Endothelial regeneration. VI. Chronic nondenuding injury in baboon vascular grafts.

The cellular lining of 4-mm polytetrafluoroethylene (PTFE) arterial bypass grafts of differing porosity implanted into baboons for a period of 3 months was investigated. Endothelial outgrowth onto the less porous (30-mu) PTFE grafts varied from approximately 1 to 3 cm, and 75% of the grafts were totally reendothelialized within 3 months. These luminal cells stained positive for Factor VIII.R.Ag. The endothelial replication in the healed grafts was significantly elevated as compared with that observed in adjacent arteries. By electron microscopy, no breaks were detected in the integrity of the endothelium and no increase in indium activity over the graft was recorded after injection of 111In-labeled platelets. To ensure that the increased cell replication was not related to regrowth, a more porous PTFE graft (60 mu) was implanted which reendothelialized within 2 weeks. Three months after implantation, the replication rate of endothelium in the graft was still significantly increased. The authors concluded that this increased replication represented a desquamating nondenuding injury and that flow characteristics along the graft might be responsible.     

Mechanisms of arterial graft healing. Rapid transmural capillary ingrowth provides a source of intimal endothelium and smooth muscle in porous PTFE prostheses.

Endothelial coverage of an exposed synthetic vascular graft surface limits thrombosis and may improve long-term graft performance. In most types of synthetic graft, luminal endothelium is derived from the cut edges of adjacent artery. In this study the authors investigated the possibility that endothelial coverage could also be obtained by ingrowth of capillaries from the outside of the graft. Porous 4-mm polytetrafluorethylene (PTFE; 60 mu internodal distance) grafts were inserted into the aortoiliac circulation of baboons and were retrieved at intervals of up to 12 weeks. Between 1 and 2 weeks after surgery a continuous sheet of cells began to appear on the surface along the entire graft. These cells stained for Factor VIII related antigen, exhibited endothelial morphology by scanning electron microscopy, were associated with capillary orifices at the luminal surface, and covered the entire graft by 4 weeks. Transmural capillaries were observed to connect the graft lumen to extravascular granulation tissue. Despite full coverage of the graft, endothelial cells continued to exhibit increased proliferation (thymidine labeling) at 12 weeks. Smooth muscle cells (pericytes) accompanied capillary endothelium into the graft lumen, exhibited vascular smooth-muscle-specific immunostaining, and proliferated under the luminal endothelium to form intima. These results indicate that under some circumstances capillary endothelium and smooth muscle cells can function in the same manner as large vessel endothelium and smooth muscle and can provide rapid coverage of porous synthetic graft surfaces in contact with the arterial circulation.     

Electron-microscopic detection of apoptotic and necrotic cell death in non-atherosclerotic areas of stenotic aortocoronary saphenous vein bypass grafts

Aortocoronary saphenous vein bypass grafts undergo structural alterations within the arterialized vein, resulting in graft stenosis and failure. Areas of the acellular intima contribute to fissuring, cracking and ulceration, while areas of the media become highly vascular but thinned. This study aimed to examine the ultrastructural features of cell death, including apoptosis and necrosis, in non-atherosclerotic areas of the stenotic aortocoronary saphenous vein bypass grafts. Thirteen stenotic vein grafts were obtained at redo coronary artery bypass grafting. The ultrastructural features of cell death were analysed by electron microscopy. Typical features of necrosis, including focal areas of cytoplasmic oedema, plasmalemmal destruction and nuclear condensation with cytoplasmic organelle destruction, were observed throughout the intima and media. Features of apoptosis, including the presence of apoptotic bodies, were also identified in the hyperplastic intima and its adjacent media. Our observations suggest that both apoptosis and necrosis occur in non-atherosclerotic areas of stenotic aortocoronary saphenous vein bypass grafts.     

