| Literature DB >> 1499739 |
M Watase1, J Kambayashi, T Itoh, Y Tsuji, T Kawasaki, E Shiba, M Sakon, T Mori, K Yashika, P H Hashimoto.
Abstract
To evaluate and compare the pathogenesis of pseudo-intimal hyperplasia (PH) of venous and arterial prostheses, a segment of the inferior vena cava (n = 16) or abdominal aorta (n = 16) was substituted by a 3 mm internal diameter polytetrafluoroethylene tube graft (PTFE, 3 cm long, 30 microns in nodal distance) in albino rabbits. At designated time intervals (3-28 days) after the replacement, graft patency was examined and the dry weights of the intraluminal deposits measured as an indicator of the degree of PH. The harvested grafts were then subjected to an ultrastructural analysis by means of light microscopy (LM), and scanning electron and transmission electron microscopy (SEM, TEM). All the grafts remained patent during the entire observation period. The PH judged by the dry weight was significantly more extensive in the venous than in the arterial prostheses. The PH on day 28, observed by light microscopes was apparently most extensive in the mid-portion of venous prostheses but in the arteria prostheses it was mostly seen at the anastomotic sites. The lining of the intraluminal surface of the prostheses with endothelial-like cells observed by SEM was faster and more extensive in venous than in arterial prostheses. The process of PH in venous prostheses observed by TEM may be divided into the following steps: early thrombosis, phagocytosis of the thrombus, appearance of fibroblasts, growth of endothelial-like cells, appearance of smooth muscle cells, and pseudointimal thickening and proliferation of fibroblasts producing collagen fibrils. The process in arterial prostheses was essentially identical to that in venous prostheses but was much slower and less extensive. From these observations, it was concluded that the formation of PH occurs much faster in venous than in arterial prostheses, although the mechanism of PH is mostly identical in venous and arterial prostheses.Entities:
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Year: 1992 PMID: 1499739 DOI: 10.1016/s0950-821x(05)80282-8
Source DB: PubMed Journal: Eur J Vasc Surg ISSN: 0950-821X