title: The influence of circulatory overload on extraalveolar microvessel endothelium of dog lung in vivo.
abstract: In an earlier study from this laboratory, morphometric evaluations of the alveolar capillary endothelium of the lungs of intact dogs were recorded after periods of sustained increases of pulmonary microvascular pressures (D. O. DeFouw, W. O. Cua, and F. P. Chinard, 1983, Microvasc. Res. 25, 56-67). In the present study ultrastructural characteristics of the extraalveolar microvessel endothelium of these dog lungs were evaluated. Small (25- to 50-microns luminal diameter) nonmuscular vessels, which adjoin the alveolar capillaries, and larger (51-200 microns) partially muscular and muscular microvessels were assessed. After increased microvascular filtration, to be expected from the increased hydrostatic pressures, fluid accumulation was found only in the connective tissue sleeves of the larger microvessels. The endothelium of these partially muscular and muscular vessels was markedly affected by fluid distension of the periendothelial interstitium. The endothelial response included the appearance of basal (abluminal) surface invaginations, de novo plasmalemmal vesicle formation, and increased numbers of cytoplasmic vacuoles. The small nonmuscular microvessels lacked both the fluid cuffs and the alterations of endothelial ultrastructure. This latter observation is consistent with the previous report from this laboratory that indicated an absence of both alveolar septal edema and increased capillary endothelial vesicle densities in these lungs (DeFouw et al., 1983). Thus, it seems likely that the conformational changes of the endothelium of the larger microvessels were related to the formation of the periendothelial fluid cuffs. The mechanisms responsible for this endothelial response have not been determined but can be explained on the basis of the testable hypothesis that they are secondary to an increase of tissue pressure associated with accumulation of tissue fluid. These changes may thus represent a secondary structural adaptation to the increased tissue pressures and may serve as a potential vesicular-vacuolar pathway across the endothelium.
authors.affiliation: Department of Anatomy, UMDNJ-New Jersey Medical School, Newark 07103-2757.
authors.forename: D O
authors.initials: DO
authors.lastname: DeFouw
authors.forename: W O
authors.initials: WO
authors.lastname: Cua
authors.forename: F P
authors.initials: FP
authors.lastname: Chinard
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003238:Connective Tissue / Q000648:ultrastructure; D004285:Dogs; D004730:Endothelium, Vascular / Q000648:ultrastructure*; D008168:Lung / Q000098:blood supply*; D008833:Microcirculation; D009131:Muscle, Smooth, Vascular / Q000648:ultrastructure