Mechanisms of vasodilatatory effect of perivascular tissue of human internal thoracic artery.
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It has beed showed that perivascular adipose tissue (PVAT) of human internal thoracic artery (ITA) releases adventitia/adipocyte-derived relaxing factor (ADRF). The precise mechanism of vasodilatatory effect of ADRF is still unknown. It was suggested that various potassium channels may be involved in the action of ADRF. The aim of this study was to assess the involvment of potassium channels in the vasorelaxing properties of ADRF in human internal thoracic artery. Human ITA rings were studied in vitro. First the ability of perivascular tissue of human ITA to release ADRF to the bath was checked. In subsequent experiments two fragments of skeletonised ITA were used to assess the involvement of various potassium channels in vasorelaxing action of PVAT. Segment of ITA, precontracted with serotonin (10(-5.5)M), was relaxed by adding PVAT to tissue bath, first without and then in the presence of appropriate potassium channel blocker. Second segment served as a control (no addition of PVAT). The magnitude of relaxation was measured and compared between preparations. This protocol was used to analyze the influence of iberiotoxin (100 nM), apamin (1 uM), 4-aminopyridine (1 mM, 5 mM), BaCl(2) (100 uM) and glibenclamide (10 uM). The addition of PVAT to precontracted skeletonized ITA caused significant vasorelaxation (54.6+/-8.03 mN versus 33.7+/-6.58 mN p=0.03). Similar effect was seen when 5 ml of aliquot from separate incubation of PVAT was added (36.3+/-5.45 mN versus 20.7+/-3.02 mN; p<0.001). PVAT dependent relaxation was blocked in the presence of Ca(+)(2) dependent potassium channel blocker iberiotoxin (47.4+/-16.67 mN versus 43.3+/-14.54 mN; p=0.36) and 4-aminopyridine (5 mM) (59.3+/-3.54 mN versus 51.6+/-4.77 mN; p=0.12). We conclude that perivascular adipose tissue of human ITA releases relaxing factor that seems to act with the involvement of Ca(+)(2) dependent potassium channels. (+info)
Structure and immunohistochemistry of the human lenticulostriate arteries.
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BACKGROUND: Data about the structure and immunohistochemistry of the lenticulostriate arteries (LSAs), although very important for medical research and clinical practice, have been rarely reported in literature. MATERIALS AND METHODS: Fourty serially sectioned LSAs were stained with hematoxilin and eosin, and prepared for immunohistochemistry. RESULTS: Our examination revealed a typical endothelial lining and a narrow subendothelial space with subintimal smooth muscle cells occasionally. The internal elastic lamina was fragmented or absent in the smallest LSAs branches. The mediacoat, with a mean diameter of 148.5 mum, contained typical smooth muscle cells which formed 14.2 layers on average and showed a positive immune reactions for alfa-actin, desmine, laminin and collagen IV. The thin adventitial coat contained fibroblasts, collagen fibers, and nerve bundles, with the strongest immunopositivity to thyrosin hydroxilase. The immune reactions against CD31 and CD34 proteins,endothelial nitric oxide synthase, S 100 protein, neurofilament protein and synaptophysin,seem to be performed in the LSAs wall for the first time. Similarly,the thickness of the LSAs wall and its coats have never been reported, nor the number of the smooth muscle cell layers. CONCLUSIONS: Our results related to the structure and immunohistochemistry of the LSAs could be important in cerebrovascular pathology, neurology and neurosurgery. (+info)
OBJECTIVE: This study aimed to compare the effects of hemocoagulase atrox and cauterization hemostasis on intimal hyperplasia and explore the effect of hemocoagulase atrox on vascular modeling in rabbit carotid artery adventitia. METHODS: A total of 27 rabbits were randomly divided into 3 groups (0d, 14d, 28d). They were anaesthetized using an intramuscular injection of phenobarbital sodium (1 ml/kg). The left and right common carotid arteries were exposed and capillary hemorrhaged after blunt dissection of the adventitia layers of common carotid arteries. Nine rabbits in each group were again randomly divided into 3 groups, in which animals were respectively treated with hemocoagulase (2 U/ml), cauterization (power = 40 w) and saline (as control). Groups of animals were euthanized at 0, 14 and 28 days after surgery. The samples were equally divided in the middle of the adventitia removal section to obtain equal parts for histologic, immunohistochemical and molecular biologic analysis. The vascular repair after adventitial stripping was observed by HE staining, Masson staining and transmission electron microscopy. The expression of carotid MCP-1, PCNA, TGF-beta1, alpha-SMA and VEGF were measured at different time points by RT-PCR and immunohistochemical staining. RESULTS: HE staining and Masson staining showed that hemocoagulase atrox had a significantly stronger effect on reducing intimal hyperplasia than the cauterization after 14 and 28 days. The results of RT-PCR showed that the expression of MCP-1, TGF-beta1, alpha-SMA and VEGF in hemocoagulase atrox-treated animals were lower than that of cauterization-treated animals. CONCLUSION: Our results suggested that hemocoagulase atrox as a topical hemostatic is safety and efficiently and it can accelerate adventitia restoration and decrease intimal proliferation. (+info)
Oncostatin M and TLR-4 ligand synergize to induce MCP-1, IL-6, and VEGF in human aortic adventitial fibroblasts and smooth muscle cells.
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