ISSN:1018-1172    

DOI:10.1159/000158880

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Bioassay studies suggest that impaired endothelium-dependent relaxation in atherosclerotic arteries is due to a reduced release of biologically active endothelium-derived relaxing factor (EDRF). We tested the hypothesis that endothelial dysfunction is caused by deficiency of the EDRF precursor L-arginine. Aortae from normal and cholesterol-fed (1%, 4 months) rabbits were excised and incubated for 1 h with 5 mML-arginine. Pretreatment with L-arginine had no effect on the relaxation to acetylchohne in normal vessels and was without effect on the impaired response of atherosclerotic arteries to acetylchohne. This finding suggests that L-arginine deficiency is unlikely the underlying cause of impaired endothelium-dependent relaxation in the aorta of cholesterol-fed rabbits.

ISSN:1018-1172    

DOI:10.1159/000158881

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The aim of this study was to evaluate the effects of aging on endothelium-dependent and endothelium-independent relaxation of rabbit thoracic aorta from New Zealand white rabbits aged 4–6 and 7–12 months. The contractile response to noradrenaline (NA) decreased with increasing age, but NA [EC50] did not vary significantly. Acetylcholine (Ach)-induced relaxation of aortic rings precontracted with NA [EC50] did not change significantly with increasing age. The relaxation induced by ATP of aortic rings, precontracted with NA [EC50], was signficantly greater in young than in adult rabbits. This difference between young and adult animals became more evident in aortic rings deprived of endothelium: in adult animals, the ATP-induced relaxation of aortic rings with endothelium was significantly greater than in the rings without endothelium. The endothelium-independent relaxation by sodium nitrite (NaNO2) at lower concentrations was significantly greater in young than in adult rabbit aortic rings precontracted with NA [EC50]. Concluding, the age-induced changes in vascular response in male New Zealand white rabbits are related to an impaired mechanism at smooth muscle le

ISSN:1018-1172    

DOI:10.1159/000158882

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

We theorized that H-8, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide, an inhibitor of cyclic nucleotide-dependent protein kinases, might be a useful probe to assess cyclic nucleotide-dependent relaxation of blood vessels. However, working in the rat caudal artery and aorta, we found that neither cyclic AMP- nor cyclic GMP-mediated relaxations were diminished by even large doses of H-8. For example, in the caudal artery, relaxation of a phenylephrine contraction by 8-bromo-cGMP (10–5M) was unaffected by H-8: control, 33 ± 6.2%; 10 µM H-8, 41 ± 12%; 30 µM H-8, 30 ± 16% (p NS). The amount of relaxation by 8-bromo-cAMP (3 × 10–4M) was actually increased by H-8: control, 29 ± 7.6%; 10 µM H-8, 34 ± 7.4%; 30 µM H-8, 80 ± 14%. In the rat aorta, H-8 also failed to diminish relaxation induced by 8-bromo-cGMP, or by atriopeptin II or sodium nitroprusside. In both caudal artery and aorta, H-8 of itself caused a dose-dependent suppression of α-adrenergic contraction: for example, in the caudal artery, with 10 or 30 µM H-8, peak contraction to phenylephrine was reduced to 70 (SEM) ± 12% or 52 ± 7% of control, respectively. The results suggest that the protein kinase inhibitor H-8 is not a useful probe to study cyclic nucleotide-de

ISSN:1018-1172    

DOI:10.1159/000158883

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

To evaluate whether intravascular phenomena contribute to local differences in growth responses of the arterial wall, we evaluated responses to organoid culture in a broad variety of arterial preparations. Arterial segments were isolated from adult, normotensive rats, sympathectomized, denuded from endothelium, and suspended in medium supplemented with serum. As judged from the nuclear incorporation of the thymidine analogue 5-bromo-2’-deoxyuridine (BrdUrd), this induced a transient stimulation of DNA synthesis in only a fraction of the arterial smooth muscle cells in all types of arteries. This intramedial DNA synthesis was more marked in renal arteries than in carotid arteries or aortae and was least pronounced in main pulmonary, femoral, and superior mesenteric artery and in mesenteric resistance-sized arteries. Organoid culture of isolated arteries did not increase the cross-sectional area of the media or the number of medial cells. It rather resulted in proliferation of smooth-muscle-like cells outside the media. In addition, smooth-muscle-like cells migrated out of the isolated arterial segments during culture. The rate of proliferation of these isolated cells did not differ between large arteries of different anatomical origin. However, isolated cells derived from mesenteric resistance arteries proliferated at a rate that was 4 times slower than that of large artery cells. The presence of endothelium significantly reduced medial DNA synthesis in carotid and renal artery segments, but not in mesenteric resistance-sized preparations. These data indicate that growth responses of the arterial wall differ quantitatively with the anatomical location and branching order of the vascular segment. In addition to the regional heterogeneity of endothelial effects on mitogenic responses of arterial smooth muscle, this seems to be due to regional differences in the susceptibility of arterial smooth muscle to exogenous growth factors. In this respect, we speculate that subsets of growth-resistant and growth-prone arterial smooth muscle cells could be heterogeneously distributed over the arterial tre

ISSN:1018-1172    

DOI:10.1159/000158884

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Excised canine carotid arteries held at constant physiologic length were cycled from –13 to +27 kPa with a constant-flow infusion pump, and the pressure-volume curves were recorded. The change in diameter on reducing the pressure from 16 to 0 kPa was determined and the strain of recoil [(diameter16 – diameter0)/diameter16] calculated. Diameter recoil was reduced from 51 % (fresh tissue) to 5 % after 3 h pressure fixation in 4 % formaldehyde and to 9% after 15 min in 2% glutaraldehyde with little further change. Lengthwise recoil was reduced from 37 to 10% after 5 min in 2% glutaraldehyde. Photographs were taken to measure outer diameter during pressure fixation. There was no change in diameter in either fixative from the first minute up to 3 days at the constant pressure of 16

ISSN:1018-1172    

DOI:10.1159/000158885

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Graded stenoses (40–64% diameter reduction) were applied to dog common carotid arteries under anesthesia, and 27 days later the poststenotic velocity field was examined using transcutaneous pulsed Doppler velocimetry. Following in situ fixation, endothelial cell area, shape and orientation was measured by digitizing endothelial cell outlines in scanning electron micrographs. Endothelial cell area in the vicinity of the stenosis throat (within ± 1 diameter) was reduced. No relation to stenosis hemodynamics was apparent. Cell area was increased 5 diameters downstream; in this region, there was turbulence due to jet break up. Cells were maximally rounded at the stenosis throat and gradually returned to upstream elongation by 5 diameters downstream. There was a region of flow separation and low velocity recirculation between the stenosis and the site of maximum turbulence, thus, downstream cell rounding was associated with flow separation. Subdivision of the experiments into four stenosis grades revealed little variation of the pattern of morphology between groups. It is possible that this is related to flow limitation with increasing grade. Elongation of endothelial cells through the entrance of the stenosis was apparent in only four experiments. Poststenotic dilatation of greater than 12 % external diameter increase was noted in only four out of the sixteen experiments. In general, the relation of cell elongation to shear stress is supported, but this relationship does not fully explain endothelial cell shape at a stenos

ISSN:1018-1172    

DOI:10.1159/000158886

出版商:S. Karger AG    

年代:1991

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158887

出版商:S. Karger AG    

年代:1991

数据来源: Karger