Weibin Du1, Lihong He2, Lixiang Wang2, Huahui Hu2, Huateng Zhou2, Guanai Bao3, Rongliang Chen2, Fuxiang Shen2, Renfu Quan4. 1. Research Institute of Orthopedics, the Affiliated Jiangnan Hospital of Zhejiang Chinese Medical University, Hangzhou, China. dwbbdm@163.com. 2. Research Institute of Orthopedics, the Affiliated Jiangnan Hospital of Zhejiang Chinese Medical University, Hangzhou, China. 3. Department of Rehabilitation, Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Hangzhou, China; Institute of Cancer and Basic Medicine (IBMC), Chinese Academy of Sciences, Hangzhou, China. 4. Research Institute of Orthopedics, the Affiliated Jiangnan Hospital of Zhejiang Chinese Medical University, Hangzhou, China. quanrenfu@126.com.
Abstract
BACKGROUND: The sustained negative pressure created by vacuum sealing drainage (VSD) on exposed vascular wounds can result in blood vessel compression, embolism, or necrosis. The objective of this research was to explore the ability of an experimental vascular protective shield combined with VSD to protect exposed vessels of the lower limbs and accelerate wound repair. METHODS: (I) The vascular protective shield was prepared; (II) the material was subjected to acute toxicity and hemolysis tests; (III) and 30 New Zealand rabbits were divided into three groups: the control, VSD-only, and combined shield-VSD groups (with ten rabbits in each group). The wound-healing rate, myocardial function, wound histopathology, expression of angiogenesis markers, and exposed vascular compression of these three groups were compared on day 7. RESULTS: (I) The internal structure of the material was smooth; and (II) no toxicity or death was observed in mice of any group. The hemolysis rate in the combined shield-VSD group was very low. (III) The combined shield-VSD group showed a higher wound-healing rate, and higher levels of cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF), than the other groups (P<0.05), along with a better tissue healing rate. (IV) Left ventricular pressure fluctuations in the combined shield-VSD group were smaller than those in the VSD-only group (P<0.05). (V) Blood vessels in the control and combined shield-VSD group were not damaged, but were damaged in the VSD-only group. CONCLUSIONS: The experimental vascular protective shield exhibited exceptional biosafety. The combination of this shield with VSD reduces influences on systolic and diastolic capacities of myocardium and avoids multiple compressions of exposed vessels, thus contributing to early vascularization of wounds and wound repair.
BACKGROUND: The sustained negative pressure created by vacuum sealing drainage (VSD) on exposed vascular wounds can result in blood vessel compression, embolism, or necrosis. The objective of this research was to explore the ability of an experimental vascular protective shield combined with VSD to protect exposed vessels of the lower limbs and accelerate wound repair. METHODS: (I) The vascular protective shield was prepared; (II) the material was subjected to acute toxicity and hemolysis tests; (III) and 30 New Zealand rabbits were divided into three groups: the control, VSD-only, and combined shield-VSD groups (with ten rabbits in each group). The wound-healing rate, myocardial function, wound histopathology, expression of angiogenesis markers, and exposed vascular compression of these three groups were compared on day 7. RESULTS: (I) The internal structure of the material was smooth; and (II) no toxicity or death was observed in mice of any group. The hemolysis rate in the combined shield-VSD group was very low. (III) The combined shield-VSD group showed a higher wound-healing rate, and higher levels of cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF), than the other groups (P<0.05), along with a better tissue healing rate. (IV) Left ventricular pressure fluctuations in the combined shield-VSD group were smaller than those in the VSD-only group (P<0.05). (V) Blood vessels in the control and combined shield-VSD group were not damaged, but were damaged in the VSD-only group. CONCLUSIONS: The experimental vascular protective shield exhibited exceptional biosafety. The combination of this shield with VSD reduces influences on systolic and diastolic capacities of myocardium and avoids multiple compressions of exposed vessels, thus contributing to early vascularization of wounds and wound repair.