A study of stress during final exam week in 20 college students with mild allergic asthma showed that their anxiety and depression scores were significantly higher and that their stress levels acted as a cofactor to increase airway inflammation after an antigen challenge. The investigators were testing the hypothesis that a relatively chronic stressful life event, such as final examinations, would enhance the airway inflammatory response to antigens. An antigen is a substance or organism that, when entering the body, causes the production of an antibody to neutralize, destroy, or weaken it. Based on a skin prick test, the mildly allergic asthmatic students received a graded inhaled antigen challenge of either ragweed, cat dander, or house dust mite–substances that would cause an immediate fall in lung function test results of at least 20 percent. The researchers found that the stress connected with a final exam was associated with enhanced eosinophilia and eosinophil-derived neurotoxin at 6 and 24 hours post-antigen challenge. Eosinophils are white blood cells that normally constitute about one-third of the total white blood cell count. An increase in the number of eosinophils commonly occurs in allergic reactions and in some inflammatory conditions. The researchers believe that this is the first study to show allergen-induced airway eosinophilia can be significantly augmented during a period of stress. In an editorial about the study in the same issue, John Bienenstock, M.D., of the Brain-Body Institute, McMaster University, Hamilton, Ontario, Canada, said that the data in the published research “very strongly support the contention that stress promoted at least some of the hallmarks of inflammation associated with asthma.” According to him, the study draws our attention to the difficulties with the quantitation of stress, and our inadequacy in determining whether and how stress may have either a greater or lesser effect in different individuals. The research and editorial appear in the second issue for April of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine.
INTRAVENOUS SILDENAFIL SIGNIFICANTLY LOWERS PULMONARY VASCULAR RESISTANCE IN AN ANIMAL MODEL OF NEONATAL PULMONARY HYPERTENSION
In an animal model of persistent neonatal pulmonary hypertension, a serious killer of newborns, the vasodilator sildenafil completely reversed vascular resistance in six affected piglets within one hour after researchers began infusing the drug. The investigators were comparing the effects of intravenous sildenafil with inhaled nitric oxide (a standard treatment) in a piglet model of neonatal pulmonary hypertension caused by meconium aspiration. Meconium is the dark green material found in the intestine of the full-term infant. When the fetus inhales meconium, the substance can block the airways and irritate the lungs. Severe meconium aspiration syndrome produces acute lung disease with rapid onset of persistent pulmonary hypertension. Current management of persistent pulmonary hypertension of the newborn includes therapies that are targeted at lowering vascular resistance, with inhaled nitric oxide as a key treatment. The six piglets that were instilled with human meconium, with a resulting increase in vascular resistance of 70 percent, had that level completely reversed within one hour of the start of sildenafil infusion. This result was in contrast to those of the controls (no change) and the six piglets treated with nitric oxide (40 percent reduction in two hours). The researchers believe that sildenafil may play an important role in the future treatment of the illness. The research appears in the second issue for April of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine.
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Journal
American Journal of Respiratory and Critical Care Medicine