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Biomedical subjects

H K Fisher

Publications and source records attributed to H K Fisher.

18 recordsLinked to original sources
PubMed1982

A study of beta-adrenergic and prostaglandin receptors in patients with aspirin-induced bronchospasm.

Nine patients with aspirin-induced bronchospasm were compared with age-matched normal controls to test the hypothesis that a defect in the beta-adrenergic system could lead to excessive dependence on prostaglandins to maintain bronchodilator function. Lymphocyte beta-receptor density and affinity were measured by 3H-dihydroalprenolol binding. Beta-receptor function was measured in terms of cyclic AMP accumulation in response to isoproterenol. Prostaglandin (PG) responsiveness was measured in terms of cyclic AMP accumulation caused by PGE1 stimulation. No difference was found in either ther number of beta-adrenergic receptors (1234 +115 vs 1213 +82) or dissociation constant (1.40 +0.23 nM vs 1.19 +0.07nM) (mean +SEM) between the asthmatic and the control group, respectively. Furthermore, neither group showed any difference in maximally stimulated cyclic AMP in response to isoproterenol and PGE 1. Thus we find no evidence of an inherent defect of beta-adrenergic receptor and function to account for the susceptibility to aspirin-induced bronchospasm.

Adult↗
PubMed1982

Sleep apnea.

Explore the source record for details and available documents.

Aged↗
PubMed1976

Site of action of inhaled 6 per cent carbon dioxide in the lungs of asthmatic subjects before and after exercise.

We studied 10 nonsmoking young adults before and after inducing asthmatic attacks by treadmill exercise. We used body plethysmography, flow-volume curves with air and a mixture of 80% helium and 20% oxygen, pressure-volume diagrams, and arterial blood gas analyses to characterize the effects of exercise and acute inhalation of 6% CO2. Even when exercise produced no change in arterial CO2 tension, inhalation of 6% CO2 relieved obstruction to airflow. It also altered the volume-pressure ralationship of the lungs so that total lung capacity was reduced within minutes, and elastic recoil was increased at fixed lung volume. A large increase in density dependence of airflow was seen in some cases, suggesting relief of obstruction in peripheral airways. Atropine sulfate did not prevent obstruction after exercise and did not prevent relief during CO2 inhalation. We concluded that CO2 inhalation can relax both central and peripheral airways in young asthmatic adults, both at rest and after exercise, and that both total lung capacity and density dependence of airflow can change acutely in these subjects.

Adolescent↗
PubMed1976

IgE-induced respiratory and circulatory changes during systemic anaphylaxis in the rabbit.

We studied systemic anaphylaxis induced by the administration of 200 mug of horseradish peroxidase into 11 anesthetized rabbits known to be producing anti-horseradish peroxidase antibodies only of the IgE class. Ventilatory changes included a transient, abrupt decrease in breathing frequency followed by increased minute ventilation; lung mechanical changes included decreased dynamic lung compliance and increased total pulmonary resistance; cardiovascular changes included pulmonary hypertension, systemic hypotension, and, frequently, a transient bradycardia. Recovery from these physiologic changes took place within 60 min. After recovery, the administration of 2 mg of horseradish peroxidase into 6 of the rabbits induced a second reaction indistinguishable from the first with respect to ventilatory and circulatory alterations; however, lung mechanical changes were less prominent. No histologic evidence of pulmonary edema or intraluminal plugging of the pulmonary edema or intraluminal plugging of the pulmonary circulation was observed by light microscopy. Although the first anaphylactic reaction was accompanied by disappearance of stainable basophils from the circulating blood, the second reaction occurred despite the absence of circulating basophils. These studies characterize further the effects of antigen challenge in rabbits producing detectable concentrations of IgE, but not other classes of antibody to the antigen.

Airway Resistance↗
PubMed1975

Pulmonary effects of paraquat in the first day after injection.

To learn whether surface force changes precede the appearance of lung edema during experimental intoxication due to paraquat, we studied rats for 1 day following injection of 27 mg/kg iv. By 24 h, surface-active material recovered by lung lavage was decreased 32 percent, and changes in lung microsections and recoil pressure at half-deflation suggested decreased alveolar stability. Despite a 25 percent loss in overall body weight, lung weight increased more than 7 percent and protein concentration in lung lavage fluid increased by 158 percent. Lung edema was demonstrated morphologically as early as we could detect changes in surfactant or lung mechanical properties. Metabolic studies with lung tissue slices incubated with 4.5 times 10-4 M paraquat showed a fourfold increase in 14CO2 formed from (1-14C) glucose, but no significant change in 14CO2 form (6-14C) glucose, suggesting increased utilization of the pentose pathway for oxidation of glucose. (1-14C) Acetate oxidation was impaired slightly, but incorporation into lipid was decreased by 70 percent. we conclude that paraquat intoxication in the rat is not a suitable model for studying uncomplicated perturbation of the surfactant system.

Acetates↗
PubMed1974

Effect of experimental pneumococcal meningitis on respiration and circulation in the rabbit.

Pathophysiological studies in bacterial meningitis in man have been limited by clinical variability and the necessity for immediate therapy. After the development of a reliable animal model of pneumococcal meningitis, we studied respiration and circulation in 25 anesthetized New Zealand white rabbits during untreated pneumococcal meningitis and in 33 healthy controls. In meningitis, we found increased lactic acid in cerebrospinal fluid (CSF). Increased ventilation, perhaps due to CSF lactic acid accumulation, resulted in respiratory alkalosis; the concomitant lowering of Pco(2) acted as a homeostatic mechanism to restore pH toward normality in the CSF. Hyperventilation increased with the duration of the illness. Cardiac output was also increased with decreased peripheral vascular resistance but with only slight reduction in mean systemic and pulmonary arterial pressures. In the final hour of life, peripheral vascular resistance fell further; ventilation declined and then abruptly ceased while cardiac activity continued. Lactic acid accumulation in the CSF, found in both experimental and human pneumococcal meningitis, may cause the hyperventilation found in this disease and may contribute to death.

Acidosis↗