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PubMed1996

Denervation, but not decentralization, reduces nerve growth factor content of the mesenteric artery.

In the present study we applied an improved nerve growth factor (NGF) extraction method to examine the effects of denervation and sympathetic decentralization on NGF levels in vascular tissue. Adult male Wistar Kyoto rats underwent mesenteric arterial denervation or splanchnic nerve transection. Four days after operation, animals were killed, and the mesenteric artery and coeliac-superior mesenteric ganglia were removed. The arterial adventitia was stripped from the media to measure NGF levels in nerve and smooth muscle separately. A high concentration of NGF was detected in the normal artery, 90% of which was in the adventitial layer. Surgical denervation significantly reduced the NGF levels in the artery and ganglia by 78 and 71%, respectively. However, within the artery the level of NGF was reduced in the adventitia but not in the media. Thus, the large reduction of NGF content resulted from the loss of nerve plexus from the artery. In contrast, decentralization did not alter the NGF content in the artery, in either the adventitia or media. Our results are in marked contrast to previous studies reporting elevated levels of NGF following denervation. This discrepancy is explained by the ability of our new procedure to extract much greater amounts of NGF from the tissue.

Animals↗
PubMed2001

Venous neointimal hyperplasia in polytetrafluoroethylene dialysis grafts.

BACKGROUND: Vascular access dysfunction is the most important cause of morbidity and hospitalization in the hemodialysis population in the United States at a cost of $1 billion per annum. Venous neointimal hyperplasia (VNH) characterized by stenosis and subsequent thrombosis accounts for the overwhelming majority of pathology resulting in polytetrafluoroethylene (PTFE) dialysis graft failure. Despite the magnitude of the problem and the enormity of the cost ($1 billion), there are currently no effective therapies for the prevention or treatment of venous neointimal hyperplasia in PTFE dialysis grafts. METHODS: Tissue samples were collected from the graft-vein anastomosis of stenotic PTFE grafts during surgical revision. Specimens were graded using standard light microscopy and immunohistochemistry for the magnitude of neointimal hyperplasia and for the expression of specific cell types, cytokines, and matrix proteins. RESULTS: VNH was characterized by the (1) presence of smooth muscle cells/myofibroblasts, (2) accumulation of extracellular matrix components, (3) angiogenesis within the neointima and adventitia, and (4) presence of an active macrophage cell layer lining the PTFE graft material. Platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) were expressed by smooth muscle cells/myofibroblasts within the venous neointima, by macrophages lining both sides of the PTFE graft, and by vessels within the neointima and adventitia. CONCLUSIONS: Our results suggest that macrophages, specific cytokines (bFGF, PDGF, and VEGF), and angiogenesis within the neointima and adventitia are likely to contribute to the pathogenesis of VNH in PTFE dialysis grafts. Interventions aimed at these specific mediators and processes may be successful in reducing the very significant human and economic costs of vascular access dysfunction.

Actins↗
PubMed1987

Evaluation of different microsurgical techniques for arterial anastomosis of vessels of diameter less than one millimeter.

The purpose of this study was to compare four different methods of microsurgical arterial anastomosis. One hundred and sixty rabbit popliteal artery anastomoses were performed. The following techniques were employed in each of four equal groups. Group 1: end-to-end technique with asymmetrical sleeving of the adventitia; Group 2: end-to-end technique with symmetrical sleeving of the adventitia and wrapping of the suture site with a collagen cuff; Group 3: end-to-end technique with symmetrical trimming of the adventitia; Group 4: end-in-end (sleeve) technique. A fifth group served as the control and omitted the division and anastomosis of the vessel. At one hour, 24 hr, three days, seven days, two weeks, six weeks, three months, and six months, the anastomosis was re-examined, and arterial segments were excised and prepared for evaluation. Long-term patency rates for the above techniques were found within the range of 87.5 to 92.5 percent. The healing process of anastomosed arteries occurred within three to seven days. A different pattern of arterial wall healing was found in the end-in-end, compared to the end-to-end, techniques. The study showed that the end-in-end technique is comparable in long-term patency rates to the conventional end-to-end technique, with significant reduction of the time needed to perform the anastomosis.

Anastomosis, Surgical↗
PubMed1982

[Repair of megaureter by tailoring in two layers while preserving vascular supply (author's transl)].

Since 1976 we tapered extremely wide obstructive or refluxive megaureters with partial fibrosis by this new technique, sometimes over 2/3 of length with ureterolysis in the upper segment. In these cases, preservation of the mesoureteric vascular supply is important in addition to the regular intramural nutrition. The mesoureteric arteries and veins spread into the adventitia and turn around in curves like a network. Exactly linear resection would cause damage. Therefore, we remove the adventitia from the lateral shape, resect beneath the abundant strip of muscularis with mucosa, trimming the megaureter downwards to a diameter of 7 to 4 mm, close the inner layer with running and interlocking 5-0 chromic suture over a splint and then readapt the adventitia. The advantages are: better arterial vascular supply, minimal thrombosis, no necrosis and no urinary leakage, less scarring and, therefore, good peristalsis.

Child, Preschool↗
PubMed1968

Studies on blood capillaries. II. Transport of ferritin molecules across the wall of muscle capillaries.

The pathway by which intravenously injected ferritin molecules move from the blood plasma across the capillary wall has been investigated in the muscle of the rat diaphragm. At 2 min after administration, the ferritin molecules are evenly distributed in high concentration in the blood plasma of capillaries and occur within vesicles along the blood front of the endothelium. At the 10-min time point, a small number of molecules appear in the adventitia, and by 60 min they are relatively numerous in the adventitia and in phagocytic vesicles and vacuoles of adventitial macrophages. Thereafter, the amount of ferritin in the adventitia and pericapillary regions gradually increases so that at 1 day the concentration in the extracellular spaces approaches that in the blood plasma. Macrophages and, to a lesser extent, fibroblasts contain large amounts of ferritin. 4 days after administration, ferritin appears to be cleared from the blood and from the capillary walls, but it still persists in the adventitial macrophages and fibroblasts. At all time points examined, ferritin molecules within the endothelial tunic were restricted to vesicles or to occasional multivesicular or dense bodies; they were not found in intercellular junctions or within the cytoplasmic matrix. Ferritin molecules did not accumulate within or against the basement membranes. Over the time period studied, the concentration of ferritin in the blood decreased, first rapidly, then slowly, in two apparently exponential phases. Liver and spleen removed large amounts of ferritin from the blood. Diaphragms fixed at time points from 10 min to 1 day, stained for iron by the Prussian Blue method, and prepared as cleared whole mounts, showed a progressive and even accumulation of ferritin in adventitial macrophages along the entire capillary network. These findings indicate: (1) that endothelial cell vesicles are the structural equivalent of the large pore system postulated in the pore theory of capillary permeability; (2) that the basement membrane is not a structural restraint in the movement of ferritin molecules across the capillary wall; (3) that transport of ferritin occurs uniformly along the entire length of the capillary; and (4) that the adventitial macrophages monitor the capillary filtrate and partially clear it of the tracer.

Animals↗
PubMed2004

Activation of arterial wall dendritic cells and breakdown of self-tolerance in giant cell arteritis.

Giant cell arteritis (GCA) is a granulomatous and occlusive vasculitis that causes blindness, stroke, and aortic aneurysm. CD4(+) T cells are selectively activated in the adventitia of affected arteries. In human GCA artery-severe combined immunodeficiency (SCID) mouse chimeras, depletion of CD83(+) dendritic cells (DCs) abrogated vasculitis, suggesting that DCs are critical antigen-presenting cells in GCA. Healthy medium-size arteries possessed an indigenous population of DCs at the adventitia-media border. Adoptive T cell transfer into temporal artery-SCID mouse chimeras demonstrated that DCs in healthy arteries were functionally immature, but gained T cell stimulatory capacity after injection of lipopolysaccharide. In patients with polymyalgia rheumatica (PMR), a subclinical variant of GCA, adventitial DCs were mature and produced the chemokines CCL19 and CCL21, but vasculitic infiltrates were lacking. Human histocompatibility leukocyte antigen class II-matched healthy arteries, PMR arteries, and GCA arteries were coimplanted into SCID mice. Immature DCs in healthy arteries failed to stimulate T cells, but DCs in PMR arteries could attract, retain, and activate T cells that originated from the GCA lesions. We propose that in situ maturation of DCs in the adventitia is an early event in the pathogenesis of GCA. Activation of adventitial DCs initiates and maintains T cell responses in the artery and breaks tissue tolerance in the perivascular space.

Adoptive Transfer↗
PubMed2006

Lymphocyte recruitment into the aortic wall before and during development of atherosclerosis is partially L-selectin dependent.

Atherosclerosis is an inflammatory disease of large arteries. Flow cytometry of aortic cell suspensions showed that B and T lymphocytes and some macrophages and dendritic cells are already present in the adventitia of normal/noninflamed mouse aortas. Adoptively transferred lymphocytes constitutively homed to the aorta and resided within the adventitia up to 7 d after transfer. Lymphocyte trafficking into normal/noninflamed or atherosclerosis-prone aortas was partially L-selectin dependent. Antigen-activated dendritic cells induced increased T lymphocyte proliferation within the aorta 72 h after adoptive transfer. During progression of atherosclerosis in apolipoprotein-E-deficient mice, the total number of macrophages, T cells, and dendritic cells, but not B cells, increased significantly. This alteration in immune cell composition was accompanied by the formation of tertiary lymphoid tissue in the adventitia of atherosclerotic aortas. These results demonstrate that lymphocytes already reside within the normal/noninflamed aorta before the onset atherosclerosis as a consequence of constitutive trafficking. Atherosclerosis induces the recruitment of macrophages and dendritic cells that support antigen presentation.

Adoptive Transfer↗
PubMed1997

Gene transfer into the carotid artery using an adventitial collar: comparison of the effectiveness of the plasmid-liposome complexes, retroviruses, pseudotyped retroviruses, and adenoviruses.

We studied the efficiency of plasmid/liposome complexes, Moloney murine leukemia virus-derived (MMLV) retroviruses, pseudotyped vesicular stomatitis virus protein-G (VSV-G)-containing retroviruses, and adenoviruses in delivering genes into the rabbit carotid artery using a silastic collar applied to the adventitia. This method was used for gene transfer because (a) it provides a gene delivery reservoir; (b) no intraluminal manipulations are performed; (c) installation of the collar induces arterial smooth muscle cell (SMC) proliferation and enhances retroviral gene transfer efficiency where target cell proliferation is required. The transfer of the beta-galactosidase (lacZ) marker gene to the adventitia and media occurred with all gene transfer systems. Adenoviruses also transferred the beta-galactosidase gene to some endothelial cells. After 5 days, adenoviral vectors produced the highest gene transfer efficiency with up to 10%+/-6% of cells showing beta-galactosidase activity. Pseudotyped VSV-G retroviruses were also effective in achieving gene transfer in 0.05%+/-0.03% of cells in the adventitia and media. Plasmid/liposome complexes and MMLV retroviruses infected 0.05%+/-0.03% and <0.01%+/-0.01% of cells, respectively. It is concluded that replication-deficient adenoviruses, VSV-G pseudotyped retroviruses, and plasmid/liposome complexes can be used for gene transfer to the arterial wall using the collar method. Because the endothelium remains anatomically present throughout the experiments, the model may be useful for the gene transfer studies involving diffusible or secreted gene products that primarily act on the endothelium. Effects on medial SMC and even endothelium can be achieved from the adventitial side, suggesting an alternative route for the delivery of therapeutically useful genes into the arterial wall.

Adenoviridae↗
PubMed1998

Advantages of sharp adventitial dissection for microvascular anastomoses.

Adventitia is usually removed from arteries to simplify microvascular anastomoses. Some surgeons peel the adventitia away bluntly whereas others trim the adventitia sharply with scissors. We used a rat cremaster flap for intravital microscopy to evaluate these two techniques. Animals with unmanipulated vessels, without anastomosis or adventitial removal, served as controls. Fifty-four rats were studied in three groups of 18 rats. Functional capillary density, red blood cell velocity, diameter of the flap's feeding artery (A1), microthrombi formation, and neutrophilic activity were studied for 5 hours following anastomosis, and 24 and 72 hours later. Histological changes in blunt and sharply prepared arteries were compared with control vessels. After blunt preparation, capillary perfusion was reduced to 61% of control values (p < 0.05) and A1 diameter was reduced to 77% of control values (p < 0.05). Capillary perfusion and A1 diameter were unchanged in sharply prepared arteries. Architectural changes in the vessel wall were more profound, and neutrophilic activity was increased in bluntly prepared arteries. In this study, sharp preparation of small arteries was beneficial compared with blunt preparation.

Anastomosis, Surgical↗
PubMed1999

Adventitial expression of recombinant endothelial nitric oxide synthase gene reverses vasoconstrictor effect of endothelin-1.

The present study was designed to determine the effect of recombinant endothelial nitric oxide synthase (eNOS) gene expression on reactivity of canine basilar arteries to endothelin-1 (ET-1). Experiments were performed ex vivo. The arteries were exposed (30 minutes at 37 degrees C) to adenoviral vectors encoding eNOS gene (AdCMVeNOS) or beta-galactosidase reporter gene (AdCMVbeta-Gal). Twenty-four hours after transduction, transgene expression was evident mainly in the vascular adventitia. Rings of control (nontransduced), AdCMVbeta-Gal- and AdCMVeNOS-transduced arteries with and without endothelium were suspended for isometric tension recording. Levels of guanosine 3',5'-cyclic monophosphate (cGMP) were measured by radioimmunoassay. During contractions to uridine 5'-triphosphate, ET-1 (10(-10) to 3x10(-9) mol/L) caused further increase in tension in control and AdCMVbeta-Gal-transduced arteries. In contrast, ET-1 caused concentration-dependent relaxations of AdCMVeNOS-transduced arteries. The relaxations to ET-1 in AdCMVeNOS-transduced arteries were endothelium-independent. They were abolished by N(G)-nitro-L-arginine methyl ester or by chemical treatment of adventitia with paraformaldehyde before gene transfer. ET-1 (10(-9) mol/L) significantly increased intracellular cGMP levels in AdCMVeNOS-transduced arteries without endothelium. In arteries transduced with AdCMVeNOS, higher concentrations (10(-9) to 3x10(-8) mol/L) of ET-2 also caused relaxations, whereas ET-3 and sarafotoxin, a selective ET(B) receptor agonist, did not produce any relaxations. The relaxations to ET-1 in AdCMVeNOS-transduced arteries were strongly reduced by BQ-123 (10(-7) mol/L), an ET(A) receptor antagonist, but were not affected by BQ-788 (3x10(-7) mol/L), an ET(B) receptor antagonist. These results suggest that genetically modified adventitia can produce nitric oxide and cause relaxations in response to ET-1 via activation of ET(A) receptors. Our findings support a novel concept that successful transfer and expression of recombinant eNOS gene can lead to a qualitative change in responsiveness to vasoconstrictor substances.

Adenoviridae↗
PubMed1997

Cellular changes induced by chronic nitric oxide inhibition in intact rat basilar arteries revealed by confocal microscopy.

BACKGROUND: Cellular aspects of remodelling have not been investigated fully in intact vessels due to lack of appropriate methodology. OBJECTIVE: To determine the cellular alterations induced by chronic inhibition of nitric oxide (NO) production in intact rat basilar arteries by combined use of perfusion myography and a laser scanning confocal microscope. METHODS: Wistar-Kyoto rats were treated with 10 mg/kg per day NG-nitro-L-arginine methyl ester (L-NAME) for 3 weeks. Basilar arteries from treated and age-matched Wistar-Kyoto rat controls were mounted on a perfusion myograph, stained with the nuclear dye Hoechst 33342 and fixed under pressure. The segments were mounted on a slide and visualized using the 364 nm line of a laser scanning confocal microscope. MetaMorph software was used to obtain optical sections from the vessel and for morphology determinations. RESULTS: L-NAME treatment induced hypertension (systolic blood pressure control 129.2+/-2.7 mmHg and SBP L-NAME treatment 176.3+/-5.2 mmHg, P< 0.001). Compared with control rat arteries, arteries from treated rats had a reduced lumen diameter, similar wall thickness and an increased wall: lumen ratio. L-NAME treatment induced specific changes in adventitia, media and intima, namely an increase in number of adventitial cells and in adventitia thickness, a reduction in number of smooth muscle cells with no change in media thickness and reductions in number of endothelial cells, size of nuclei and luminal surface area. CONCLUSIONS: Hypertension induced by chronic inhibition of NO production is associated with eutrophic remodelling of rat basilar artery. However, within this overall maintenance of constant volume, there are marked cellular changes in adventitia, media and intima. The separate contributions of inhibition of NO production and hypertension to the remodelling process need to be elucidated.

Animals↗
PubMed1999

Gene therapy for cerebrovascular disease.

OBJECTIVE: To review the principles of and the experimental and clinical results of gene therapy for cerebrovascular disease. METHODS: Literature review. RESULTS: Vectors for gene transfer into the brain or into the cerebral vasculature include naked plasmid deoxyribonucleic acid, cationic liposomes, and viruses such as adenovirus, retrovirus, adeno-associated virus, and herpes simplex virus. Experiments using these vectors showed that intra- or perivascular application to systemic arteries can lead to transfection and expression of a foreign transgene in the adventitia and the endothelium. Intrathecal administration can lead to transfection and foreign transgene expression in leptomeningeal cells as well as in fibroblasts of blood vessel adventitia. Biological effects demonstrated thus far include increased nitric oxide production by transfection of cerebral arterial adventitia with adenovirus expressing nitric oxide synthase. Adenoviruses carrying foreign genes have been used to decrease neuronal damage in cerebral ischemia and to decrease blood pressure in spontaneously hypertensive rats. Vectors and therapeutic applications for gene therapy are evolving rapidly. CONCLUSION: Gene therapy for cerebrovascular disease is likely to have clinical application in the near future and will have a major impact on neurosurgery. Neurosurgeons will need to be aware of the literature in this area.

Animals↗
PubMed1995

Sequential immunological targeting of chronic experimental arterial allograft.

Arterial wall is the main site involved in the chronic rejection process. The rat aortic allograft model was used here to characterize and describe the sequential evolution of the different targets and effectors of arterial wall immunological injury and response during arterial allograft rejection. Rat abdominal aortae were isografted or allografted from Brown-Norway to Lewis rats. Endothelial and smooth muscle cell injury and humoral and cellular immunological effectors were characterized from 0 to 60 days after transplantation using a battery of specific antibodies. The intimal proliferative response was also characterized over this time. Isografted Brown-Norway aorta adventitia had very few cellular components, which suggests that donor adventitia would be poorly antigenic in allografts. In contrast, allograft adventitia was the site of a major inflammatory cell invasion in which the expression of an adhesion molecule by colonizing capillary endothelial cells could play a main role. This adventitial infiltration continued as long as medial smooth muscle persisted. The luminal endothelial cells disappeared early, probably associated with macrophage margination. In contrast, medial smooth muscle cell disappearance occurred later and was specifically targeted by immunoglobulins. Intimal proliferation was the most delayed phenomenon, involving both inflammatory cell infiltration at an early stage and later myofibroblastic proliferation, and could be related to the specific expression of growth factors in this layer. The rat aortic allograft model appeared useful for characterizing specific targets and effectors of chronic arterial graft rejection, demonstrating an early stage of endothelial injury and the presence of immunoglobulins involved in chronic medial smooth muscle cell injury.

Animals↗
PubMed2006

Effects of time of contact and concentration of caustic agent on generation of injuries.

OBJECTIVES: Solid caustic soda (CS) ingestion levels continue high in Brazil. The aggressiveness of a caustic agent depends, among other factors, on its concentration and time of contact with mucosa. However, the interdependence of these factors in the production of caustic lesion in the esophageal mucosa is not known, especially regarding CS as the strongest corrosive agent. We analyze the effects of concentration and time of contact on the aggressiveness of CS to the esophagus of live animals. STUDY DESIGN/METHODS: One milliliter of CS at concentrations between 1.83% and 73.33% was applied to rats. The solution was kept in contact with the mucosa for 10 to 120 minutes. Internal and external organ aspects were analyzed and the epithelium, submucosa, muscle layer, and adventitia were analyzed microscopically RESULTS: Epithelial necrosis was observed at all concentrations. Among the necrotic layers, the submucosa was observed starting at the 7.33% concentration, and the muscular layer and adventitia were observed at 14.66% concentration. Damage to the pulmonary parenchyma and trachea occurred at 33.66% after 10 minutes, and perforation of the esophagus was observed only after 120 minutes. After 10 minutes, important corrosive lesions installed in the esophageal layers, expanding in depth and superficial extension. The use of heparin had no effect on the production of lesions. CONCLUSIONS: Ten minutes were sufficient to provoke necrosis, and longer contact increased the area of necrosis. Solution concentration levels were more important in damage production: 1.83% was sufficient for epithelial necrosis, 7.33% caused submucosal necrosis, and 14.66% muscle and adventitia necrosis; 33.66% solutions caused lung and trachea damage after 10 minutes and esophageal perforation after 120 minutes.

Animals↗
PubMed1998

Guidance of intracoronary radiation therapy based on dose-volume histograms derived from quantitative intravascular ultrasound.

Application of ionizing radiation to prevent restenosis in atherosclerotic vessels treated by balloon angioplasty is a new treatment under investigation in interventional cardiology and radiology. There is variability in dose prescription, and both gamma- and beta-emitters are used, leading to a wide range of dose distribution over the arterial vessel wall. We present a new modality of dosimetry based on a method that three-dimensional (3-D) image reconstruction of electrocardiogram (ECG)-gated intravascular ultrasound (IVUS) images. Dose volume histograms (DVH) are used to describe the cumulative distribution of dose over two specific volumes: i) at the level of the luminal surface, defined with a thickness of 0.1 mm from the automatically detected contour of the highly echogenic blood-vessel interface, and ii) the adventitia volume is computed considering a 0.5-mm thickness from the echogenic media-adventitia interface. DVH provide a tool for reporting the actual delivered dose at the site believed to be the target: the adventitia, and to detect excessive radiation which could lead to vascular complications. Simulation of a gamma-emitter or of a radioactive source train in the center of the lumen are possible. The data obtained from the first ten patients included in the beta-irradiation trial (BERT 1.5) conducted in our institution are presented, supporting the use of DVH based on quantitative IVUS measurements for optimal dose prescription in vascular interventional radiation therapy.

Brachytherapy↗
PubMed1990

Immunohistochemical characterization of inflammatory cells associated with advanced atherosclerosis.

