Other smoking-affected pulmonary diseases.

Cigarette smoking is the leading cause of preventable death in the United States. Smoking adversely affects many organ systems, but especially the lung. Carcinoma of the lung and chronic obstructive pulmonary disease account for most smoking-associated respiratory morbidity and mortality, and their association with smoking is both well established and widely recognized. Cigarette smoking also is associated with differences in the incidence, severity, or natural history of a broad array of other respiratory illnesses, ranging from the common cold to pneumothorax, pulmonary hemorrhage, and various interstitial lung diseases. Interestingly, while the general effect of smoking on respiratory diseases is adverse, in the cases of sarcoidosis and hypersensitivity pneumonitis smoking may actually be associated with a decrease in the incidence of disease. In this article, the author briefly discusses some of the pulmonary and systemic effects of smoking that might mediate its effects on an array of lung diseases, then comprehensively reviews less common or less well-recognized smoking-affected lung diseases such as pulmonary infections, spontaneous pneumothorax, Goodpasture's syndrome, eosinophilic granuloma and other interstitial lung diseases, and pulmonary metastatic disease.

The preflight evaluation. A comparison of the hypoxia inhalation test with hypobaric exposure.

STUDY OBJECTIVES: We sought to compare arterial oxygen partial pressure (PaO2) relationships between a 15.1% hypoxia inhalation test (HIT) at sea level and a hypobaric chamber exposure equivalent to 2,438 m (8,000 feet) of altitude above sea level in patients with chronic obstructive pulmonary disease (COPD) and healthy subjects. DESIGN: Comparison of physiologic variables before and during intervention. SETTING: A referral-based pulmonary disease clinic at a US Army medical center in a metropolitan area. SUBJECTS: The study included three groups: group 1, 15 patients, 3 women and 12 men, with COPD (forced expiratory volume in the first second [FEV1, mean +/- SD], 41 +/- 14% of predicted); group 2, 9 healthy men; and group 3, 18 men with COPD (FEV1, 31 +/- 10% of predicted) previously reported in detail. INTERVENTIONS: We evaluated each group at sea level followed by one of two different types of hypoxic exposures. Group 1 received exposure to 15.1% oxygen at sea level, the HIT. Groups 2 and 3 received hypobaric chamber exposure equivalent to 2,438 m (8,000 feet) above sea level. MEASUREMENTS AND MAIN RESULTS: For all three groups combined, the arterial oxygen tension at sea level (PaO2SL) explained significant variability in PaO2 during hypoxic exposure according to the following formula: PaO2 during exposure = 0.417 (PaO2SL)] + 17.802 (n = 42; r = 0.756; p < 0.001). Neither the type of hypoxic exposure (HIT vs hypobaric), status as patient vs control, sex, nor age explained significant variability in PaO2 during hypoxia exposure after inclusion of PaO2SL as a covariate in analysis of variance. Subsequent analysis revealed that forced expiratory spirometric variables FEV1 and FEV1 to FVC ratio served as second order covariates with PaO2SL to improve description of PaO2 during hypoxia exposure for the combined samples (n = 42; p < 0.05). Analysis of residuals from regression analysis revealed approximately normal distribution. CONCLUSIONS: The PaO2 relationships did not differ between the 15.1% HIT at sea level and hypobaric exposures of 2,438 m (8,000 feet) above sea level. Normal subjects and patients with COPD formed a single relationship. The present study extends descriptive models to a larger range of subjects. Regression models have definable accuracy in predicting PaO2 during hypoxia exposure that increases with inclusion of spirometric variables.

Diaspirin crosslinked hemoglobin (DCLHb): control of pressor effect with anti-hypertensive agents.

Diaspirin crosslinked hemoglobin (DCLHb) administration elevates mean arterial pressure (MAP). The purpose of this study was to determine whether commonly used antihypertensive agents could control this pressor effect in rats. Awake rats were injected intravenously (i.v.) with 280 mg/kg of DCLHb. Fifteen minutes later when MAP was 25-30% above baseline and heart rate (HR) was reciprocally decreased, prazosin (2 mg/kg;an alpha adrenergic blocker), nitroglycerine (NTG; 10-150 mcg/min; a nitrovasodilator), nicardipine (0.204-0.08 mg/hr; a calcium channel blocker) or labetalol (5 mg/kg; an alpha/beta adrenergic blocker) was administered i.v. All four classes of antihypertensive agents promptly restored MAP to baseline. Coincident with the return of MAP to baseline, HR was restored to baseline in prazosin and NTG treated animals, however, bradycardia persisted in those animals treated with nicardipine and labetalol, most likely due to the negative chronotropic properties of these agents. We conclude that the pressor effect of DCLHb can be readily controlled with at least four different classes of commonly used antihypertensive agents.