Arterial pO sub(2) stimulates intimal hyperplasia and serum stimulates inward eutrophic remodeling in porcine saphenous veins cultured ex vivo

Ex vivo culture of arteries and veins is an established tool for investigating mechanically induced remodeling. Porcine saphenous veins (PSV) cultured ex vivo with a venous mechanical environment, serum-supplemented cell-culture medium and standard cell-culture conditions (5% CO sub(2) and 95% balan...

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Veröffentlicht in:Biomechanics and modeling in mechanobiology 2011-04, Vol.10 (2), p.161-175
Hauptverfasser: Joddar, Binata, Shaffer, Rebecca JG, Reen, Rashmeet K, Gooch, Keith J
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Sprache:eng
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Zusammenfassung:Ex vivo culture of arteries and veins is an established tool for investigating mechanically induced remodeling. Porcine saphenous veins (PSV) cultured ex vivo with a venous mechanical environment, serum-supplemented cell-culture medium and standard cell-culture conditions (5% CO sub(2) and 95% balance air ~140 mmHg pO sub(2)) develop intimal hyperplasia (IH), increased cellular proliferation, decreased compliance and exhibit inward eutrophic remodeling thereby suggesting that nonmechanical factors stimulate some changes observed ex vivo. Herein we explore the contribution of exposure to greater than venous pO sub(2) and serum to these changes in cultured veins. Removing serum from culture medium did not inhibit development of IH, but did reduce cellular proliferation and inward eutrophic remodeling. In contrast, veins perfused using reduced pO sub(2) (75 mmHg) showed reduced IH. Among the statically cultured vessels, veins cultured at arterial pO sub(2) (95 mmHg) and above showed IH as well as increase in proliferation and vessel weight compared to fresh veins; veins cultured at venous pO sub(2) did not. Taken together, these data suggest that exposure of SV to arterial pO sub(2) stimulates IH and cellular proliferation independent of changes in the mechanical environment, which might provide insight into the etiology of IH in SV used as arterial grafts.
ISSN:1617-7959
1617-7940
DOI:10.1007/s10237-010-0224-8