Corticosteroids are often used in the outpatient treatment of acute exacerbation of chronic obstructive pulmonary disease (COPD). To date, there are few data documenting the benefit of this practice. The objective of this randomized, double-blind, placebo-controlled trial was to assess the efficacy of corticosteroids in the outpatient treatment of COPD exacerbations. Twenty-seven patients presenting with acute COPD exacerbation were studied. In addition to continuing their previous medications and increasing their use of beta-agonists, patients were randomized to receive a 9-d tapering dose of either oral prednisone or placebo. Treatment with prednisone rather than placebo resulted in a more rapid improvement in arterial PO2 (PaO2) (1.12 mm Hg/d versus -0.03 mm Hg/day; p = 0.002), alveolar-arterial oxygen gradient (A-aDO2) (-1.16 mm Hg/d versus -0.03 mm Hg/day; p = 0.04), FEV1 (0.05 L/d versus 0.00 L/d; p = 0.006), and peak expiratory flow (PEF) (0.15 L/s/d versus 0.04 L/s/d; p = 0.009). Prednisone also resulted in fewer treatment failures (p = 0.002) and in a trend toward more rapid improvement in dyspnea scale scores. Outpatient treatment of acute COPD exacerbation with prednisone accelerates recovery of PaO2, A-aDO2, FEV1, and PEF, reduces the treatment failure rate, and improves subjective dyspnea.

The death rate from asthma is highest in old age and continues to rise, despite diagnostic and therapeutic advances.'3 Acute attacks of asthma in older people with chronic asthma may be very rapidly fatal4 and have been said to have a poorer prognosis than in the young.5 Of the many potential reasons for the higher mortality from asthma in old age, the possibility of impaired awareness of the severity of an acute asthmatic attack by the elderly patient, his physician, or both has been little investigated. Petheram et al 6 showed that during acute exacerbations of asthma elderly patients have less pronounced pulsus paradoxus and tachycardia than younger patients with similar airway obstruction and blood gas abnormalities. They argued that this might theoretically result in undertreatment of the elderly asthmatic patient during an acute attack. Treatment might also be inadequate if the severity of the attack were also underestimated by the patient. This may indeed be the case in the elderly. Elderly asthmatic patients tend to deteriorate for longer periods at home before admission,6 and when challenged with inhaled methacholine they do not report dyspnoea or wheeze to be troublesome despite a minimum fall in one second expiratory volume (FEV,)

The bronchial vasculature is the systemic arterial blood supply to the lung. Although small relative to the pulmonary blood flow, the bronchial vasculature serves important functions and is modified in a variety of pulmonary and airway diseases.Congestion of the bronchial vasculature may narrow the airway lumen in inflammatory airway diseases, and formation of new bronchial vessels (angiogenesis) is implicated in the pathology of a variety of chronic inflammatory, infectious and ischaemic pulmonary diseases. The remarkable ability of the bronchial vasculature to remodel has implications for disease pathogenesis.The contributions of the bronchial vasculature to the pathogenesis of pulmonary disease are reviewed in this article. Eur Respir J 1997; 10: 1173-1180. The bronchial circulation is ideally situated to play an important role in lung defence and in the pathogenesis of a number of airway diseases. The bronchial microvasculature provides nutrient blood flow to the airway epithelium and is important for proper functioning of the mucociliary escalator. Bronchial blood flow is responsive to changes in neural and humoral stimuli and plays a role in conditioning of inspired air. The focus of this review is the potential involvement of the bronchial vasculature in contributing to the pathogenesis of a variety of airway diseases. In particular, we have focused on the possibility of airway narrowing as a consequence of bronchial vascular congestion, and the remarkable proliferative capacity of the bronchial vessels in response to a variety of pulmonary diseases. Bronchial vascular congestionHyperaemia of the bronchial vasculature is often included in descriptions of the pathology of asthma. An example of hyperaemia of the bronchial vasculature is shown in figure 1. This photomicrograph shows a crosssection of a human airway from a patient who died of asthma. The apparent increase in the size and number of vessels inside and outside the smooth muscle layer is clearly visible, suggesting that vascular dilation and proliferation (angiogenesis) could be important components of the airway wall remodelling in asthmatic patients. The airway vasculature is of considerable interest in asthma because it can contribute to the excessive airway narrowing, which is characteristic of this disease. A diagram of an airway ( fig. 2) illustrates the two bronchial vascular plexuses: the peribronchial plexus, located in the adventitial space between the muscle and the surrounding lung parenchyma; and the submucosal vascular plexus, located beneath the epithelial layer. Dilation, exudation or transudation from these vessels could contribute to the excessive airway narrowing observed in asthma. Relaxation of the bronchial vascular smooth muscle and/or an increase in the intravascular pressure will lead to congestion of these vessels. This bronchial vascular congestion could result in a reduction in the area of the airway lumen and/or an increase in the outer diameter of the airway. The latter effect could uncouple the airway smoo...

We studied the effects of left pulmonary artery (LPA) ligation on the bronchial circulatory system (BCS) by using a sheep model. LPA was ligated in the newborn lambs soon after birth (n = 8), and when the sheep were approximately 3 yr of age anatomic studies revealed marked angiogenesis in BCS. Bronchial blood flow and cardiac output were studied by placing flow probes around the bronchial and pulmonary arteries in four adult sheep. After LPA ligation, bronchial blood flow increased from 35 +/- 6 to 134 +/- 42 ml/min in approximately 3 wk (P < 0.05). We also studied gas-exchange functions of BCS approximately 3 yr after the ligation of LPA in newborn lambs (n = 4) and used a control group (n = 12) in which LPA was ligated acutely. In the left lung, O2 uptake after acute ligation was 16 +/- 3 ml/min and was similar to the chronic model, whereas CO2 output in the control group was 27 +/- 3 ml/min compared with 79 +/- 12 ml/min in the chronic preparation (P < 0.05). We conclude that LPA ligation causes marked angiogenesis in BCS that is capable of performing some gas-exchange functions.

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