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1. |
Two-Dimensional Tortuosity of the Superficial Femoral Artery in Early Atherosclerosis |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 181-191
Örjan Smedby,
Nils Högman,
Sven Nilsson,
Uno Erikson,
Anders G. Olsson,
Goran Walldius,
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摘要:
Tortuosity of an artery can disturb fluid mechanics and cause flow separation, which might in turn promote atherogenesis. This study discusses theoretically several quantitative measures of arterial tortuosity and curvature in two dimensions and tests them with computations from digitized femoral arteriograms. When reproducibility, sensitivity to scaling and computational procedure, and agreement between the measures were all taken into account, the total curvature and distance factor were considered the most suitable measures. Significant correlations were found between tortuosity and atherosclerosis measures, but the interpretation of this finding is not straightforward.
ISSN:1018-1172
DOI:10.1159/000158993
出版商:S. Karger AG
年代:1993
数据来源: Karger
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2. |
Morphogenic Effects of Endothelin-1 on Vascular Smooth Muscle Cells |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 192-201
Alfred W.A. Hahn,
Stefan Regenass,
Therese J. Resink,
Frances Kern,
Fritz R. Bühler,
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摘要:
Endothelin-1 (ET-1), a vasoconstrictor peptide produced by endothelial and vascular smooth muscle cells (VSMC) might play a role in vascular remodelling. To investigate the proposed ‘mitogenic’ potential of ET-1, we examined the effects of chronic exposure of VSMC to ET-1 on cell cycle, growth/proliferation and differentiation under essentially mitogen-free culture conditions. Bulk cultures of thoracic aortic VSMC of spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats, although exhibiting genetically determined differences in growth/proliferation (due to shortened Gl and G2 phases in SHR VSMC), respond in a similar manner to ET-1 exposure: long-term exposure (12-15 days) of VSMC from both sources to ET-1 in nonmitogenic medium did not promote cycling of cells. On the contrary, ET-1 attenuated the cycling of VSMC which had already cycled beyond the S phase. For cells which had not cycled beyond the S phase, ET-1 interrupted progression through the cell cycle at the late Gl/early S phase. The specific ability of SHR VSMC to grow in mitogen-free medium was abolished by ET-1 most likely via down-regulation of platelet-derived growth factor (PDGF)-α receptors. Subsequent to ET-1 exposure, VSMC expressed increased levels of mRNA and protein for smooth-muscle-specific α-actin. However, expression of smooth muscle α-actin did not predominate over β-actin as observed for adult contractile VSMC in vivo. The ET-1-induced expression of smooth-muscle-specific α-actin mRNA was dose dependent (EC50 approx. 2 × 10-9M), and α-actin protein expressed was associated with organized ac
ISSN:1018-1172
DOI:10.1159/000158994
出版商:S. Karger AG
年代:1993
数据来源: Karger
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3. |
Protein Kinase C Involvement in the Regulation of Angiogenesis |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 202-208
N.E. Tsopanoglou,
E. Pipili-Synetos,
M.E. Maragoudakis,
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摘要:
Using the chick chorioallantoic membrane as a model system for the study of angiogenesis, we have shown that promoters of protein kinase C (PKC) such as 4-β-phorbol-12-myristate-13-acetate (4- β-PMA) and 1,2-dioctanoyl-sn-glycerol (DiC8) stimulated angiogenesis. This effect was specific since 4-α-PMA and 1,2-dioleoyl-sn-glycerol, which either do not activate or cannot reach PKC, were devoid of angiogenic activity. Furthermore, Ro 31-8220, a specific inhibitor of PKC, suppressed both basal and 4-β-PMA- or DiC8-induced angiogenesis. Similar results were obtained with the commonly used inhibitor of PKC, l-(5-isoquinoline-sulfonyl)-2-methylpiperazine and with tricyclodecan-9-yl-xanthogenate, an antitumor agent which has been suggested to be an inhibitor of PKC. Activation of PKC may be, therefore, an important signalling pathway in the initiation and control of the angiogenic respo
ISSN:1018-1172
DOI:10.1159/000158995
出版商:S. Karger AG
年代:1993
数据来源: Karger
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4. |
Eicosapentaenoic Acid Potentiates the Production of Nitric Oxide Evoked by lnterleukin-1β in Cultured Vascular Smooth Muscle Cells |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 209-217
Valerie B. Schini,
William Durante,
Sebastian Catovsky,
Paul M. Vanhoutte,
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摘要:
Experiments were designed to determine whether the ω3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-lβ in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1β evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1β in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1β in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L-arginine (an inhibitor of nitric oxide synthase), transforming growth factor β1 platelet-derived growth factorAB and thrombin. The addition of interleukin-1β -activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1β and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in vascular smoot
ISSN:1018-1172
DOI:10.1159/000158996
出版商:S. Karger AG
年代:1993
数据来源: Karger
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5. |
Renal versus Femoral Hemodynamic Response to Endothelium-Derived Relaxing Factor Synthesis Inhibition |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 218-223
David H. Sigmon,
Oscar A. Carretero,
William H. Beierwaltes,
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摘要:
