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PubMed2005

Pathologic characteristics and surgical indications of superacute type A intramural hematoma.

BACKGROUND: The treatment policy for acute intramural hematoma involving the ascending aorta remains controversial. METHODS: This study compared the pathologic characteristics of intramural hematoma with those of acute aortic dissection with a false lumen. The study group comprised 69 patients with intramural hematoma and 156 with acute aortic dissection who underwent emergency operation between 1995 and 2003. RESULTS: Patients were significantly older in the intramural hematoma group than in the dissection group (67.7 +/- 7.2 years compared with 59.8 +/- 11.6 years; p < 0.0001). Pericardial hemorrhage was present in a higher proportion of patients in the intramural hematoma group than in the dissection group (66.7% compared with 50.6%; p = 0.0257). Three patients (4.3%) died in the intramural hematoma group, whereas 26 patients (16.7%) died in the dissection group (p = 0.011). Histopathologic examination showed no difference in the severity of medial changes, but the site of dissection differed. The thickness of the residual media of the adventitia side was 0.21 +/- 0.12 mm in the intramural hematoma group compared with 0.32 +/- 0.22 mm in the acute aortic dissection group. Dissection was significantly nearer the adventitia in the intramural hematoma group (p = 0.0016). CONCLUSIONS: Dissection is nearer the adventitia in intramural hematoma than in dissection, leading to a greater probability of rupture. These results suggest that operation as soon as possible after the onset of intramural hematoma will contribute to improved survival.

Acute Disease↗
PubMed2007

Surgical management of lung cancer invading the aorta or the superior vena cava.

OBJECTIVE: Invasion of mediastinal structures (T4) is considered as an absolute contraindication to surgical management of non-small cell lung cancer (NSCLC). The authors studied the role of surgical treatment in case of direct aortic and superior venous caval involvement. PATIENTS: From 1995 to 2000, 13 patients with left lung NSCLC invading descending aorta and 9 patients with right upper lobe NSCLC and superior vena cava (SVC) invasion were subjected to thoracotomy for lung resection. Surgery was indicated in case of absence of intraluminal extension. All patients were cN2 negative. The pathology results and 5-year survival were recorded and analyzed. RESULTS: In three cases (23%) the tumor was adhered to the parietal pleura overlying descending aorta, which was resected en block with tumor-associated lung parenchyma. Aortic adventitia invasion by tumor led to local resection of adventitia (<1cm(2)) in nine patients (69%). Invasion deeper than adventitia was encountered in one case (8%), which was managed with aortic partial occlusion, resection of aortic wall and repair of the defect with Gore graft patch. In three patients (33%) the SVC wall was involved by the tumor 1-3cm in length and 2-4mm of the circumference. The defect was repaired with direct suturing. In five patients (56%) the area of SVC wall that was invaded was 3cmx2cm. The defect was repaired with Dacron patch. In 1 patient (11%) an arterial 14 graft was end-to-end interposed. All resections were radical (R0). Neither associated postoperative complications nor operative mortality was recorded. Five-year survival was 30.7% for the cases with aortic invasion and 11% for the ones with SVC involvement. CONCLUSIONS: Radical surgical resection of lung tumors with localized aortic invasion can be considered after exclusion of N2 involvement.

Aorta↗
PubMed2005

Adventitial dysfunction: an evolutionary model for understanding atherosclerosis.

Endothelial and smooth muscle dysfunctions are widely implicated in the pathogenesis of atherosclerosis. Modern mechanical and pharmacologic treatments aim to remodel abnormalities of the vessel intima and media. We hypothesize that adventitial dysfunction comprises the dominant source of atherosclerosis by originating many endothelial and smooth muscle abnormalities. The autonomic nervous system innervates the adventitia, and autonomic dysfunction induces many end-organ dysfunctions including inflammation and thrombosis. The link between diabetes and atherosclerosis may operate through adventitial autonomic neuropathy. Smoking may promote atherosclerosis by inducing adventitial autonomic dysfunction related to nicotine-mediated compensatory upregulation of sympathetic bias independent of endothelial injury induced by purported tobacco toxins. While hypertension is thought to cause atherosclerosis, the two conditions may instead represent independent consequences of autonomic dysfunction. The link between aging and atherosclerosis may operate through adventitial dysfunction induced by autonomic dysregulations. Exercise may ameliorate atherosclerosis by restoring adventitial autonomic function, thereby normalizing adventitial regulation of medial and intimal biology. Feed-forward adventitial vascular baroreceptor and chemoreceptor dysregulation may further exacerbate atherosclerosis as intimal plaque interferes with these sensors. Since penetrating external physical injury likely represented a dominant selective force during evolution, the adventitia may be preferentially equipped with sensors and response systems for vessel trauma. The convergent response of adrenergia, inflammation, and coagulation, which is adaptive for physical trauma, may be maladaptive today when different stressors trigger the cascade. Endoluminal therapies including atherectomy, angioplasty, and stent deployment involve balloon expansion that traumatizes all layers of the vessel wall. These interventions may paradoxically reinitiate the cascade of atherogenesis that begins with adventitial dysfunction and leads to restenosis. Methods to reduce adventitial trauma, a maladaptive trigger of adventitial dysfunction, may reduce the risk of restenosis. We envision novel mechanical and biopharmaceutical solutions that target the adventitia to prevent or treat atherosclerosis including novel drug delivery strategies, exo-stents that wrap vessels, and neuromodulation of vessels.

Animals↗
PubMed2006

Adventitial inflammation: a possible pathogenic link to the instability of atherosclerotic plaque.

A variety of cells, including fibroblasts, mast cells, macrophages, and ganglionic cells, are present in coronary artery adventitia. In the infarct-related coronary arteries of myocardial infarction patients, the majority of mast cells are found in the outer layer of the adventitia. Neurogenic stimulation of mast cells in the adventitia of coronary arteries may release vasoactive compounds, such as histamine and leukotrienes, which can contribute to the complex neurohormonal response that leads to abnormal coronary vasoconstriction. Lymphocytes and bacteria are also present mainly in the adventitial layer. Chlamydia pneumoniae is directly involved in the development of adventitial and plaque inflammation (pan-arteritis), leading to plaque rupture. Adventitial O(2)(-) may also play an extensive role in the control of vascular tone. Therefore, adventitial inflammation may play a pivotal role for atherosclerotic lesion development and atheroma instability.

Arteritis↗
PubMed2002

Imaging of the left anterior descending coronary artery by high-frequency transthoracic and epicardial echocardiography.

Left anterior descending coronary artery (LAD) wall thickness and external diameter are significantly increased in patients with coronary artery disease compared with normal subjects. High-resolution, 2-dimensional transthoracic echocardiography (HR-2DTTE) can be used to measure LAD wall thickness and is sensitive enough to detect these differences. However, HR-2DTTE measurements of the LAD wall thickness are larger than measurements obtained by intravascular ultrasound and histology. We hypothesize that this difference is due to inclusion of the third vascular layer, which may represent adventitia, by HR-2DTTE, and that this layer must be increasing in thickness with the development of atherosclerosis. We evaluated the contribution of this third layer to the wall thickness of the normal and atherosclerotic LAD imaged by HR-2DTTE using high-frequency epicardial echocardiography (HFEE). Thirteen patients with coronary atherosclerosis and 5 patients with normal coronary arteries underwent preoperative HR-2DTTE and intraoperative HFEE. HR-2DTTE and HFEE measurements of the wall thickness correlated well. The wall thickness was significantly greater in patients with coronary atherosclerosis than in patients with normal coronary arteries by both HR-2DTTE and HFEE. With HFEE, the average intima plus media thickness and the average thickness of adventitia were greater in patients with coronary atherosclerosis than in patients with normal coronary arteries. A third vascular layer, which likely includes adventitia, represents a significant portion of the LAD wall thickness imaged by HR-2DTTE and HFEE, and its thickness increases significantly with the development of atherosclerosis.

Case-Control Studies↗
PubMed1977

Coronary arterial narrowing in Takayasu's aortitis.

A patient with Takayasu's aortitis and angina pectoris due to severe narrowing of the right and left coronary arterial ostia is described. Takayasu's arteritis produces a panaortitis, with thickening of the adventitia predominating, and an inflammatory cell infiltrate involving the adventitia, outer media and vasa vasorum. Narrowing of the coronary arteries in this disease is due to extension into these arteries of the processes of proliferation of the intima and contraction of the fibrotic media and adventitia that occur in the aorta. The distal coronary arteries usually do not manifest arteritis and are normal in caliber. Angina pectoris may be the first symptom of the disease if the coronary arteries are the initial site of severe arterial narrowing. The coronary arterial bypass graft operation is effective therapy for treating coronary arterial narrowing due to Takayasu's arteritis.

Adult↗
PubMed2003

Does skeletonization compromise the integrity of internal thoracic artery grafts?

BACKGROUND: There are few reports that demonstrate the chronologic changes in the functional integrity of the internal thoracic artery (ITA) wall after skeletonization. We investigated the impact of skeletonization on ITA wall integrity by immunohistochemical analyses in acute and chronic phases. METHODS: Nine mongrel dogs underwent bilateral ITA dissection with one skeletonized vessel and the other pedicled. The following studies were performed 1 week (acute phase, n = 3) and 12 weeks (chronic phase, n = 6) after ITA harvesting. All specimens of the ITAs were stained by antibodies against von Willebrand Factor (VWF), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and proliferating cell nuclear antigen (PCNA). After observation with confocal laser scanning microscopy, quantitative analyses of the staining signal for VWF and eNOS expressed on endothelial cells were performed. RESULTS: There were significantly more microvessels positive for VWF in the adventitia of skeletonized ITAs than in the adventitia of pedicled ITAs but the expression of PCNA in both groups was minimal, as in normal vessels. iNOS was not detected in any specimen. The intensity of VWF and eNOS expressed by endothelial cells had no significant differences between groups at either phase. CONCLUSIONS: The functional integrity of skeletonized ITA was similar to that of pedicled ITA in both acute and chronic phases. Although skeletonization induced neovascularization in the adventitia it did not induce proliferation of smooth muscle cells in the media, which is supposed to be a feature of vascular remodeling.

Animals↗
PubMed2001

Vascular-associated lymphoid tissue (VALT) involvement in aortic aneurysm.

Vascular-associated lymphoid tissue (VALT) consisting of accumulations of immunocompetent and antigen presenting cells has recently been recognised in the arterial wall. In this study, we investigated the involvement of VALT in immune responses in abdominal aortic aneurysms (AAAs). Tissue samples were collected during operations from 31 patients with atherosclerotic infrarenal abdominal aortic aneurysms ranging in diameters from 5 to 8 cm. The specimens were immediately frozen and examined using single and double immunohistochemical staining. T-cell subpopulations, B-cells, dendritic cells and macrophages were identified using cell type specific antibodies. Cell contacts were examined by electron microscopy. Most inflammatory infiltrates were found in the adventitia. T-cells were the predominant cell type in a majority of inflammatory infiltrates but in seventeen cases, typical lymphoid follicles with B-cells forming germinative centres were also observed. In eight cases, the lymphoid follicles aggregated in lymph node-like structures. Dendritic cells were present within all inflammatory infiltrates and contacted lymphocytes. The present observations show that in aortic aneurysm, VALT is involved in immune responses and its activation mostly occurs in the adventitia. The formation of lymphoid follicles and lymph node-like structures in the adventitia suggests that VALT might locally serve the entire complex of both cellular and humoral immune responses in the aneurysmal wall.

Aged↗
PubMed1998

Nitric oxide, prostacyclin and cyclic nucleotide formation in externally stented porcine vein grafts.

Non-restrictive, porous, external stents inhibit neointima formation in porcine vein grafts. Since the mechanisms underlying these effects are unknown we investigated the impact of this external stent on factors known to inhibit vascular smooth muscle cell proliferation: prostacyclin (PGI2), nitric oxide (NO), cAMP and cGMP formation in different regions of stented and unstented porcine vein grafts. Paired stented and unstented saphenous vein-carotid artery interposition grafting was carried out in Landrace pigs. One month after surgery, the vessels were excised and the formation of PGI2, cAMP and cGMP determined using radioimmunoassay and nitric oxide synthase (NOS) distribution studied using autoradiography and histochemistry. There were no significant differences between PGI2, cAMP and cGMP (nitroprusside-stimulated) formation in the medial/intimal regions of grafts of stented vein graft and ungrafted saphenous vein whereas all were significantly reduced in unstented vein graft. A23187-stimulated cGMP formation (mediated by NO release) and NOS content was significantly greater in the medial/intimal region of stented and unstented vein graft compared to ungrafted saphenous vein, indicating induction of endothelial NOS (eNOS) in both types of graft. This normalisation of the PGI2-cAMP axis and guanylyl cyclase activity in the medial/intimal region may contribute to the beneficial impact of the external stent on vein graft thickening. The increase in eNOS in both stented and unstented vein grafts mitigates against this isoform as playing a role in mediating the inhibitory effect of the stent on neointima formation. In the adventitia of both stented and unstented grafts there was an increase in PGI2, cAMP and cGMP formation compared to ungrafted saphenous vein, the production being greater in the stented compared to the unstented graft. In the adventitia of stented veini grafts, NOS, detected with NAPDH diaphorase staining, was associated with microvessels as well as with inflammatory cells. Taken together, these data are suggestive of a role for PGI2 and NO in promoting microangiogenesis in the adventitia of stented vein grafts which may in turn minimize graft hypoxia, an established contributory factor to neointima formation.

Animals↗
PubMed1997

Pulmonary artery structural changes in pulmonary hypertension complicating congenital diaphragmatic hernia.

Primary pulmonary hypertension is characterized by the presence of smooth muscle cells in nonmuscular compartments or segments of the vessel and the abnormal deposition of collagen in both the small muscular arteries and arterioles and the large elastic arteries. Victorian blue van Gieson staining and Immunostaining with anti-alpha smooth muscle actin (ASMA) were performed on lung tissues obtained during autopsy from 21 patients who had congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) and 10 control patients who died of sudden infant death syndrome (SIDS). The degree of medial thickening and adventitial thickening was measured in pulmonary arteries by image analysis and compared statistically. There was a significant increase in adventitial as well as medial thickness in arteries of all sizes in CDH patients compared with control patients (P < .001). The most striking increase occurred in arteries with an external diameter (ED) of less than 75 microns. Calculation of the areas of the various components in the wall of each vessel showed that for smaller vessels (< 75 microns ED), the area of the lumen was smaller and the area of the media and adventitia was larger in CDH patients compared with control patients (P < < .001). In vessels greater than 75 microns ED, the areas of media in CDH was the same as in controls and the area of adventitia in CDH was significantly larger than controls (P < .001). The present study provides evidence that an increase in adventitial thickness and adventitial area occurs in pulmonary arteries in CDH patients complicated by PPH. The structural changes in the adventitia of the pulmonary arteries may be an important factor in the development of PPH in patients with CDH.

Actins↗
PubMed1995

Comparison of endothelial function between in situ and reversed vein graft: differences in endothelium-dependent responses.

BACKGROUND: The endothelium releases endothelium-derived relaxing factors that are potent vasodilators and inhibitors of platelet aggregation. Experiments were performed to determine whether the endothelium-dependent responses differed between in situ and reversed vein grafts. The influence of valve disruption or of dissection of the adventitia was also examined. METHODS: Segments of canine jugular veins were grafted into the carotid arteries during procedures such as reversed grafting, in situ grafting with valve disruption, in situ grafting without valve disruption, and in situ grafting with dissection of adventitia. After 4 weeks the endothelium-dependent responses of the grafts were examined by isometric tension recording. RESULTS: In the reversed and in situ vein graft with valve disruption, acetylcholine caused endothelium-independent contractions, whereas in the in situ vein graft without valve disruption acetylcholine-induced endothelium-dependent relaxations were preserved. Adenosine diphosphate (ADP) caused comparable endothelium-dependent relaxations in the in situ vein graft irrespective of valve disruption. In the reversed vein graft ADP-induced relaxations were significantly impaired. In the in situ vein graft with dissection of the adventitia, relaxations in response to acetylcholine and ADP were significantly reduced. CONCLUSIONS: These results suggest that endothelial function, in terms of endothelium-derived relaxing factors in the in situ vein graft, can be preserved and that adventitial dissection in the in situ vein graft should be minimized to preserve endothelial function.

Acetylcholine↗
PubMed2000

Three-dimensional automatic quantitative analysis of intravascular ultrasound images.

Intravascular ultrasound (IVUS) has established itself as a useful tool for coronary assessment. The vast amount of data obtained by a single IVUS study renders manual analysis impractical for clinical use. A computerized method is needed to accelerate the process and eliminate user-dependency. In this study, a new algorithm is used to identify the lumen border and the media-adventitia border (the external elastic membrane). Setting an initial surface on the IVUS catheter perimeter and using active contour principles, the surface inflates until virtual force equilibrium defined by the surface geometry and image features is reached. The method extracts these features in three dimensions (3-D). Eight IVUS procedures were performed using an automatic pullback device. Using the ECG signal for synchronization, sets of images covering the entire studied region and corresponding to the same cardiac phase were sampled. Lumen and media-adventitia border contours were traced manually and compared to the automatic results obtained by the suggested method. Linear regression results for vessel area enclosed by the lumen and media-adventitia border indicate high correlation between manual vs. automatic tracings (y = 1.07 x -0.38; r = 0.98; SD = 0.112 mm(2); n = 88). These results indicate that the suggested algorithm may potentially provide a clinical tool for accurate lumen and plaque assessment.

Algorithms↗
PubMed1999

Arterialization of human vein grafts is associated with tenascin-C expression.

OBJECTIVES: This study was performed to test the hypothesis that tenascin-C (TN-C), an extracellular matrix (ECM) protein with counteradhesive chemotactic and vascular growth-promoting effects, is expressed in "arterialized" human saphenous vein grafts (SVGs). BACKGROUND: Tenascin-C is expressed in the vessel wall after vascular injury in the experimental model, where it has been implicated in the formation of neointima. Overexpression of TN-C has also been implicated in the development and progression of pulmonary hypertension. Saphenous vein grafts are exposed to hemodynamic stress when interposed in the arterial circulation and mechanical stress upregulates expression of TN-C, whereas stress-relaxation suppresses its synthesis. We hypothesized that the hemodynamic stress of increased arterial pressure could also induce TN-C expression in SVG. METHODS: We examined the expression of TN-C protein and mRNA in normal vein and "arterialized" human SVG using immunohistochemistry and in situ hybridization, respectively. RESULTS: TN-C protein was not detected in control human saphenous veins; however, it was uniformly and strongly expressed in the adventitia and media of patent human vein grafts, with minimal or no expression in the neointima (n = 27, 100%). In situ hybridization showed that TN-C mRNA was not detected in the neointima, but was strongly upregulated in the adventitia and media, corroborating immunostaining data (n = 10, 100%). Unlike patent SVG, TN-C was not expressed in the adventitia of occluded grafts, except for a low level of expression around the newly formed vessels in neointima (n = 5, 100%). Smooth muscle cell-specific staining demonstrated that the lack of expression of TN-C in occluded vein grafts is not due to the lack of presence of smooth muscle cells in the graft. CONCLUSIONS: These findings suggest that placement of a venous graft in the arterial system leads to expression of TN-C, which may in turn facilitate graft remodeling. Conversely, loss of flow and intravascular pressure, associated with vein graft occlusion, is accompanied by disappearance of TN-C expression.

Arteries↗
PubMed1996

Chronic rejection of concordant aortic xenografts in the hamster-to-rat model.

Several groups have demonstrated that it is possible to obtain long-term graft survival of concordant xenografts. One of the important questions that remains is whether xenografts are susceptible to chronic rejection. To answer this question we used the aorta transplantation model. One centimetre of hamster aorta was interposed in the abdominal aorta of Lewis rat recipients. The recipients were either untreated (group 1), or treated with 10 mg/kg cyclosporine (CsA), given intramuscularly three times a week (group 2). Rats were sacrificed at day 7, 14, 21, 28, 56 and 84 and the thickness of the intima, the media and the adventitia was measured. Furthermore, the cellularity of the media and the adventitia was assessed by counting the number of nuclei per 0.05 mm2 and immunohistochemistry of the aortic grafts was performed. Graft arteriosclerosis developed in aortic xenografts of both group 1 and group 2. In group 1, intimal lesions were already present from day 21 onwards in all rats, whereas in group 2 they were present only in 33% (2/6) of the rats. At day 84 all the grafts in group 1 were totally occluded, while those in group 2 were still open. The thickness of the media was slightly increased in both groups during the whole observation period, mainly due to edema. Although a few infiltrating macrophages could be seen, the number of nuclei per 0.05 mm2 of the media remained constant during the first 21 days, but declined sharply from day 21 onwards, as a consequence of disappearing myocytes. Thickness of the adventitia in both groups increased after transplantation due to infiltrating macrophages and T cells, reaching a peak at day 14. After day 14 the adventitial thickness in group 1 decreased rapidly to reach values comparable to group 2 from day 28 onwards. In conclusion, graft arteriosclerosis, as a sign of chronic rejection, occurs in concordant aortic xenografts. The lesions in the xenografts develop extremely rapidly, and compared to data from the literature, faster than in aortic allografts. The process of chronic rejection in aortic xenografts can be reduced by CsA.

Animals↗
PubMed2000

Immunophenotypic analysis of the aortic wall in Takayasu's arteritis: involvement of lymphocytes, dendritic cells and granulocytes in immuno-inflammatory reactions.

The present study was undertaken to examine the cellular composition of the aortic wall in Takayasu's arteritis and to investigate the association of different cell types in the immuno-inflammatory reactions of this disease. Specimens of aortic wall affected by Takayasu's arteritis were obtained from 10 patients (five male, five female), aged 32 to 68 years (mean 49.5 years) at elective operation. The mean duration of disease was 6.5 years (range 2 months to 13 years). Specimens were embedded in paraffin and the sections stained with antibodies to CD3 (to identify T cells), CD20 (B cells), S-100 (dendritic cells), CD15 (granulocytes), CD68 (macrophages), alpha-SMA (smooth muscle cells) and von Willebrand factor (endothelial cells). Immunohistochemical examination demonstrated that all specimens showed histological alteration with the replacement of the muscular and elastic layers of the media and adventitia by dense fibrous tissue, and were characterized by varying degrees of inflammatory cell infiltration. In five cases, inflammatory nodules consisting of numerous T cells and B cells were observed in the adventitia. Within the inflammatory nodules, as well as around areas of neovascularization in the deep portion of the intima, lymphocytes were co-localized with dendritic cells. In addition, in the adventitia, the accumulation of a large number of granulocytes was observed. The present study demonstrates that immune inflammation is a typical feature of Takayasu's disease, and that the interactions between dendritic cells and lymphocytes may be important in the control of the immune reactions in this vascular pathology.

Adult↗
PubMedDate not supplied

Interactive computerized microscopy as a tool for quantifying vascular remodelling effects of diabetes and V1a receptor antagonist SR 49059 on rat mesenteric arterial bed.

A methodology using interactive computerized microscopy (ICM) was developed to quantify in the mesenteric arterial bed the morphometric changes associated with diabetes and the influence of treatment with SR 49059, an antagonist of vasopressin V1a receptors. Four groups of rats were studied: untreated normal (N) or streptozotocin- (60 mg/kg i.v.) induced diabetic (D), and treated (0.4 mg/g SR 49059 included in food) normal (NT) or diabetic (DT) animals. Treatment was initiated 4 days after diabetes induction and continued for 3 weeks. Nested (hierarchical) analysis of variance of ICM data was performed on raw diameter or after logarithmic normalization of area and nuclei values. Diabetes was associated with an increase in arterial diameters, and in total vessel, wall, media, adventitia, and lumen areas. The same parameters, with the exception of the lumen, were also increased in DT as compared to D. The number of nuclei in the media or adventitia was increased in D as compared to N, and in DT as compared to D. In summary, ICM is allowed to further characterize the vascular mesenteric changes and describe for the first time the enlargement of adventitia associated with diabetes. Our study also suggested that the blockade of Via receptors is unable to prevent diabetes-related vascular changes, although the slight increase in food intake associated with SR 49059 treatment may have had an indirect influence on angiopathy development.

Animals↗
PubMed2000

Calcium phosphate precipitates augment adenovirus-mediated gene transfer to blood vessels in vitro and in vivo.

Adenovirus (Ad)-mediated gene transfer to blood vessels is relatively inefficient, probably because binding of adenovirus to the endothelium and adventitia seems to be limited. Association of calcium phosphate (CaPi) precipitates with adenovirus improves efficiency of gene transfer to some cells in culture and to mouse lung in vivo. In this study, we tested the hypothesis that CaPi is useful for adenovirus-mediated gene transfer to blood vessels. In fibroblast and endothelial cells in culture, Ad:CaPi coprecipitates greatly increased transgene expression. Ad:CaPi also enhanced transgene expression in both adventitia and endothelium of carotid arteries and aortae from rabbits studied ex vivo. After injection of Ad:CaPi into the cisterna magna of rabbits in vivo, the transgene product was markedly increased in leptomeninges of the ventral brain stem, including the adventitia of the basilar artery. We also examined mechanisms of enhanced gene transfer. Binding of adenovirus to fibroblast and endothelial cells in culture, and to the basilar artery in vivo, as determined using Southern blot analysis, was augmented by CaPi. Antibody to adenoviral fiber knob did not inhibit augmented transgene expression by Ad:CaPi. The finding suggests that improved adenoviral binding occurs primarily via a fiber-independent pathway. Thus, CaPi precipitates are useful for improvement of adenovirus-mediated gene transfer to blood vessels in vitro and in vivo.

3T3 Cells↗
PubMed1999

Epithelioid hemangioma of the temporal artery clinically mimicking temporal arteritis.

A rare case of epithelioid hemangioma (angiolymphoid hyperplasia with eosinophilia) arising in the right temporal artery of a 68-year-old Japanese woman was investigated. The patient had been treated with corticosteroids (Predonine 5 mg/day p.o.) for 4 years for idiopathic thrombocytopenic purpura. Headaches in the right temporal region with repeated high fevers first appeared 1 year prior to the biopsy of a nodule at the artery. The clinical diagnosis was temporal arteritis (giant cell arteritis). The specimen consisted of a short segment of the superior arterial branch having a sheet-like proliferation of the epithelioid endothelial cells in the lumen, which was almost occluded, focal rupture of the media, and marked proliferation of the capillaries (neovascularization) radiating out from the media to the adventitia. There were scattered foci of inflammatory cell infiltration composed mainly of small lymphocytes in the adventitia, but there were no histological changes suggestive of giant cell arteritis. The lesion was thus characterized by the proliferation of epithelioid endothelial cells in the lumen of the artery, and neovascularization between the media and adventitia. The histological features were very close to epithelioid hemangioma except for the absence of an eosinophilic reaction. The long-term administration of corticosteroids may have suppressed it. The authors believe this is the first case of epithelioid hemangioma arising from the temporal artery without a history of trauma. It showed some unique features both clinically and histopathologically, which contributed to the study of the yet not clearly classified vascular proliferative lesion, epithelioid hemangioma.

Aged↗