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Enhanced peripheral vasodilation in humans after a fatty meal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第2期36卷 417-422页

作者： Raitakari, OT Lai, N Griffiths, K McCredie, R Sullivan, D Celermajer, DS Royal Prince Alfred Hosp Dept Cardiol Camperdown NSW 2050 Australia Royal Prince Alfred Hosp Dept Clin Biochem Camperdown NSW 2050 Australia Univ Sydney Dept Med Sydney NSW 2006 Australia Turku Univ Cent Hosp Dept Clin Physiol FIN-20520 Turku Finland

OBJECTIVES We sought to study the effects of a fatty meal on vascular reactivity, including endothelial function and maximal vasodilation. BACKGROUND Recent reports regarding the physiological changes in peripheral vasculature after eating a fatty meal have been controversial. METHODS Twelve volunteers were studied before, 3 h after, and 6 h after a high-fat meal (1030 kcal, 61 g fat) rich in saturated fatty acids, and 10 were restudied after a similar meal rich in monounsaturated fatty acids. Endothelial function was assessed as flow-mediated dilatation (FMD) in the brachial artery using ultrasound. Resting and postischemic forearm blood flow (FBF) were recorded using venous occlusion strain-gauge plethysmography, before, and every 10 to 15 s after, 5 min upper arm ischemia. RESULTS Brachial artery basal diameter, resting FBF and postischemic hyperemia increased after high-fat meats (all p < 0.001), whereas FMD did not change. The increase in resting FBF correlated with increases in postprandial insulin (r = 0.80, p < 0.002) and triglyceride (r = 0.77, p < 0.005) levels. CONCLUSIONS We concluded that eating a fatty meal induces vasodilation and increases resting and stimulated FBF and that these observations are probably mediated by postprandial changes in insulin and/or triglyceride levels. The metabolic changes that occur after meals are not associated with impaired endothelial nitric oxide release in the conduit arteries, (C) 2000 by the American College of Cardiology.

关键词：动脉/生理学胆固醇/血液膳食脂肪类/药理学内皮血管/药物作用前臂/血液供给高半胱氨酸/血液充血/病理生理学体积描记术饭后期间/生理学局部血流血管舒张/药物作用青少年成年人女(雌)性人类男(雄)性

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Diadenosine polyphosphates cause contraction and relaxation in isolated rat resistance arteries

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期294卷 1175-1181页

作者： Steinmetz, M Schlatter, E Boudier, HAJS Rahn, KH De Mey, JGR Univ Munster Med Poliklin D-48129 Munster Germany Univ Maastricht Cardiovasc Res Inst Maastricht Dept Pharmacol & Toxicol Maastricht Netherlands

The effects of diadenosine polyphosphates (APnA;n = 3-6) and adenine nucleotides on contractile reactivity of isolated rat mesenteric resistance arteries (MrA) and superior epigastric arteries (SEA), which display a dense and sparse autonomic innervation, respectively, were evaluated. All agonists examined, except adenosine and AMP, induced contractions. The rank order of potency was similar in both arteries: alpha,beta-methylene ATP (alpha,beta-meATP) > AP5A > AP6A > AP4A > ATP > ADP > APBA. Contractions were stable during several minutes in SEA but highly transient in MrA. They were reduced after exposure to 10 mu M alpha,beta-meATP and by 10 mu M of the P2X antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid. During phenylephrine (10 mu M)-induced contractions, the agonists induced a further contraction in SEA. In MrA, however, further contraction was followed by marked relaxation. The rank order of relaxing potency was comparable to that of the contractile potency of agonists. Also, the relaxing effects of APnA were blunted by 10 mu M pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and after exposure to alpha,beta-meATP. In vitro and in vivo sympathectomy with 6-hydroxydopamine and removal of the endothelium did not modify the effects of APnA in MrA. Thus, the contractile effects of APnA in resistance arteries 1) are due to a P2X purinoceptor-mediated stimulation of the smooth muscle;2) depend on the length of the phosphate chain;acid 3) are followed by endothelium-independent relaxing effects in MrA but not SEA, which may involve receptors that are similar to those mediating contraction. The regional heterogeneity of APnA effects cannot be attributed to a direct neurogenic influence.

关键词：腺嘌呤核苷酸类/药理学腺嘌呤核苷酸类/生理学腺苷/药理学腺苷二磷酸/药理学腺苷一磷酸/药理学腺苷三磷酸/药理学二核苷磷酸类/药理学二核苷磷酸类/生理学内皮血管/生理学腹壁动脉/药物作用腹壁动脉/生理学肠系膜动脉/药物作用肠系膜动脉/生理学肌收缩/药物作用肌松弛/药物作用肌平滑血管/药物作用肌平滑血管/生理学磷酸吡哆醛/类似物和衍生物磷酸吡哆醛/药理学大鼠近交WKY 受体嘌呤能P2/拮抗剂和抑制剂受体嘌呤能P2/生理学交感神经切除术血管阻力动物男(雄)性大鼠

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Utilizing granulocyte colony-stimulating factor to enhance vascular graft endothelialization from circulating blood cells

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ANNALS OF VASCULAR SURGERY 2002年第3期16卷 314-320页

作者： Shi, Q Bhattacharya, V Hong-De Wu, M Sauvage, LR Providence Seattle Med Ctr Hope Heart Inst Seattle WA 98122 USA Univ Washington Sch Med Dept Surg Seattle WA 98195 USA

Cells in the blood circulating through a vascular graft can contribute to endothelialization of its flow surface. We hypothesized that granulocyte colony-stimulating factor (G-CSF) could enhance this process by increasing circulating bone marrow progenitor cells. Ten dogs received composite grafts that were shielded from any source of endothelialization other than the circulating blood. On the seventh postoperative day and for 7 days thereafter, five dogs were injected subcutaneously with 10 mug/kg/day of human G-CSF. The additional five dogs, used as controls, received no G-CSF. Grafts were retrieved at 4 weeks. All dogs recovered promptly postoperatively. White cell counts in G-CSF dogs increased by an average of 9.5-fold at the end of treatment, and had returned to normal before retrieval. All grafts remained patent. G-CSF grafts had significantly higher endothelialization than the controls (82.2 +/- 9.2% vs. 23.7 +/- 4.4%, p = 0.0004), with extensive flow surface neointima, covered with a single layer of endothelium verified by FVIII/vWF and CD34 staining. Control grafts had virtually no neointima and were covered with a thin layer of fibrin coagulum. Significantly more endothelial-lined microvessels were also found in the G-CSF grafts than in the controls. Dogs treated with G-CSF have increased endothelialization of synthetic vascular grafts due to increased circulating bone marrow progenitor cells.

关键词：人工血管血管假体植入内皮血管/药物作用粒细胞集落刺激因子/药理学造血干细胞/药物作用白细胞计数血管未闭动物狗女(雌)性男(雄)性

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Ethanol enhances basal and flow-stimulated nitric oxide synthase activity in vitro by activating an inhibitory guanine nucleotide binding protein

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期289卷 1293-1300页

作者： Hendrickson, RJ Cahill, PA Sitzmann, JV Redmond, EM Georgetown Univ Med Ctr Dept Surg Pasquerilla Healthcare Ctr Washington DC 20007 USA

The aim of this study was to determine the effect of ethanol on endothelial nitric oxide synthase (eNOS), the enzyme responsible for the production of the important vasoactive agent nitric oxide. The effect of ethanol (0.8-160 mM) on both basal and flow-stimulated eNOS activity was determined using cultured bovine aortic endothelial cells (EC), In "static" EC ethanol dose-dependently increased basal eNOS activity with a maximum response (similar to 2.0-fold increase) achieved at 40 mM in the absence of any effect on cell viability or nitric oxide synthase protein expression. Pertussis toxin (PTX) pretreatment significantly inhibited the ethanol-induced increase in basal eNOS activity. EC exposed to steady laminar flow exhibited a flow- and time-dependent increase in eNOS activity. Ethanol significantly enhanced the laminar flow-induced eNOS response from 0.62 +/- 0.1 to 1.06 +/- 0.06 pmol [C-14]citrulline/mg/min, a response that was inhibited by PTX, PTX-catalyzed ribosylation of Gi alpha substrates, an index of G-protein functional activity, was increased in laminar flow-exposed EC compared with static controls and was further enhanced by ethanol treatment. Likewise, EC exposed to low (similar to 0.5 dynes/cm(2)) and high (similar to 12 dynes/cm(2)) pulsatile flow demonstrated increased eNOS activity, an effect that was associated with increased PTX-catalyzed ribosylation of Gi alpha substrates, Ethanol enhanced the low flow response in a PTX-sensitive manner. These data demonstrate a stimulatory effect of ethanol on basal and flow-stimulated eNOS activity, mediated in part by a mechanism involving a PTX-sensitive G protein.

关键词：主动脉细胞存活/药物作用细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活乙醇/药理学 GTP结合蛋白质α亚单位 Gi-Go/代谢 GTP结合蛋白质类/药物作用 GTP结合蛋白质类/代谢动力学一氧化氮合酶/代谢一氧化氮合酶Ⅲ型百白咳毒素应力物理时间因素毒力因子鲍特菌属/药理学动物牛

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The endothelial component of cannabinoid-induced relaxation in rabbit mesenteric artery depends on gap junctional communication

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期520卷 539-550页

作者： Chaytor, AT Martin, PEM Evans, WH Randall, MD Griffith, TM Univ Wales Coll Med Dept Diagnost Radiol Cardiovasc Sci Res Grp Cardiff CF4 4XN S Glam Wales Univ Wales Coll Med Dept Biochem Med Cardiovasc Sci Res Grp Cardiff CF4 4XN S Glam Wales Univ Nottingham Sch Med Sch Biomed Sci Queens Med Ctr Nottingham NG7 2UH England

1. We have shown that the endocannabinoid anandamide and its stable analogue methanandamide relax rings of rabbit superior mesenteric artery through endothelium-dependent and -independent mechanisms that are unaffected by blockade of NO synthase and cyclooxygenase. 2. The endothelium-dependent component of the responses was attenuated by the gap junction inhibitor 18 alpha-glycyrrhetinic acid (18 alpha-GA;50 mu m), and a synthetic connexin-mimetic peptide homologous to the extracellular Gap 27 sequence of connexin 43 ((43)Gap 27, SRPTEKTIFII;300 mu M) By contrast, the corresponding connexin 40 peptide ((40)Gap 27, SRPTEKNVFIV) was inactive. 3. The cannabinoid CB1 receptor antagonist SR141716A (10 mu M) also attenuated endothelium-dependent relaxations but this inhibition nas not observed with the CB, receptor antagonist LY320135 (10 mu M) Furthermore, SR141716A mimicked the effects of (43)Gap 27 peptide in blocking Lucifer Yellow dye transfer between coupled COS-7 cells (a monkey fibroblast cell line), whereas LY320135 was without effect, thus suggesting that the action of SR141716A was directly attributable to effects on gap junctions. 4. The endothelium-dependent component of cannabinoid-induced relaxation was also attenuated by AM404 (10 mu M), an inhibitor of the high-affinity anandamide transporter, which was without effect on dye transfer. 5. Taken together, the findings suggest that cannabinoids derived from arachidonic acid gain access to the endothelial cytosol via a transporter mechanism and subsequently stimulate relaxation by promoting diffusion of an endothelium-derived hyperpolarizing factor to adjacent smooth muscle cells via gap junctions. 6. Relaxations of endothelium-denuded preparations to anandamide and methanandamide were unaffected by (43)Gap 27 peptide, 18 alpha-GA, SR141716A, AM404 and indomethacin and their genesis remains to be established.

关键词：乙酰胆碱/药理学花生四烯酸类/药理学苯呋喃类/药理学 COS细胞大麻酚类/拮抗剂和抑制剂大麻酚类/药理学内源性大麻酚类缝隙接合部/药物作用缝隙接合部/生理学甘草次酸/类似物和衍生物甘草次酸/药理学吲哚美辛/药理学异喹啉类肠系膜上动脉/药物作用肠系膜上动脉/代谢肌松弛肌平滑血管/药物作用肌平滑血管/代谢 NG-硝基精氨酸甲酯/药理学苯福林/药理学哌啶类/药理学多不饱和脂肪酸酰胺类吡唑类/药理学受体大麻酚受体药物/拮抗剂和抑制剂受体药物/代谢动物男(雄)性兔

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Differences in neointima formation between impervious and porous polytetrafluoroethylene vascular patch material

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ANNALS OF VASCULAR SURGERY 2002年第4期16卷 407-412页

作者： Wong, P Hopkins, S Vincente, D Williams, K Macri, N Berguer, R Wayne State Univ Harper Hosp Div Vasc Surg Detroit MI 48201 USA

The aim of this study was to compare the neointima formation and blood loss of an impervious ePTFE with those of the porous ePTFE patch. Ten mongrel dogs were selected for the study. Both the impervious and porous ePTFE patches were implanted into the common iliac arteries in each dog. The blood loss of each patch was recorded and the patches were explanted 30-60 days later for microscopic analysis. The arteries with either the impervious or the porous ePTFE patch were all patent at the end of the study. The impervious ePTFE patch had a significant reduction in blood loss when compared with the porous ePTFE patch (rho = 0.04). The neointima covering both patches showed no statistically significant difference in its thickness or in its cellular composition. It has been speculated that wall porosity is essential for tissue ingrowth, endothelial cell proliferation, and neointima formation. In this study, the impervious ePTFE patch did not inhibit neointima formation. Our study shows that graft porosity does not improve neointima formation or patency. Neointimization of the impervious ePTFE patch is the result of pannus ingrowth and deposition of circulating blood elements. There is a statistically significant reduction in blood loss (p = 0.04) with impervious ePTFE patch, compared with that of the porous ePTFE patch.

关键词：生物相容性材料/药理学失血手术人工血管内皮血管/药物作用内皮血管/生理学髂动脉/外科学聚四氟乙烯/药理学多孔性动物狗

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RGD-dependent vacuolation and lumen formation observed during endothelial cell morphogenesis in three-dimensional fibrin matrices involves the α_vβ₃ and α₅β₁ integrins

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AMERICAN JOURNAL OF PATHOLOGY 2000年第5期156卷 1673-1683页

作者： Bayless, KJ Salazar, R Davis, GE Texas A&M Univ Ctr Hlth Sci Dept Pathol & Lab Med College Stn TX 77843 USA

Recent data have revealed the involvement of the alpha(v)beta(3) integrin in angiogenesis. However, few studies to date have provided, a convincing role for this receptor in in vitro assays of endothelial cell morphogenesis where defined steps can be examined. Here, we present data showing that two integrins, alpha(v)beta(3) and alpha(5)beta(1), regulate human endothelial cell vacuolation and lumen formation in three-dimensional fibrin matrices. Cells resuspended in fibrin formed intracellular vacuoles that coalesced into lumenal structures. These morphogenic events were completely inhibited by the simultaneous addition of anti-alpha(v)beta(3) and anti-alpha(5) integrin antibodies. Complete blockade was also accomplished with a combination of the cyclic Arg-Gly-Asp (cRGD) peptide and anti-alpha(5) integrin antibodies. No blockade was observed with the control Arg-Gly-Glu (RGE) peptide alone or in combination with control antibodies. Finally, we were able to demonstrate regression of vacuoles and lumens several hours after the addition of cRGD peptides combined with anti-alpha(5) integrin antibodies. These effects were not observed with control peptides alone or in combination with control antibodies. We report here the novel involvement of both the alpha(v)beta(3) and alpha(5)beta(1) integrins in vacuolation and lumen formation in a fibrin matrix, implicating a role for multiple integrins in endothelial cell morphogenesis.

关键词：抗体单克隆/药理学细胞培养技术/方法细胞系内皮血管/细胞学内皮血管/药物作用内皮血管/代谢纤维蛋白/药理学新生血管化生理性/药物作用寡肽类/药理学肽类环/药理学受体纤连蛋白/免疫学受体纤连蛋白/生理学受体玻连蛋白/免疫学受体玻连蛋白/生理学时间因素空泡/药物作用空泡/代谢人类

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4-(3-chloro-4-methoxybenzyl) aminophthalazines: Synthesis and inhibitory activity toward phosphodiesterase 5

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JOURNAL OF MEDICINAL CHEMISTRY 2000年第13期43卷 2523-2529页

作者： Watanabe, N Adachi, H Takase, Y Ozaki, H Matsukura, M Miyazaki, K Ishibashi, K Ishihara, H Kodama, K Nishino, M Kakiki, M Kabasawa, Y Eisai & Co Ltd Tsukuba Res Labs Tsukuba Ibaraki 3002635 Japan

We synthesized various 4-(3-chloro-4-methoxybenzyl)aminophthalazines substituted at the 1- and 6-positions and evaluated their inhibitory activity toward phosphodiesterase 5 (PDE5) and their vasorelaxant activity in isolated porcine coronary arteries precontracted with prostaglandin F2 alpha (10(-5) M). The preferred substituents at the 1-position of the phthalazine were 4-hydroxypiperidino, 4-hydroxymethylpiperidino, 4-(2-hydroxyethyl)piperidino, and 4-oxopiperidino. Among these compounds, [4-(3-chloro-4-methoxybenzyl)amino-1-(4-hydroxy)piperidino]-6-phthalazinecarbonitrile monohydrochloride (13) exhibited potent PDE5 inhibitory activity (IC50 = 0.56 nM) with > 1700-fold high selectivity over other PDE isozymes (PDE1-4). Compound 13 exhibited the most potent vasorelaxant action (EC50 = 13 nM) in this series of compounds. Compound 13 reduced mean pulmonary arterial pressure by 29.9 +/- 3.1% when administered intravenously at 30 mu g/kg to the chronically hypoxic rats and had an apparent oral bioavailability of about 19.5% in rats and was selected for further biological evaluation.

关键词： 3' 5'-环GMP磷酸二酯酶类抗高血压药/化学合成抗高血压药/化学抗高血压药/药代动力学抗高血压药/药理学生物利用度血压/药物作用冠状血管/药物作用冠状血管/生理学环核苷酸磷酸二酯酶类 5型地诺前列素/药理学高血压肺性/药物疗法高血压肺性/病理生理学肌松弛/药物作用肌平滑血管/药物作用肌平滑血管/生理学磷酸二酯酶抑制剂/化学合成磷酸二酯酶抑制剂/化学磷酸二酯酶抑制剂/药代动力学磷酸二酯酶抑制剂/药理学磷酸二酯水解酶类/代谢酞嗪类/化学合成酞嗪类/化学酞嗪类/药代动力学酞嗪类/药理学哌啶类/化学合成哌啶类/化学哌啶类/药代动力学哌啶类/药理学喹唑啉类/药理学大鼠 Sprague-Dawley 构效关系猪血管舒张药/化学合成血管舒张药/化学血管舒张药/药代动力学血管舒张药/药理学动物男(雄)性大鼠

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Nitric oxide synthase 3-dependent vascular remodeling and circulatory dysfunction in cirrhosis

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AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 1985-1993页

作者： Fernández-Varo, G Ros, J Morales-Ruiz, M Cejudo-Martín, P Arroyo, V Solé, M Rivera, F Rodés, J Jiménez, W Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Hormonal Lab E-08036 Barcelona Spain Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Liver Unit E-08036 Barcelona Spain Univ Barcelona Hosp Clin Barcelona Inst Invest Biomed August Pi i Sunyer Dept Pathol E-08036 Barcelona Spain Inst Reina Sofia Invest Nefrol Barcelona Spain

Vascular remodeling is an active process that consists in important modifications in the vessel wall. Endothelium derived nitric oxide (NO) plays a major role in this phenomenon. We assessed wall thickness (WT), total wall area (TWA), lumen diameter, and total nuclei number/cross-section (TN) in cirrhotic rats with ascites;and in control rats. A second group of cirrhotic rats received the NO synthesis inhibitor, L-NAME, or vehicle daily for 11 weeks and systemic hemodynamics, arterial compliance, aortic NO synthase 3 (NOS3) protein expression, and vascular morphology were analyzed. Cirrhotic vessels showed a significant reduction in WT, TWA, and TN as compared to control vessels. Long-term inhibition of NOS activity in cirrhotic rats resulted in a significant increase in WT, TWA, and TN as compared to cirrhotic rats receiving vehicle. NOS3 protein abundance was higher in aortic vessels of nontreated cirrhotic animals than in controls. This difference was abolished by chronic treatment with L-NAME. NOS inhibition in cirrhotic rats resulted in higher arterial pressure and peripheral resistance and lower arterial compliance than cirrhotic rats receiving vehicle. Therefore, vascular remodeling in cirrhosis with ascites is a generalized process with significant functional consequences that can be negatively modulated by long-term inhibition of NOS activity. (Am J Pathol 2003, 162:1985-1993)

关键词：主动脉腹/药物作用主动脉腹/病理学主动脉腹/病理生理学主动脉胸/药物作用主动脉胸/病理学主动脉胸/病理生理学动脉/药物作用动脉/病理学动脉/病理生理学腹水/酶学腹水/病理生理学血液循环/药物作用内皮血管/药物作用内皮血管/病理学内皮血管/病理生理学酶抑制剂/药理学纤维化肠系膜动脉/药物作用肠系膜动脉/病理学肠系膜动脉/病理生理学 NG-硝基精氨酸甲酯/药理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅲ型大鼠 Wistar 肾动脉/药物作用肾动脉/病理学肾动脉/病理生理学血管中膜/药物作用血管中膜/病理学血管中膜/病理生理学动物男(雄)性大鼠

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Vascular actions of 17β-oestradiol in rat aorta and mesenteric artery

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JOURNAL OF AUTONOMIC PHARMACOLOGY 1999年第5期19卷 291-299页

作者： Browne, M Connolly, C Docherty, JR Royal Coll Surg Ireland Dept Physiol Dublin 2 Ireland

1 It has been proposed that the cardiovascular protective actions of 17 beta-oestradiol may involve calcium antagonistic actions. We have examined the effects of 17 beta-oestradiol on contractions to noradrenaline and KCl in male rat small mesenteric artery and aorta. 2 In rat mesenteric artery, 17 beta-oestradiol (10 mu m) significantly reduced the maximum contraction to noradrenaline (67.7 +/- 5.8% of control) and KCl (38.8 +/- 3.1% of control) without affecting potency. 3 In rat aorta, 17 beta-oestradiol (10 mu m) also significantly reduced contractions to noradrenaline (77.5 +/- 4.8% of control), and the effects were mimicked by droloxifene (10 mu m). The effect of oestrogen was not prevented by the protein synthesis inhibitor cycloheximide (10 mu m). In experiments carried out in calcium-free solution in which calcium stores were depleted, 17 beta-oestradiol (10 mu m) significantly reduced the contraction to calcium restoration in rat aorta. 4 In aorta from female rats, 17 beta-oestradiol (10 mu m) significantly reduced contractions to noradrenaline (73.6 +/- 10.8% of control), but this effect of oestrogen was not prevented by cycloheximide (10 mu m). 5 In summary, 17 beta-oestradiol diminishes the maximum contractile response to noradrenaline in both rat small mesenteric artery and aorta, an effect which at least in the aorta is mimicked by the oestrogen receptor antagonist/partial agonist droloxifene, and may be due to restriction of calcium entry by a nongenomic action.

关键词：主动脉/药物作用钙/拮抗剂和抑制剂钙/生理学药物相互作用内皮血管/药物作用雌二醇/药理学肠系膜动脉/药物作用肌收缩/药物作用肌松弛/药物作用肌平滑血管/药物作用去甲肾上腺素/药理学氯化钾/药理学大鼠 Wistar 血管收缩药/药理学动物女(雌)性男(雄)性大鼠

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