Increased resistance in postobstructive pulmonary vasculopathy: structure-function relationships.
Postobstructive pulmonary vasculopathy (POPV) was produced by chronic ligation (120 days) of the left main pulmonary artery of seven dogs. To explain the abnormal physiological changes found using arterial and venous occlusion (AVO) in POPV (J. Appl. Physiol. 69: 1022-1032, 1990), the light-microscopic morphology, morphometry (n = 5), and ultrastructure (n = 6) of ligated left lower lobes were compared with contralateral control right lower lobes. First, there was a proliferation of bronchial vessels around pulmonary vessels and airways to explain bronchial blood flow rates of 330 ml/min in left lower lobes. The walls of the bronchial vessels contained smooth muscle with minimal elastic tissue and prominent myoendothelial junctions. Second, focal bronchopulmonary anastomoses were seen in pulmonary arteries approximately equal to 100 microns diam, which is consistent with our conclusion that the major site of communication is at the precapillary level and suggests that the limit between arterial and middle segments defined by AVO may lie in arteries of approximately equal to 100 microns. Third, to explain the increased arterial resistance in POPV, the pulmonary arteries had an increased percent medial muscle thickness, peripheral muscularization, and focal intimal thickening but had no plexiform lesions. The ultrastructure of the arteries revealed new intimal cells and numerous myoendothelial junctions rarely found in controls. Capillaries and veins were only subtly altered. Fourth, the hyperreactivity of arteries to serotonin and of veins to histamine found using AVO was partially explained by the increased medial thickness and decreased diameter but may also be due to increased receptor concentration or related to the myoendothelial junctions. We conclude that most of the hemodynamic alterations in POPV are related to morphological abnormalities and that this model has clinical and experimental relevance in the study of bronchopulmonary vascular interactions.
Department of Pathology, McGill University, Montreal, Quebec, Canada.
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Michel
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Hakim
D000402:Airway Obstruction / Q000150:complications* / Q000473:pathology; D000818:Animals; D001980:Bronchi / Q000473:pathology / Q000503:physiopathology; D002196:Capillaries / Q000473:pathology / Q000648:ultrastructure; D004285:Dogs; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D008168:Lung / Q000473:pathology; D008171:Lung Diseases / Q000473:pathology / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D011651:Pulmonary Artery / Q000473:pathology / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology*; D011667:Pulmonary Veins / Q000473:pathology / Q000503:physiopathology; D014652:Vascular Diseases / Q000473:pathology / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology*