摘要:

Responses to 5-hydroxytryptamine (5HT) were compared in large [2.1–3.0 mm outside diameter (OD)], medium (1.5–1.8 mm OD) and small (0.5–1.0 mm OD) isolated canine coronary arteries. 5HT produced contraction of large and medium arteries, with the maximal response averaging 35.1 ± 4.0 and 21.0 ± 3.3%, respectively, of the contraction to 100 mM KCl. Endothelial removal increased the response to 5HT, with the maximal response averaging 43.6 ± 12.6 and 32.4 ± 7.5%, respectively, of the 100 mM KCl contraction. Small arteries did not contract significantly to 5HT in the presence or absence of endothelium. However, 5HT (10–6 M) contracted small arteries that were contracted with 30 mM KCl, averaging 130 ± 3% of the original contraction to KC1. This further contraction to 5HT was slightly potentiated by removal of the endothelium. We conclude that, unlike larger epicardial arteries, coronary arteries <1 mm OD are unresponsive to 5HT under resting conditions. Failure of small arteries to contract to 5HT cannot be explained by an inhibitory influence of the endothelium. However, 5HT enhances the contraction of small arteries to K+, and this response tends to be augmented by endothe

ISSN:1018-1172    

DOI:10.1159/000158639

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Vein-to-artery grafts develop areas of endothelial loss with fibrin and leukocytes which lead to early thrombosis and may lead to subsequent atherosclerosis of the graft. En face monolayers were prepared which removed >90% of vascular intima. Unevenly distributed leukocytes and endothelial cells were counted using a standardized sampling of calibrated oil immersion fields of 0.01 mm2. Nongrafted veins had 14 ± 1 evenly arranged endothelial cells per field without gaps or leukocytes, while 10-min grafts had 13 ± 2 with rare leukocytes. Four-hour grafts from normal dogs had 9 ± 2 endothelial cells with gaps and 97 ± 37 neutrophils and 44 ± 25 monocytes. Leukopenic dogs (vinblastine-treated) had normal numbers of endothelial cells (14 ± 1) with scanty leukocytes. We conclude that leukocytes cause endothelial loss in vein-to-artery grafts that can be prevented by intense leukopenia. This may lead to practical approaches to protecting such grafts in h

ISSN:1018-1172    

DOI:10.1159/000158640

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

We have characterized the dilation response to increased blood flow in the canine femoral and saphenous arteries. An arteriovenous shunt was created and changes in arterial diameter measured by sonomicrometer crystals. Increasing shunt flow approximately 10-fold caused a 9% increase in femoral and 15 % increase in saphenous artery diameter. The dilation response consisted of a transient decrease in diameter, followed by a rapid dilation and a slow return to control when flow was decreased. The increased diameter was not a result of decreased transmural pressure or alterations in pulse pressure. After removing the endothelial cells, the vessels did not dilate to increased flow or topical acetylcholine (10–5 M), but responses to norepinephrine (10–5 M) and sodium nitroprusside (10–4 M) were unaltered. Indomethacin, theophylline or propranolol did not affect the flow-induced dilation. Quinacrine, an inhibitor of phospholipase A2, attenuated the dilation response in a dose-dependent manner. We conclude that increased blood flow affects endothelial cells, causing an active dilation of arterial smooth m

ISSN:1018-1172    

DOI:10.1159/000158641

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Morphometric measurements on different arteries at the light-microscopic level and ultrastructural studies of the mesenteric arteries were carried out in salt-sensitive (DS) and salt-resistant (DR) Dahl rats given a high-salt (8%) or low-salt (0.4%) diet for 6–7 weeks. Hypertension was produced in DS rats given high-salt diet (DS-H), while only moderate hypertension was produced in DS rats given low-salt diet (DS-L). Blood pressure in DR rats given high salt (DR-H) and low salt (DR-L), however, was normal. Cross-sectional area of the media was increased significantly in the superior mesenteric artery (an elastic artery), large mesenteric arteries (muscular arteries) and small mesenteric arteries (small muscular arteries or arterioles) from DS-H rats. In all the vessel types, this increase was positively correlated with the increase in blood pressure. In the superior mesenteric artery, medial wall increase was probably due to an increase in intercellular space, and/or hypertrophy of the smooth muscle cells. Similarly, increase in the media of small mesenteric arteries was probably due to hypertrophy of the smooth muscle cells. In contrast, increase in the media of large mesenteric arteries was related to hyperplasia of the smooth muscle cells. Damage to endothelial cells was noted in the 3 vessel types from DS-H. Intimal lesions composed of myointimal cells were found in the superior mesenteric arteries of all the rat groups. Our results showed that the incidence of these lesion formations was higher in the following order: DS-&H>DS-&L> DR-&H> DR-L, suggesting that the degree of hypertension (DS vs. DR rats) and the amount of salt in the diet (DR-H vs. DR-L) may be some of the factors contributing to the development of these lesions. We conclude that hyperreactivity of the arteries due to increase in medial smooth muscle mass (e.g. muscular arteries), and/or probably impaired relaxation capability of the arteries in the DS-H rats due to endothelial cell damage, may contribute to the elevation of BP in the Dahl model of genetic hypertensio

ISSN:1018-1172    

DOI:10.1159/000158642

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Endothelium-dependent relaxations to acetylcholine have been identified in mammalian arteries and veins. To determine the occurrence of such relaxations in other classes of vertebrates, rings of descending aortas of turtles, cayman and bullfrogs and ventral aortas of trout were suspended for isometric force measurements. Acetylcholine and the calcium ionophore A23187 initiated concentration-dependent relaxations in aortas from cayman and bullfrogs contracted with norepinephrine. These relaxations were not affected by meclofenamate, were reversed by methylene blue and abolished by endothelium removal. Acetylcholine caused concentration-dependent contractions in aortas (with and without endothelium) from trout and turtles; these tissues contracted minimally to norepinephrine. In the aortas of the trout contracted with acetylcholine, the calcium ionophore A23187 initiated endothelium-dependent relaxations which were reversed by methylene blue and abolished by meclofenamate. A23187 contracted turtle aortas; an effect reduced by endothelium removal. These data demonstrate endothelium-dependent relaxations and contractions in blood vessels of reptiles, amphibians and teleosts. Thus, endothelium-dependent modulation of the responses of the vascular smooth muscle represents a cardiovascular regulatory mechanism which appears early in vertebrate phylogeny.

ISSN:1018-1172    

DOI:10.1159/000158643

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Three types of vasorelaxants were used to test the responses of canine veins isolated from 13 different sites: isoproterenol, papaverine and nitroglycerin. Strips were preconstricted with methoxamine (5 × 10–6–10–5 M), KC1 (50 mM) and PGF2α (1 µg/ml), and were relaxed by cumulative addition of relaxants. Isoproterenol caused more than 80% relaxation after preconstriction with methoxamine in cephalic, external jugular, azygos, renal, femoral, lateral saphenous veins and the supradiaphragmatic and infrarenal portions of the inferior vena cava, all of which are veins of the body wall. Pulmonary and splenic veins also showed marked relaxation with isoproterenol. However, maximal relaxation responses of portal, mesenteric veins and segment C of the inferior vena cava (a portion between liver and renal veins), which are embryologically related to the digestive tube, were less than 30%. Similar regional differences in the relaxation responses to isoproterenol were obtained after preconstriction with KC1 or PGF2α. Papaverine and nitroglycerin caused nearly uniform relaxation in all veins, although relaxations of segment C of the inferior vena cava were slightly less than those of other veins. These results indicated that there is a regional difference in the relaxation responses of the canine venous system to isoproterenol, and such a difference may be related to its embr

ISSN:1018-1172    

DOI:10.1159/000158644

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Effects of nicorandil on contractile responses to α1- and α2adrenoceptor agonists were examined in isolated rabbit aorta. Nicorandil (10–6 or 10–5M) inhibited contractile responses to clonidine (CL) and BHT-920 in a concentration-dependent manner, but had no effect on the response to methoxamine (MO). Nifedipine (10–6 and 10–5M) had no significant effect on responses to CL and MO, but it had a noticeable inhibitory effect on the response to BHT-920. In tissues pretreated with phenoxybenzamine, nicorandil (10–5M) inhibited the residual response to MO, and nifedipine (10–5M) inhibited responses to MO and CL. The relationship between maximum contraction and percent receptor occupancy was found to be nonlinear for MO, but was near linear for CL and BHT-920. The inhibitory effect of prazosin (pA2 of about 9) on MO and CL was much greater than that of yohimbine (pA2 of about 6). Nicorandil had no apparent or slight inhibitory effect on responses to potassium and Ca2+, and this inhibitory effect was much less than that of nifedipine. These results indicate that the responses induced by MO, CL, and BHT-920 in the rabbit aorta are due to activation of α1-adrenoceptors. It is also suggested that nicorandil minimally affects voltage-dependent Ca2+ influx and that differential effects of nicorandil on the responses to α1 and α2 agonists may be the result of differeneces in the amount of receptor reserve that exist for MO, CL, and BHT-920 in t

ISSN:1018-1172    

DOI:10.1159/000158645

出版商:S. Karger AG    

年代:1986

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158646

出版商:S. Karger AG    

年代:1986

数据来源: Karger