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Simulation of a cold-stressed finger including the effects of wind, gloves, and cold-induced vasodilatation

JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME 1998年第3期120卷 389-394页

作者： Shitzer, A Bellomo, S Stroschein, LA Gonzalez, RR Pandolf, KB Technion Israel Inst Technol Dept Mech Engn IL-32000 Haifa Israel USA Environm Med Res Inst Natick MA 01760 USA

The thermal response of fingers exposed to cold weather conditions has been simulated Energy balance equations were formulated, in a former study, for the tissue layers and the arterial, venous, and capillary blood vessels. The equations were solved by a finite difference scheme using the Thomas algorithm and the method of alternating directions. At this stage of development the model does not include any autonomic control functions. Model simulations assumed an electrical heating element to be embedded in the glove layers applied on the finger. A 1.3 W power input was calculated for maintaining finger temperatures at their pre-cold exposure level in a 0 degrees C environment. Alternate assumptions of nutritional (low) and basal thigh) blood flows in the finger demonstrated the dominance of this factor in maintaining finger temperatures at comfortable levels. Simulated exposures to still and windy air at 4.17 m/s (15 km/h), indicated the profound chilling effects of wind on fingers in cold environments. Finally, the effects of variable blood flow in the finger, known as "cold-induced vasodilatation," were also investigated. Blood flow variations were assumed to be represented by periodic, symmetric triangular waves allowing for gradual opening-closing cycles of blood supply to the tip of the finger. Results of this part of the simulation were compared with measured records of bare finger temperatures. Good conformity was obtained for a plausible pattern of change in bloodflow, which was assumed to be provided in its entirety to the tip of the finger alone.

关键词：算法动脉/生理学体温毛细血管/生理学衣物冷温度指/血液供给指/生理学模型理论血管舒张/生理学静脉/生理学风人类

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Impaired endothelial function following a meal rich in used cooking fat

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第4期33卷 1050-1055页

作者： Williams, MJA Sutherland, WHF McCormick, MP de Jong, SA Walker, RJ Wilkins, GT Univ Otago Dept Med Dunedin New Zealand

OBJECTIVES The purpose of this study was to test the hypothesis that intake of used cooking fat is associated with impaired endothelial function. BACKGROUND Diets containing high levels of lipid oxidation products may accelerate atherogenesis, but the effect on endothelial function is unknown. METHODS Flow-mediated endothelium-dependent dilation and glyceryl trinitrate-induced endothelium-independent dilation of the brachial artery were investigated in 10 men. Subjects had arterial studies before and 4 h after three test meals: 1) a meal (fat 64.4 g) rich in cooking fat that had been used for deep frying in a fast food restaurant;2) the same meal (fat 64.4 g) rich in unused cooking fat, and 3) a corresponding low fat meal (fat 18.3 g) without added fat. RESULTS Endothelium-dependent dilation decreased between fasting and postprandial studies after the used fat meal (5.9 +/- 2.3% vs. 0.8 +/- 2.2%, p = 0.0003), but there was no significant change after the unused fat meal (5.3 +/- 2.1% vs. 6.0 +/- 2.5%) or low fat meal (5.3 +/- 2.3% vs. 5.4 +/- 3.3%). There was no significant difference in endothelium-independent dilation after any of the meals. Plasma free fatty acid concentration did not change significantly during an), of the meals. The level of postprandial hypertriglyceridemia was not associated with change in endothelial function. CONCLUSIONS Ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function. These findings suggest that intake of degradation products of heated fat contribute to endothelial dysfunction. (J Am Coil Cardiol 1999;33:1050-5) (C) 1999 by the American College of Cardiology.

关键词：膳食脂肪类/副作用内皮血管/病理生理学脂质过氧化作用/生理学饭后期间/生理学甘油三酯类/血液血管舒张/生理学成年人人类男(雄)性中年人

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Lipids and the endothelium

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CARDIOVASCULAR RESEARCH 1999年第2期43卷 308-322页

作者： Dart, AM Chin-Dusting, JPF Alfred Hosp Alfred Baker Med Unit Melbourne Vic Australia Baker Med Res Inst Melbourne Vic Australia

