Human alveolar capillaries undergo angiogenesis in pulmonary veno-occlusive disease.

The bronchial circulation undergoes angiogenesis in several pathological conditions, such as lung neoplasm and bronchiectasis, but whether the pulmonary circulation can do this has been questioned. A woman treated with mitomycin C and 5-fluorouracil developed progressive, fatal pulmonary hypertension over 5 months. In addition to light and transmission electron microscopic examination of her lung, her pulmonary vasculature was cast and the casts were studied with scanning electron microscopy. Light microscopy showed that she had pulmonary veno-occlusive disease and angiomatoid capillary growth in the alveolar walls. Transmission electron microscopy confirmed the presence of pulmonary hypertension and showed thickened endothelial basement membrane. Scanning electron microscopy of the cast blood vessels showed distortion and destruction of alveolar capillaries prohibiting the passage of erythrocytes. Large new capillaries developed on top of, and were connected to, the shrivelled capillaries that made up the alveolar wall. The new capillaries were larger and fewer, which reduced the alveolar-capillary interface. Arteries and veins were irregularly narrowed and the veins had broad muscularity. Oedema was present, and the pulmonary lymphatics were extensively cast, especially in the lobular septa, but the lymphatics had a normal appearance. It appears that this patient suffered extensive capillary damage and venous occlusion and that the response was extensive new capillary formation, sometimes in angiomatoid configurations, and hypertrophy of pulmonary veins and arteries. Casting the microvasculature and viewing it with scanning electron microscopy identified new alveolar capillaries in this patient with acquired pulmonary hypertension.

Pulmonary venous sphincter constriction is attenuated by alpha-adrenergic antagonism.

Pulmonary veins of rats have regular thin bands of constriction (sphincters) that deepen when the animals are given a blow to the head that is sufficient to cause pulmonary edema. Pulmonary edema caused by a stimulus to the brain is attenuated by alpha-adrenergic blockade. This study tested the hypothesis that alpha-adrenergic antagonism decreases this contraction in pulmonary veins. Male and female Sprague-Dawley rats were given prazosin, an alpha 1-specific antagonist, phentolamine, a combined alpha 1- and alpha 2-antagonist, or saline 10 min before their lungs were cast and they were given a blow on the head. The casts were fractured, causing the veins to break at the site of the constriction. Depth of contraction expressed as a percentage was 1 minus the ratio of the inner (constricted) and outer (total) diameters of the vein at the fracture. Resin that escaped the vascular space to cast alveoli and lymphatics was also measured. The average contraction of the veins at the site of the sphincters was 7.9 +/- 1.1% in the saline group, 5.4 +/- 0.7% in the phentolamine group, and 4.8 +/- 0.7% in the prazosin group (p < 0.05), although about a third of the constrictions were less than 2% in all groups. Arteries had no contraction. Contraction was greater in heavier and male animals, which were variables that interacted with the agent the animals were given in a multivariate analysis. Contrary to the hypothesis, lymphatic casts were greater in the animals receiving alpha-blockers (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)