转染组织纤溶酶原激活物及内皮型一氧化氮合酶基因的内皮细胞和平滑肌细胞共同种植于人工血管对内膜增生的影响

背景：前期研究表明,双层细胞种植能有效提高内皮细胞保留率,将组织纤溶酶原激活物基因转染到内皮细胞中能提高其细胞溶解纤维蛋白的能力。 目的：采用双细胞种植及修饰内皮的组织纤溶酶原激活物基因提高内皮细胞保留率和抗栓能力,通过内皮型一氧化氮合酶基因调控平滑肌细胞的增殖,观察对小口径人工血管通畅率的影响。 方法：以4种不同组合细胞(内皮细胞+平滑肌细胞SMC,内皮细胞/组织纤溶酶原激活物+平滑肌细胞,内皮细胞+平滑肌细胞/内皮型一氧化氮合酶,内皮细胞/组织纤溶酶原激活物+平滑肌细胞/内皮型一氧化氮合酶)种植在PTFE管腔面。将新西兰大白兔随机分成4组,4种人工血管经旁路分别移植在4组兔的腹主动脉上。 结果与结论：移植后60 d,种植内皮细胞+平滑肌细胞组和内皮细胞+平滑肌细胞/内皮型一氧化氮合酶组内膜厚度无明显差异(P > 0.05)。与内皮细胞/组织纤溶酶原激活物+平滑肌细胞/内皮型一氧化氮合酶组相比,未转染内皮型一氧化氮合酶组(内皮细胞/组织纤溶酶原激活物+平滑肌细胞）内膜明显增厚(P < 0.05);未转染组织纤溶酶原激活物组(内皮细胞+平滑肌细胞/内皮型一氧化氮合酶)内膜较薄(P < 0.05)。提示组织纤溶酶原激活物基因转染可以促进血管内膜增生导致血管狭窄,但同时转入内皮型一氧化氮合酶基因可以抑制组织纤溶酶原激活物的促进平滑肌细胞增殖及内膜增生的作用。     

Intimal hyperplasia and hemodynamic factors in arterial bypass and arteriovenous grafts: a review

Stenosis at the graft–vein junction caused by intimal hyperplasia (IH) is the major cause of failure of vascular access grafts used for hemodialysis. There is a strong relationship between hemodynamic factors and formation of IH. The hemodynamic pattern and the location of IH are different in arterial bypass grafts (ABGs) compared with arteriovenous grafts (AVGs). In an ABG, end-to-side anastomosis of the expanded polytetrafluoroethylene graft and artery produces hemodynamic changes around the junction. IH develops at the arterial floor and the toe and heel of the distal anastomosis. Low shear stress and oscillating shear forces at the arterial floor and the heel plus a high wall sheer stress (WSS) gradient at the toe probably promote IH development. Compliance mismatch between the graft and artery causes turbulence that may contribute to IH formation. The blood flow rate in AVGs is 5–10 times greater than that in ABGs. High flow causes turbulence that injures endothelial cells and eventually results in IH. The peak WSS in AVGs is about 6N/m², much higher than that in ABGs. Excessively high WSS may effect IH formation in AVGs. Several venous cuff or patch anastomotic designs have been used in attempts to regulate hemodynamic factors in grafts. In ABGs, these designs appear to help decrease IH formation. In AVGs, however, they generally have not improved patency rates. In a high-flow system such as an AVG, more drastic changes in anastomotic design may be required.     

Evaluation of electrostatically endothelial cell seeded expanded polytetrafluoroethylene grafts in a canine femoral artery model

(1) PURPOSE: The purpose of this study was to evaluate the extent (luminal coverage) of the endothelial cell (EC) lining/neointimal development and the thromboresistance of electrostatically EC seeded small diameter e-PTFE vascular grafts. (2) METHODS: This evaluation consisted of harvesting autologous, canine jugular vein ECs, electrostatically EC seeding the e-PTFE grafts (4 mm GORE-TEX, Length = 6 cm), implanting the grafts in a canine femoral artery model for six weeks, and excising the graft for histological and scanning electron microscopy evaluations. (3) RESULTS: The results of the histological evaluation (mid-graft region only) indicated that the electrostatic EC seeding significantly affected neointimal development (p < 0.01) and the degree of thrombus formation (p < 0.001) within the EC seeded grafts versus the untreated control grafts. Scanning electron microscopy examination demonstrated a mature, confluent endothelium with a "cobblestone" appearance on the EC seeded graft luminal surface. The control grafts demonstrated an equal distribution of SMCs through the graft wall while the electrostatically EC seeded graft sections exhibited an uneven SMC cellular distribution which was skewed toward the graft luminal surface. (4) CONCLUSIONS: The presence of electrostatic EC seeding significantly (p < 0.01) enhanced the development of a neointima and reduced the incidence of thrombosis in e-PTFE grafts implanted in a canine femoral artery model. Results of the mid-graft SMC migration measurements indicate that the electrostatic EC seeding had a significant (p < 0.001) impact on the acute healing of the standard wall e-PTFE vascular graft specimens.     

Analysis of chronic rejection and obliterative arteriopathy. Possible contributions of donor antigen-presenting cells and lymphatic disruption.

Sequential analysis of changes that lead to chronic rejection was undertaken in an animal model of chronic rejection and obliterative arteriopathy. Brown Norway rats are pretreated with a Lewis bone marrow infusion or a Lewis orthotopic liver allograft and a short course of immunosuppression. They are challenged 100 days later with a Lewis heterotopic heart graft without immunosuppression. The heart grafts in both groups undergo a transient acute rejection, but all rats are operationally tolerant; the heart grafts are accepted and remain beating for more than 100 days. Early arterial remodeling, marked by arterial bromodeoxyuridine incorporation, occurred in both groups between 5 and 30 days during the transient acute rejection. It coincided with the presence of interstitial (but not arterial intimal) inflammation and lymphatic disruption and resulted in mild intimal thickening. Significant arterial narrowing occurred only in the bone-marrow-pretreated rats between 60 and 100 days. It was associated with T lymphocyte and macrophage inflammation of the heart graft that accumulated in the endocardium and arterial intima and adventitia near draining lymphatics. There also was loss of passenger leukocytes from the heart graft, up-regulation of cytokine mRNA and major histocompatibility class II on the endothelium, and focal disruption of lymphatics. In contrast, long-surviving heart grafts from the Lewis orthotopic liver allograft pretreated group are near normal and freedom from chronic rejection in this group was associated with persistence of donor major histocompatibility class-II-positive hematolymphoid cells, including OX62+ donor dendritic cells. This study offers insights into two different aspects of chronic rejection: 1) possible mechanisms underlying the persistent immunological injury and 2) the association between immunological injury and the development of obliterative arteriopathy. Based on the findings, it is not unreasonable to raise the testable hypothesis that direct presentation of alloantigen by donor antigen-presenting cells is required for long-term, chronic-rejection-free allograft acceptance. In addition, chronic intermittent lymphatic disruption is implicated as a possible mechanism for the association between chronic interstitial allograft inflammation and the development of obliterative arteriopathy.     

原位静脉动脉化与静脉动脉间置后静脉的实验形态学研究

目的：探讨原位静脉动脉化与静脉动脉间置后，静脉的组织学和超微结构变化。在１８只犬后肢设计原位大隐静脉动脉化，静脉动脉间置实验模型，对原位大隐静脉动脉化和静脉动脉间置后不同时间（２、４、８、１６ｗ）静脉管壁的变化，进行了实验形态学观察。结果：①原位静脉动脉化后早期内皮细胞损伤较轻微，中、晚期主要表现为管腔内皮细胞损伤较轻微，管腔的扩张和中膜平滑肌的增生，肥厚；②静脉动脉间置早期内皮细胞有广泛脱落，中膜平滑肌细胞肿胀，细胞间积液，中晚期变化主要为内皮不规则增生，肥厚，中膜平滑肌不同程度的增生与纤维化，使血管腔呈现不同程度的狭窄。结论：原位静脉动脉化后静脉呈现结构上的“动脉化”倾向，并且较静脉动脉间置更有利于保持血管的通畅。     

The aortic intima. II. Repair of the aortic lining after mechanical denudation.

This article reports the ultrastructure of the aortic lining during the repair of mechanically denuded aortic intima in the rat. Three main features were observed: a) Although platelets form a pavement on the exposed components of the aortic intima, platelet thrombi do not form on the denuded surface. b) During the first weeks after injury, a temporary false endothelial lining is formed by modified intimal smooth muscle cells. While the modified smooth muscle cells do not constitute a continuous cell layer, they are like true endothelial cells in that platelets do not adhere to the cell membrane of either cell type. c) A continuous layer of true endothelial cells is formed within 2 months after the original injury. Even after reestablishment of a continuous endothelium, however, abnormalities persist in the form of incompletely formed intercellular junctions. This abnormal endothelium is associated with areas of intimal smooth muscle cell proliferation. These observations are compatible with two alternative interpretations of the role of endothelial injury in the intimal proliferation seen following injury to the vessel wall: a) persistent defects in the endothelium may result in proliferation of underlying arterial smooth muscle cells or b) the proliferation, in converse, may in some manner delay the healing process of the overlying endothelium.     

Restitution of aortic wall after sustained necrotizing transmural ligation injury. Role of blood cells and artery cells.

Partial ligation of the rabbit abdominal aorta with fine silk suture for 48 hours produced a circular band of transmural necrosis. On release of the ligature, blood cells from the lumen and from adventitial vasa vasorum, as well as cells derived by mitosis from the adjacent surviving endothelium and media, participated in the restitution of a continuous endothelial lining and an intact media containing well-differentiated smooth muscle cells within normal medial lamellar units. Initial deposition of a layer of blood platelets on the fibrillar material coating the denuded lumenal surface was followed by ingress from the lumen of polymorphonuclear granulocytes and mononuclear cells. These changes preceded the appearance of mitoses in surviving endothelial and medial smooth muscle cells at the margin of injury. By 24 hours, poorly differentiated cells had accumulated in the central portion of the intima and inner media. Similar cells formed a more extensive, nearly complete lumenal layer which was eventually continuous with and indistinguishable from the adjacent uninjured endothelium. By 7 days, smooth muscle cells repopulated the media, and a collection of less differentiated cells persisted between the restored endothelium and media. By 28 days, the only deviation from normal arterial structure was the persistence at the point of ligature of intimal thickening, consisting of smooth muscle cells and collagen and elastin fibers. Though still present at 6 weeks, this zone became increasingly compact and layered. There was no evidence that fibrin thrombus formation was a consistent feature of the initial reaction or that it played a role in the healing process or in the formation of the intimal lesion. Despite complete circumferential necrosis at the site of ligature, there was no evidence of medial rupture or intramural hemorrhage.     

Endothelial regeneration. VIII. Interaction of smooth muscle cells with endothelial regrowth

This study examined the ability of arterial endothelial cells to repopulate arterial grafts which were devoid of luminal smooth muscle cells and in arterial grafts which had an established pseudoendothelium comprised of smooth muscle cells. These studies were designed to explore the hypothesis that smooth muscle cells when forming a pseudoendothelium can retard endothelial cell regrowth. Segments of denuded glutaraldehyde-fixed carotid arteries and of viable autologous carotid arteries with a pseudoendothelium of smooth muscle cells were implanted end to end into the rabbit carotid arteries and left for 6 or 12 weeks. Endothelial outgrowth onto these arterial grafts was extremely limited (approximately 3 mm) regardless of the preparation and was equal to that observed in a carotid artery denuded of endothelium with a balloon catheter. Endothelial cell replication was significantly elevated in these implanted carotid segments at all times studied with the majority of the replicating cells not located at the leading edge of endothelium. The location of these cells suggests this replication was not associated with regrowth. Finally, the ability of denuded arteries to support endothelial cell adherence was tested in vitro by plating [3H]thymidine bovine endothelial cells on segments of excised arteries which had been denuded of endothelium for 2 and 12 weeks. No difference in plating efficiency was observed. These studies suggest that the presence of smooth muscle cells on the luminal surface of denuded arteries was not responsible for the cessation of endothelial regrowth.     

Experimental evaluation of a gelatin-coated polyester graft used as an arterial substitute

Protein coating and endothelial cell preseeding have been proposed and studied as improvements to arterial prostheses. In this paper, an impervious polyester vascular graft which had been coated with cross-linked gelatin was compared to a porous one over a period of up to 8 months in dogs. This evaluation involved in vivo methods using radio tracers to study patency and thrombogenicity and in vitro controls of the healing processes. The main advantages offered by coated grafts over uncoated include the absence of preclotting and better biointegration.     

Histologic findings after in vivo placement of small intestine submucosal vascular grafts and saphenous vein grafts in the carotid artery in dogs.

A small caliber vascular graft from porcine small intestine submucosa (SIS) was implanted in a canine carotid artery (n = 24) and compared with an autogenous saphenous vein graft that was implanted in the contralateral carotid artery. In this study, four grafts were evaluated at the following times after surgery: 2, 7, 14, 28, 90, and 180 days. One SIS graft thrombosed at 2 days, two SIS and two saphenous vein grafts were thrombosed at 90 days, and one SIS and one saphenous vein graft were thrombosed at 180 days. At 2 days after implant, the luminal surface of the SIS graft was covered by a thin (30 mu) fibrin meshwork. By 14 days after surgery, endothelial cells on the fibrin meshwork were staining for FVIII-related antigen. Smooth muscle cells were observed in the new intima (fibrin meshwork) by 28 days. At 90 days, both types of graft had arterialized with an intima covered by endothelium, a smooth muscle media, and marked adventitial fibrosis. Similar histology was observed at 180 days. These results indicate that this SIS graft was similar to saphenous vein graft in the dog.     

A system for the direct co-culture of endothelium on smooth muscle cells

The development of a functional, adherent endothelium is one of the major factors limiting the successful development of tissue engineered vascular grafts (TEVGs). The adhesion and function of endothelial cells (ECs) on smooth muscle cells (SMCs) are poorly understood. The goal of this research was to optimize conditions for the direct culture of endothelium on SMCs, and to develop an initial assessment of co-culture on EC function. The co-culture consisted of a culture substrate, a basal adhesion protein, a layer of porcine SMCs, a medial adhesion protein, and a layer of porcine ECs. Conditions that led to successful co-culture were: a polystyrene culture substrate, a quiescent state for SMCs, subconfluent density for SMC seeding and confluent density for EC seeding, and fibronectin (FN) for the basal adhesion protein. EC adhesion was not enhanced by addition of FN, collagen I, collagen IV or laminin (LN) to the medial layer. 3-D image reconstruction by confocal microscopy indicated that SMCs did not migrate over ECs and the cells were present in two distinct layers. Co-cultures could be consistently maintained for as long as 10 days. After exposure to 5 dyne/cm(2) for 7.5 h, ECs remained adherent to SMCs. PECAM staining indicated junction formation between ECs, but at a lower level than that observed with EC monocultures. Co-culturing ECs with SMCs did not change the growth rate of ECs, but EC DiI-Ac-LDL uptake was increased. Thus, a confluent and adherent layer of endothelium can be directly cultured on quiescent SMCs.     

A histological, ultrastructural and immunohistochemical study of superficial temporal arteries and middle meningeal arteries in moyamoya disease.

Pathologic changes in superficial temporal arteries (STA) and middle meningeal arteries (MMA) biopsied from 15 patients with moyamoya disease (MD) who had undergone cerebro-temporal arterio-synangiosis were studied histologically, ultrastructurally and immunohistochemically. The main pathologic features were: proliferation of smooth muscle cells (SMCs) and thickening of the intima, degeneration and destruction of SMCs in the media and intima, and the presence of condensed organelles in necrosed SMCs or the interstitium among SMCs, or both outside and within the elastica interna (EI). The EI had become thin, porous, fragmented and was even absent in some segments. These changes are different from those of other forms of angiopathy, but identical with those at the ends of internal carotid arteries (ICA) reported by us previously, being pathognomonic for MD. These changes in the STA and MMA reveal that MD involves not only the ICA but also the intra- and extracranial branches of external carotid arteries. The medial necrosis of SMCs seems to be the primary injury of the arterial wall in MD. STA tissue blocks from two cases of MD were stained immunohistochemically. By electron microscopy, IgG-, IgM-, and C3-positive granules were observed on the ER of endothelial and intimal cells. Further studies on more cases are needed to determine whether an immunoreaction has occurred in these arteries.     

Immunocytochemical investigation of atherosclerotic changes observed in aortocoronary bypass vein grafts using monoclonal antibodies

The authors have performed immunocytochemical surveys on atherosclerotic changes observed in saphenous vein aortocoronary bypass grafts, comparing the changes occurring in coronary and aortic lesions. The two monoclonal antibodies used in this study were obtained by T. Tsukada. One of them, named HHF35, exhibited specificity to smooth muscle cells; the other, named HAM56, was specific to macrophages. These immunocytochemical studies clearly demonstrated that cells encountered within the fibrous intimal thickening in the vein graft were inevitably smooth muscle cell in origin. Macrophages were seldom seen in the grafts examined. In contrast to vein grafts, macrophages were noted within the intima of all specimens from arterial atherosclerotic lesions obtained from the same patients. These studies suggest a difference in the progression of intimal thickening between the venous graft and the arterial atherosclerotic lesions.     

