TY - JOUR
T1 - Kinetics of altered angiotensin II responses in experimental vein grafts
AU - Davies, Mark G.
AU - Hagen, Per Otto
N1 - Funding Information:
Received 11 May 1995; accepted 1 July 1996. The technical assistance of E. Barber is appreciated. Microsutures were a gift of Ethicon Inc., Somerville, NJ, USA. This study was supported by the U.S. Public Health Service Grant no. HL 15448. Mark G. Davies is supported by an NIH Fogarty International Research Fellowship (TW 04810) and holds a Royal College of Surgeons in Ireland Surgical Travelling Fellowship and a Trinity College Dublin Postgraduate Scholarship. This paper was presented at the 1 It h Annual Scientific Sessions of the Academy of Surgical Research (Alburquerque, NM; 30 September to 2 October 1995). Address correspondence to Per-Otto Hagen, PhD, Duke University Medical Center, P.O. Box 3473, Durham, NC 27710, USA. E-mail: hagen003@mc.duke.edu
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1996
Y1 - 1996
N2 - Following vein grafting, responses in the arterial vein bypass grafts to angiotensin II, a Known mitogen, increase. It is not known when these changes occur or whether these changes are due to alterations in endothelial cell function, excision/implantation of the vessel, or exposure to arterial hemodynamics. Two studies were designed to examine these questions. New Zealand white rabbits underwent excision of the external jugular vein, common carotid artery, an external jugular veno-venous bypass (VVG) or a common carotid veno-arterial bypass (VAG). Half the jugular veins and carotid arteries were mechanically denuded of their endothelium. All vein grafts were harvested at 28 days. A set of VAG was also harvested at 1, 3, 7, and 14 days. Isometric tension studies to angiotensin II (10-10 to 10-4 M) were performed on rings from each jugular vein, carorid artery, and vein graft. Jugular veins had a triphasic response to angiotensin II. Deendothelialized jugular veins had a triphasic response with an increased first phase and a much reduced second phase. Carotid arteries (6.87 ± 0.18 and 6.15 ± 0.18; with and without endothelium; means ± SEM, -log10[EC50]; p < .05), VVG (6.69 ± 0.15), and VAG (7.42 ± 0.29; p < .05 compared to VVG) showed a monophasic response to angiotensin II at 28 days. This monophasic response in VAG to angiotensin II was recordable at 7 days postoperatively and there was no further change in its sensitivity between 14 and 28 days. These results suggest that the induction of altered angiotensin II responses is dependent on exposure to the arterial circulation, that alterations in VAG responses occur within the first 7 days of vein grafting and that VAG at 28 days become more sensitive to angiotensin II than the carotid vessels into which they are placed. These changes in smooth muscle cell sensitivity to a known smooth muscle cell mitogen (angiotensin II) may contribute to the development of intimal hyperplasia in the veno-arterial graft.
AB - Following vein grafting, responses in the arterial vein bypass grafts to angiotensin II, a Known mitogen, increase. It is not known when these changes occur or whether these changes are due to alterations in endothelial cell function, excision/implantation of the vessel, or exposure to arterial hemodynamics. Two studies were designed to examine these questions. New Zealand white rabbits underwent excision of the external jugular vein, common carotid artery, an external jugular veno-venous bypass (VVG) or a common carotid veno-arterial bypass (VAG). Half the jugular veins and carotid arteries were mechanically denuded of their endothelium. All vein grafts were harvested at 28 days. A set of VAG was also harvested at 1, 3, 7, and 14 days. Isometric tension studies to angiotensin II (10-10 to 10-4 M) were performed on rings from each jugular vein, carorid artery, and vein graft. Jugular veins had a triphasic response to angiotensin II. Deendothelialized jugular veins had a triphasic response with an increased first phase and a much reduced second phase. Carotid arteries (6.87 ± 0.18 and 6.15 ± 0.18; with and without endothelium; means ± SEM, -log10[EC50]; p < .05), VVG (6.69 ± 0.15), and VAG (7.42 ± 0.29; p < .05 compared to VVG) showed a monophasic response to angiotensin II at 28 days. This monophasic response in VAG to angiotensin II was recordable at 7 days postoperatively and there was no further change in its sensitivity between 14 and 28 days. These results suggest that the induction of altered angiotensin II responses is dependent on exposure to the arterial circulation, that alterations in VAG responses occur within the first 7 days of vein grafting and that VAG at 28 days become more sensitive to angiotensin II than the carotid vessels into which they are placed. These changes in smooth muscle cell sensitivity to a known smooth muscle cell mitogen (angiotensin II) may contribute to the development of intimal hyperplasia in the veno-arterial graft.
KW - Angiotensin II
KW - Endothelium
KW - Smooth muscle cells
KW - Vein grafts
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U2 - 10.3109/08941939609025859
DO - 10.3109/08941939609025859
M3 - Article
C2 - 8981215
AN - SCOPUS:0030480786
VL - 9
SP - 423
EP - 432
JO - Journal of Investigative Surgery
JF - Journal of Investigative Surgery
SN - 0894-1939
IS - 6
ER -