Systemic inhibition of endothelium-derived relaxing factor (EDRF) synthesis leads to acute hypertension and increased peripheral vascular resistance. The changes in vascular resistance are not evenly distributed to all vascular beds. In this study, we compared the renal and femoral hemodynamic responses to EDRF synthesis inhibition. Renal blood flow (RBF) and femoral blood flow (FBF) were assessed in the presence and absence of DuP 753, an angiotensin II receptor antagonist. Inhibition of EDRF synthesis by a bolus dose of Lw-nitroarginine methyl ester (L-NAME) increased blood pressure (BP) by 21 ± 1 mm Hg(p < 0.001) and decreased RBF by 32 ± 5% (from 5.9 ± 0.5 to 3.9 ± 0.3 ml/min/g kidney weight; p < 0.005) while FBF remained unchanged (9.5 ± 0.4 versus 9.4 ± 0.4 ml/min). Renal vascular resistance (RVR) increased by 83 ± 16% (p < 0.001), compared with only a 24 ± 6% increase in femoral vascular resistance (FVR; p < 0.005). To eliminate the influence of systemic hypertension, we returned organ perfusion pressure to pre-L-NAME levels by partial aortic constriction. The kidney maintained RBF by decreasing RVR by 8 ± 2% (p < 0.02), while FBF decreased by 15 ± 5% (p < 0.01). When rats were pretreated with DuP 753, L-NAME still increased BP by 22 ± 2 mm Hg, but RVR increased by only 26 ± 5%(from 13.2 ± 1.6 to 16.8 ± 2.7;p < 0.01) and RBF did not change. DuP 753 had no effect on the femoral vascular response to L-NAME. FBF did not change (9.3 ± 0.2 versus 9.8 ± 0.7), while FVR increased by 23 ± 3% (from 8.7 ± 0.3 to 10.8 ± 0.6; p < 0.001). These results suggest that EDRF is a more important regulator of RBF than of FBF. We conclude that the kidney has a disproportionate reliance on EDRF to maintain R
ISSN:1018-1172
DOI:10.1159/000158997
出版商:S. Karger AG
年代:1993
数据来源: Karger
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6. |
Contractility of the Rabbit Abdominal Aorta 4 Days after Endothelium Denudation |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 224-230
Anna Holécyová,
Mária Gerová,
V. Smieško,
S. Doležel,
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摘要:
The purpose of this study was to evaluate contractility ofthe rabbit abdominal aorta 4 days after de-endothelialization by balloon catheter. The isometric tension of ring-segments in response to vasoactive agents was monitored. A significant enhancement of contraction to noradrenaline and serotonin was found in aortas 4 days after endothelium denudation as compared with controls with endothelium. The enhancement, however, did not differ from that found already in acutely denuded vessels (immediate denudation). No significant difference in contractility to potassium chloride was found in either group of denuded preparations as compared with controls. The sensitivity to all three vasoactive agents (EC50) was not influenced by denudation. These results indicate that changes in the contractility of denuded vessels are predominantly a consequence of lacking the endothelium as a producer of endothelium-derived relaxing factor. The access of mitogens to the media does not seem to interfere with the magnitude of contraction 4 days after denudation.
ISSN:1018-1172
DOI:10.1159/000159001
出版商:S. Karger AG
年代:1993
数据来源: Karger
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7. |
Arginine Vasopressin Increases Perinuclear [Ca2+] in Single Cultured Vascular Smooth Muscle Cells of Rat Aorta |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 231-238
Hideyoshi Fujihara,
Satoru Fukuda,
Tsuyoshi Tanaka,
Hiroaki Kanazawa,
Naoshi Fujiwara,
Koki Shimoji,
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摘要:
The effects of arginine vasopressin (AVP, 10-7M) on the spatial dynamics of intracellular [Ca2+] in single cultured smooth muscle cells of the rat aorta were studied by digital imaging microscopy using the fluorescent Ca2+ indicator fura-2. The nuclear and cytosolic regions were distinguished by the fluorescent image excited at 380 nm. Changes in intracellular [Ca2+] were expressed as percent increases in the ratios of fluorescence intensity at 500 nm excited by 340 and 380 nm. AVP increased the nuclear and cytosolic [Ca2+] in Ca2+-containing (control) (285 ± 27 and 172 ± 22%, respectively) or Ca2+-free (203 ± 26 and 121 ± 15%, respectively) solutions. However, caffeine (20 mM) and ryanodine (20 µM)greatly attenuated the [Ca2+] increase induced by AVP in both regions (61 ± 21 and 42 ± 15%, respectively). On the ratio image, the nuclear region was discriminated from other regions at the peak response to AVP in preparations treated with caffeine and ryanodine, whereas the outline of the nuclear region was indistinct in untreated preparations. The finding implies that caffeine- and ryanodine-responsive Ca2+ storage sites may exist in the region surrounding the nucleus. The results suggest that the region surrounding the nucleus may be one of the important Ca2+ storage sites with regard to the responses of rat aortic smooth muscle cells
ISSN:1018-1172
DOI:10.1159/000158998
出版商:S. Karger AG
年代:1993
数据来源: Karger
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8. |
Reduction of Vein Graft Intimal Hyperplasia by ex vivo Treatment with Desferrioxamine Manganese |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 239-239
M.J. Underwood,
R.S. More,
M.M. Thompson,
A.H. Gershlick,
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ISSN:1018-1172
DOI:10.1159/000158999
出版商:S. Karger AG
年代:1993
数据来源: Karger
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9. |
Reply |
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Journal of Vascular Research,
Volume 30,
Issue 4,
1993,
Page 240-240
P.O. Hagen,
M.G. Davies,
R.W. Schuman,
J.J. Murray,
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PDF (231KB)
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ISSN:1018-1172
DOI:10.1159/000159000
出版商:S. Karger AG
年代:1993
数据来源: Karger
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