Changes in the Organization of the Smooth Muscle Cells in Rat Vein Grafts

Mechanical tensile stress in vein grafts increases suddenly under the influence of arterial blood pressure. In this study, we examined the influence of increased tensile stress on the organization of the smooth muscle cells (SMCs) in the neointima and media of the rat vein grafts. An autogenous jugular vein was grafted into the abdominal aorta of the rat, and changes in the organization of the vein graft SMCs were studied by observing the distribution of SMC actin filaments and nuclei at 3 min and 1, 5, 10, and 30 days after surgery. In a normal jugular vein, the average wall circumferential tensile stress was ~ 3 kPa at an internal pressure of 3 mm Hg. The SMCs, that contained long, slender actin filamentous bundles, were oriented mainly in the circumferential direction of the vessel, and constituted a 2- to 3-cell-thick medial layer underneath the endothelium. In a vein graft, the wall circumferential tensile stress suddenly increased by ~ 140 times compared with the control level. In response to this suddenly increased stress, the SMC layer was stretched into a structure with scattered pores and disrupted SMC actin filamentous bundles within 3 min. This initial change was followed by a rapid reduction in the density of the SMC nuclei and actin filaments within 1 day and progressive SMC proliferation, that was associated with medial thickening and a change in the SMC orientation from 5 to 30 days. Further studies showed that a local inflation of normal jugular veins to 120 mm Hg for 3 min induced a similar change as found in the vein grafts, whereas the organization of the SMCs was not significantly changed in vein-vein grafts, that did not experience a change in tensile stress. These results suggested that increased tensile stress contributed to the initial damage of the SMCs and played a role in the regulation of medial SMC remodeling in vein grafts. © 1998 Biomedical Engineering Society. PAC98: 8722-q, 8745-k     

Experimental Aortic Intimal Thickening: II. Endothelialization and Permeability

Experimental aortic intimal thickening has been induced in rabbits by two types of injury, suture placement and electrocautery. Scanning electron microscopy showed that endothelialization of the suture plaque was completed at about 10 days following injury. New endothelial cells had no particular orientation or were oriented at right angles to the adjacent normal aortic endothelium. Realignment parallel with the aortic axis had occurred by 21 days after induction of the lesion. Orientation patterns of new endothelial cells over irregularly shaped cautery-induced intimal thickening were difficult to ascertain. Aortic permeability studies were accomplished by using the tracers horseradish peroxidase (HRP) and ferritin. Several naturally occurring intimal thickenings in normal aortas had greater permeability for HRP than did adjacent normal intima. An enhanced penetration of both tracers was observed in mature intimal lesions produced by both experimental procedures compared to adjacent morphologically normal aortic intima. HRP molecules entered the thickened aortic intima in increased amounts through interendothelial junctions and by endothelial pinocytotic vesicles; ferritin molecules were seen only in pinocytotic vesicles. Increased penetration of HRP was observed for as long as 27 weeks after injury, while that of ferritin was observed only for 3 weeks. The enhanced permeability of the thickened intima as compared to normal for these two tracers of considerably different sizes strongly suggests an increased permeability of endothelium overlying intimal thickening for naturally circulating macromolecules.     

Tissue engineering of recellularized small-diameter vascular grafts

A tissue-engineered small-diameter arterial graft would be of benefit to patients requiring vascular reconstructive procedures. Our objective was to produce a tissue-engineered vascular graft with a high patency rate that could withstand arterial pressures. Rat arteries were acellularized with a series of detergent solutions, recellularized by incubation with a primary culture of endothelial cells, and implanted as interposition grafts in the common femoral artery. Acellular grafts that had not been recellularized were implanted in a separate group of control animals. No systemic anticoagulants were administered. Grafts were explanted at 4 weeks for definitive patency evaluation and histologic examination; 89% of the recellularized grafts and 29% of the control grafts remained patent. Elastin staining demonstrated the preservation of elastic fibers within the media of the acellular grafts before implantation. Immunohistochemical staining of explanted grafts demonstrated a complete layer of endothelial cells on the lumenal surface in grafts that remained patent. Smooth muscle cells were observed to have repopulated the vessel walls. The mechanical properties of the matrix were comparable to native vessels. Such a strategy may present an alternative to autologous harvest of small vessels for use in vascular bypass procedures.     

Vascular graft healing: I. FTIR analysis of an implant model for studying the healing of a vascular graft.

FTIR analysis of sequential biopsy samples of the primary and replacement segments obtained from 70 to 80-cm long carotid-femoral bypass grafts implanted bilaterally in the dog indicate that the healing pattern is similar over the entire length of these grafts. Preliminary analysis of the spectra also indicates that the major developments in the formation of the biological layer appear to occur during the first 4 weeks after implantation. Collagen IV could be detected by both FTIR and antibody staining in the 8-week samples. Thus, this study supports the application of FTIR attenuated total reflectance to determine the components of the biological tissue that forms on an implanted vascular graft surface.