title: Mesenteric lymphatic vessels adapt to mesenteric venous hypertension by becoming weaker pumps.
abstract: Lymphangions, the segments of lymphatic vessels between two adjacent lymphatic valves, actively pump lymph. Acute changes in transmural pressure and lymph flow have profound effects on lymphatic pump function in vitro. Chronic changes in pressure and flow in vivo have also been reported to lead to significant changes in lymphangion function. Because changes in pressure and flow are both cause and effect of adaptive processes, characterizing adaptation requires a more fundamental analysis of lymphatic muscle properties. Therefore, the purpose of the present work was to use an intact lymphangion isovolumetric preparation to evaluate changes in mesenteric lymphatic muscle mechanical properties and the intracellular Ca(2+) in response to sustained mesenteric venous hypertension. Bovine mesenteric veins were surgically occluded to create mesenteric venous hypertension. Postnodal mesenteric lymphatic vessels from mesenteric venous hypertension (MVH; n = 6) and sham surgery (Sham; n = 6) animals were isolated and evaluated 3 days after the surgery. Spontaneously contracting MVH vessels generated end-systolic active tension and end-diastolic active tension lower than the Sham vessels. Furthermore, steady-state active tension and intracellular Ca(2+) concentration levels in response to KCl stimulation were also significantly lower in MVH vessels compared with those of the Sham vessels. There was no significant difference in passive tension in lymphatic vessels from the two groups. Taken together, these results suggest that following 3 days of mesenteric venous hypertension, postnodal mesenteric lymphatic vessels adapt to become weaker pumps with decreased cytosolic Ca(2+) concentration.
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas;
authors.forename: R M
authors.initials: RM
authors.lastname: Dongaonkar
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas;
authors.forename: T L
authors.initials: TL
authors.lastname: Nguyen
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas; cquick@tamu.edu.
authors.forename: C M
authors.initials: CM
authors.lastname: Quick
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas;
authors.forename: C L
authors.initials: CL
authors.lastname: Heaps
authors.affiliation: Large Animal Clinical Sciences, Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas; and.
authors.forename: J
authors.initials: J
authors.lastname: Hardy
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas;
authors.forename: G A
authors.initials: GA
authors.lastname: Laine
authors.affiliation: Department of Medical Physiology, Texas A&M Health Science Center, Texas A&M University, College Station, Texas.
authors.forename: E
authors.initials: E
authors.lastname: Wilson
authors.affiliation: Michael E. DeBakey Institute, Texas A&M University, College Station, Texas;
authors.forename: R H
authors.initials: RH
authors.lastname: Stewart
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism; D002417:Cattle; D004195:Disease Models, Animal; D005260:Female; D008196:Lymph / Q000378:metabolism; D042601:Lymphatic Vessels / Q000378:metabolism / Q000503:physiopathology*; D008642:Mesenteric Veins / Q000503:physiopathology*; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000378:metabolism / Q000503:physiopathology*; D011312:Pressure; D013997:Time Factors; D014690:Venous Pressure
chemical_list: D002118:Calcium
keywords: edema; interstitial fluid balance; stress