Atherosclerosis Alters Loading-Induced Arterial Damage: Implications for Robotic Surgery.
BACKGROUND
Lack of intra-operative haptic information during robotic surgery increases the risk for unintended tissue overload and damage. Knowledge about the acute and chronic fundamental relationship between force load and induced damage in healthy and diseased arteries is crucial to enable intra-operative haptic feedback or shared autonomy and improve patient safety.


METHODS
Arteries of wildtype and atherosclerotic mice were clamped in vivo for 2 minutes (0.0N, 0.6N or 1.27N). Histological analysis (Verhoeff's-Van Gieson, Osteopontin, CD45, CD105) was performed immediately, or after 6 hours, 2 weeks or 1 month. Endothelium-dependent and-independent vasodilatation was assessed immediately or 1 month after clamping.


RESULTS
Endothelium dependent vasodilatation is worse after clamping of wildtype arteries, but is restored after one month. Clamping also results in flattening of the innermost elastic membrane of both genotypes, which is reversed over time for wildtype arteries but not for vessels from atherosclerotic mice. Higher osteopontin content in wildtype and LDLR-/- mice after 2 weeks suggests a phenotypic switch of the medial smooth muscle cells (SMCs), an effect that is reversed after 1 month. While inflammation in the intima diminishes, medial CD45 content rises through time in both genotypes. CD105 staining shows that even manipulation without clamping results in endothelial cell loss in both LDLR+/+ and LDLR-/- mice.


CONCLUSIONS
Arterial clamping induces different acute and long-term injury to the vessel wall of atherosclerotic and healthy arteries.
Department of Cardiovascular Sciences, KU Leuven, Research Unit Experimental Cardiac Surgery, Herestraat 49 -Box 7003, 3000 Leuven, Belgium.
Rachel
R
Geenens
Department of Mechanical Engineering, KU Leuven, Celestijnenlaan 300 -Box 2419, BE-3001 Heverlee, Belgium.
Nele
N
Famaey
Department of Mechanical Engineering, KU Leuven, Celestijnenlaan 300 -Box 2419, BE-3001 Heverlee, Belgium.
Andy
A
Gijbels
Department of Cardiovascular Sciences, KU Leuven, Research Unit Experimental Cardiac Surgery, Herestraat 49 -Box 7003, 3000 Leuven, Belgium.
Silke
S
Verhelle
Department of Oncology-Vesalius Research Centre, KU Leuven-VIB, Herestraat 49 -Box 912, 3000 Leuven, Belgium.
Stefan
S
Vinckier
Department of Mechanical Engineering, KU Leuven, Celestijnenlaan 300 -Box 2419, BE-3001 Heverlee, Belgium.
Jos
J
Vander Sloten
Department of Cardiovascular Sciences, KU Leuven, Research Unit Experimental Cardiac Surgery, Herestraat 49 -Box 7003, 3000 Leuven, Belgium.
Paul
P
Herijgers
D000818:Animals; D001158:Arteries / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology* / Q000473:pathology; D003250:Constriction; D003251:Constriction, Pathologic / Q000150:complications* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D053495:Osteopontin / Q000378:metabolism; D065287:Robotic Surgical Procedures; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology; D014664:Vasodilation / Q000502:physiology*
C506896:Spp1 protein, mouse; D053495:Osteopontin