title: Pulmonary embolism: analysis of endothelial pore sizes in canine lung.
abstract: The effect of glass-bead microemboli (diameter 100 micron, range 77-125 micron) in the absence of fibrinolysis inhibition on pulmonary hemodynamics and microvascular permeability was determined in anesthetized, microfilaria-free dogs acutely prepared for the collection of lung lymph. Pulmonary vascular resistance, pulmonary capillary pressure (Pc), lymph flow (QL), and the ratio of lymph (CL) to plasma (Cp) protein concentrations were measured after 0.2 (n = 4), 0.4 (n = 6), or 0.6 (n = 3) g/kg beads. In all cases, emboli increased resistance and QL severalfold (P less than 0.05), while CL/Cp remained unchanged. In part, the increase in QL could be attributed to an increase in Pc compared with control (12.4 +/- 2.2 vs. 6.7 +/- 0.6 mmHg, P less than 0.05). Furthermore, since the solvent-drag reflection coefficient (sigma f) for total proteins approaches the osmotic reflection coefficient (sigma d) at high QL, sigma d was estimated under these conditions with sigma f approximately equal to sigma d approximately equal to 1 - (CL/Cp)min. The sigma d was decreased (P less than 0.05) after 0.4 and 0.6 g/kg beads to 0.55 +/- 0.03 and 0.50 +/- 0.07, respectively, when compared with that in control lungs (sigma d = 0.62 +/- 0.02; Parker et al., Circ. Res. 48: 549-561, 1981). A pore-stripping analysis demonstrated that after emboli the pulmonary endothelial barrier could be described by a population of small (80 A) and large (350 A) pores. However, the number of large to small pores was 1:1,195, compared with 1:195 in control lungs, suggesting an increased contribution of extra-alveolar vessels upstream of the emboli.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.
authors.forename: M I
authors.initials: MI
authors.lastname: Townsley
authors.forename: J C
authors.initials: JC
authors.lastname: Parker
authors.forename: G L
authors.initials: GL
authors.lastname: Longenecker
authors.forename: M L
authors.initials: ML
authors.lastname: Perry
authors.forename: R M
authors.initials: RM
authors.lastname: Pitt
authors.forename: A E
authors.initials: AE
authors.lastname: Taylor
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D001798:Blood Proteins / Q000378:metabolism; D002196:Capillaries / Q000473:pathology / Q000503:physiopathology; D002199:Capillary Permeability; D004285:Dogs; D004730:Endothelium, Vascular / Q000473:pathology*; D005342:Fibrinolysis; D005898:Glass; D008168:Lung / Q000098:blood supply*; D008196:Lymph / Q000378:metabolism; D008208:Lymphatic System / Q000503:physiopathology; D008214:Lymphocytes / Q000473:pathology; D008863:Microspheres; D009504:Neutrophils / Q000473:pathology; D011506:Proteins / Q000378:metabolism; D011655:Pulmonary Embolism / Q000473:pathology* / Q000503:physiopathology; D013929:Thromboxane B2 / Q000097:blood; D014655:Vascular Resistance
chemical_list: D001798:Blood Proteins; D011506:Proteins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha