Cycloheximide↗
PubMed1987

Correlation of histamine H1 receptor function and [3H]mepyramine binding in porcine tracheal tissue.

In order to validate the use of [3H]mepyramine as a radioligand to label airway histamine H1 receptors, the results of radioligand binding experiments using porcine tracheal tissue membranes were compared with the results of physiologic studies measuring histamine-induced trachealis muscle contraction. Close agreement was found between histamine-induced [3H]mepyramine binding inhibition and histamine concentration-contraction-response curves. Close agreement was also found between the KD of mepyramine-induced [3H]mepyramine binding inhibition and the K beta of mepyramine antagonism of muscle contractions stimulated by 10(-4) M histamine. [3H]Mepyramine binding was found to be rapid, reversible, saturable and stereospecific. Only H1 agonists and antagonists displayed potent [3H]mepyramine binding inhibition in competition binding studies. The results fulfill criteria for histamine H1 receptor identification by radioligand binding with [3H]mepyramine.

Aminopyridines↗
PubMed1987

Bilateral diaphragm paralysis treated with cuirass ventilation.

The therapeutic effects of cuirass ventilation were studied in two patients with bilateral diaphragm paralysis. Negative inspiratory and positive expiratory pressure applied to the cuirass shell was transmitted to the abdominal and thoracic cavities. Diaphragm excursion was enhanced. Nocturnal cuirass ventilation appears to be an ideal treatment for bilateral diaphragm paralysis.

Adult↗
PubMed1987

Hemoptysis in sarcoidosis.

The medical records of 433 patients with sarcoidosis were reviewed to determine the prevalence and significance of hemoptysis in this disease. Twenty-five patients (6%) were found to have hemoptysis. Nineteen of the 25 patients had mild hemoptysis, four had moderate, and two had massive hemoptysis. The clinical, roentgenographic, and laboratory features in patients with hemoptysis were compared with those from an age, race, and sex matched control group of sarcoidosis patients without hemoptysis. With the exception of eye involvement which occurred with greater frequency in control patients, no significant differences were found between the two groups. While bronchoscopy may be useful in establishing a diagnosis of endobronchial sarcoidosis, identification of a specific bleeding site is not likely in the absence of massive hemoptysis or localized radiographic abnormalities. Corticosteroid therapy may be useful to control hemoptysis in some patients.

Adult↗
PubMed1982

Nutritional assessment of patients with chronic obstructive pulmonary disease and acute respiratory failure.

In order to determine the likelihood of pre-existing nutritional deficits in medical patients with acute respiratory failure, a nutritional assessment survey was performed on 18 control patients with stable COPD and nine patients with COPD and acute respiratory failure. Significant differences were noted with the respiratory failure group having deficits in percentage of ideal body weight (mean difference 19 percent), triceps skinfold thickness (mean difference 4.4 mm), and arm muscle circumference (mean difference 3.3 cm). Significant deficits were also found in measurements of serum transferrin and retinol binding proteins, creatinine height index and total lymphocyte counts. Body protein and fat stores were markedly depleted in almost half of the patients with respiratory failure. These data suggest that protein-calorie malnutrition is likely to be present in patients with COPD and acute respiratory failure. Nutritional support for this population should be initiated at the onset of the illness. Nutritional repletion should be considered one goal of such therapy.

Acute Disease↗
PubMed1980

Iatrogenic malnutrition in patients receiving ventilatory support.

In a retrospective review of 26 medical patients with respiratory failure necessitating ventilatory support for at least six days, we found that the average daily vitamin, protein, and calorie intake was inadequate in almost all cases. Nutritional support for patients undergoing mechanical ventilation is often neglected and could be greatly improved.

Adult↗