During repair of 12 atherosclerotic abdominal aortic aneurysms, fresh samples of aneurysm wall were obtained. Histology confirmed the presence of advanced atherosclerosis associated with medial thinning and a variable aortic adventitial chronic inflammatory cell infiltrate. Monoclonal antibodies were used to identify the inflammatory cells throughout the aortic wall. The majority of lymphocytes in the aortic adventitia were B-cells. B-cells were not present in atheromatous plaques. T-cells, predominantly T-helper cells, were found in atheromatous plaques and in aortic adventitia. The majority of lymphocytes and macrophages in aortic adventitia and most vascular endothelial cells were HLA-DR positive. Ki-67 staining was found in B-cells and T-helper cells, indicating that these cells were proliferating. Occasional lymphocytes were BerH2 positive, indicating that some lymphocytes were activated. These findings suggest that chronic periaortitis is an active, immunologically mediated, local complication of advanced human atherosclerosis.

Aged↗
PubMed1996

Structure of small blood vessels in the testes of infertile men.

In the testis, 'hyalinization' of the lamina propria of seminiferous tubules is often accompanied by similar changes within the walls of testicular blood vessels. The aim of our study was to investigate the structure of small blood vessels in hyalinized human testes by means of immunohistochemistry, electron microscopy and image analysis methods. Results of immunohistochemical analysis indicated that, despite hyalinization, testicular small blood vessels retained positive immunostaining for desmin and actin. Their basement membranes remained immunopositive for collagen IV and laminin. No proliferative (Ki-67) activity was observed in the blood vessel walls in testes from both control and infertile men. P-170 glycoprotein was found to be expressed only in primary spermatocytes. No difference in expression and localization of this antigen was observed between control and affected testes. Electron microscopy revealed a number of testicular arterioles with a notably narrow lumen due to enlarged endothelial cells in infertile men. Such arterioles also had a thickened subendothelial layer and an abundant tunica adventitia rich in connective tissue fibres and ground substance. Some venules in hyalinized testes displayed increased connective fibres and ground substance in the subendothelial layer, between the smooth muscle cells of the tunica media and the tunica adventitia. However, no changes were found in the capillary network, when compared to controls. Image analysis data showed a statistically significant increase in the surface of tunica intima and adventitia of arterioles and tunica media of venules. It is concluded that hyalinization mostly affects testicular arterioles and venules, but not capillaries. Our immunohistochemical data indicate that the 'nature' and/or extent of hyalinization in testicular small blood vessels differs from that described previously for the lamina propria of seminiferous tubules.

Adult↗
PubMed2005

Morphological and immunocytochemical investigations on mast cells in porcine ureter.

Morphological, morphometric, histochemical and immunocytochemical investigations on mast cells, located in the wall of ureter of 8 months aged pigs were performed. Mast cells were found in all three layers of ureteral wall, but their distribution was irregular and the number unequal. It was established that alcian blue (AB)-positive mast cells were significantly more than toluidine blue (TB)-positive mast cells. A statistically significant smaller number of both AB and TB-stained mast cells were observed in the tunica mucosa. The largest number of mast cells was found in the tunica muscularis. In the adventitia, mast cells were higher in number in the main connective tissue than in the connective tissue near the blood vessels. Mast cells stained with TB showed variably expressed gamma-metachromasia, which was best visible in those situated in the lamina propria of the mucosa. The prevailing parts of mast cells, however, were AB-positive after AB-safranin staining. This was mostly found in mast cells of the tunica muscularis and in mast cells of perivascular location in the tunica adventitia. Immunocytochemically, mast cells were found to be positive for histamine and vasoactive intestinal polypeptide in the muscle coat, and to histamine in the adventitia, as well. On the basis of obtained results it was presumed that the mast cells in porcine ureter most probably took part not only in keeping of local homeostasis, but played also an important role of mobility of smooth muscle cells in the middle layer of ureter on one hand, and, on the other, in the adventitial blood vessels.

Alcian Blue↗