The normal endothelium is characterised by the production of a number of molecules which affect the contractile state of adjacent myocytes and the behavior of formed elements within the blood stream, and by the absence of cell surface adhesion molecules. In addition, endothelial cells are important modulators of coagulation and fibrinolysis. Whilst effects of lipids have been documented on many of these endothelial processes, there is particularly strong evidence for effects on the vasodilatation mediated by endothelium derived nitric oxide and on the interaction between leukocytes and the endothelial surface. Both LDL cholesterol and triglyceride rich lipoproteins impair endothelium dependent vasodilatation. The effects of LDL cholesterol are primarily evident for lipoprotein particles that have been oxidised with evidence for effects of specific constituents of oxidised LDL, such as lysophosphatidylcholine (LPC). LDL effects have been demonstrated at numerous sites of the nitric oxide signaling pathway including receptor-G protein coupling, nitric oxide synthase and NO bioactivity, with evidence for enhanced superoxide formation and the consequent production of the less potent dilator peroxynitrite. The effects of lipids on endothelium dependent vasodilatation can be reversed not only by reducing the level of elevated lipids levels but also by provision of the NOS substrate, L-arginine and by the provision of antioxidants, although the mechanism for these effects are not fully elucidated. The adhesion of leukocytes to the endothelial surface is stimulated by low density and triglyceride rich lipoproteins. As with endothelium dependent vasodilatation, the effects of LDL cholesterol are primarily evident for low-density lipoprotein particles that have been oxidised, and many of the effects of oxidised LDL can be mimicked by LPC. HDL can overcome pro-adhesive effects of oxidised LDL. The effects of LDL on leukocyte adhesion are secondary to the expression of adhesion

关键词：心血管疾病/代谢细胞黏附分子/代谢内皮血管/免疫学内皮血管/代谢白细胞/代谢脂类代谢一氧化氮/代谢血管舒张/生理学动物人类

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Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第24期96卷 14136-14141页

作者： Járai, Z Wagner, JA Varga, K Lake, KD Compton, DR Martin, BR Zimmer, AM Bonner, TI Buckley, NE Mezey, E Razdan, RK Zimmer, A Kunos, G Virginia Commonwealth Univ Med Coll Virginia Dept Pharmacol & Toxicol Richmond VA 23298 USA NIMH Genet Lab Bethesda MD 20892 USA Organix Inc Woburn MA 01801 USA

Cannabinoids, including the endogenous ligand arachidonyl ethanolamide (anandamide), elicit not only neurobehavioral but also cardiovascular effects. Two cannabinoid receptors, CBI and CBZ, have been cloned, and studies with the selective CB1 receptor antagonist SR141716A have implicated peripherally located CBI receptors in the hypotensive action of cannabinoids. In rat mesenteric arteries, anandamide-induced vasodilation is inhibited by SR141716A, but other potent CBI receptor agonists, such as HU210, do not cause vasodilation, which implicates an as-yet-unidentified receptor in this effect. Here we show that "abnormal cannabidiol" (Abn-cbd) is a neurobehaviorally inactive cannabinoid that does not bind to CBI receptors, yet causes SR141716A-sensitive hypotension and mesenteric vasodilation in wild-type mice and in mice lacking CBI receptors or both CB1 and CBZ receptors. Hypotension by Abn-cbd is also inhibited by cannabidiol (20 mu g/g), which does not influence anandamide- or HU-210-induced hypotension. In the rat mesenteric arterial bed, Abn-cbd-induced vasodilation is unaffected by blockade of endothelial NO synthase, cyclooxygenase. or capsaicin receptors, but it is abolished by endothelial denudation. Mesenteric vasodilation by Abn-cbd, but not by acetylcholine, sodium nitroprusside, or capsaicine, is blocked by SR141716A (1 mu M) or by cannabidiol (10 mu M). Abn-cbd-induced vasodilation is also blocked in the presence of charybdotoxin (100 nM) plus apamin (100 nM), a combination of Kf-channel toxins reported to block the release of an endothelium-derived hyperpolarizing factor (EDHF). These findings suggest that Abn-cbd and cannabidiol are a selective agonist and antagonist, respectively, of an as-yet-unidentified endothelial receptor for anandamide, activation of which elicits NO-independent mesenteric vasodilation. possibly by means of the release of EDHF.

关键词：花生四烯酸类/药理学大麻二酚/药理学大麻酚类/拮抗剂和抑制剂大麻酚类/代谢内源性大麻酚类内皮血管/代谢肠系膜动脉/药物作用肠系膜动脉/生理学小鼠近交C57BL 小鼠近交ICR 小鼠基因敲除一氧化氮/代谢哌啶类/药理学多不饱和脂肪酸酰胺类钾通道/代谢前列腺素内过氧化物合酶类/代谢吡唑类/药理学受体大麻酚 CB2 受体大麻酚受体药物/遗传学受体药物/生理学血管舒张/生理学血管舒张药/药理学动物小鼠

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Comparative study of ACE-inhibition, angiotensin II antagonism, and calcium channel blockade on flow-mediated vasodilation in patients with coronary disease (BANFF study)

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第1期35卷 60-66页

作者： Anderson, TJ Elstein, E Haber, H Charbonneau, F Univ Calgary Dept Med Div Cardiovasc Calgary AB Canada McGill Univ Montreal PQ Canada Parke Davis & Co Ann Arbor MI USA

OBJECTIVES To determine the effect of angiotensin-converting enzyme (ACE) inhibition on brachial flow-mediated vasodilation. BACKGROUND Quinapril, an ACE inhibitor with high affinity, has been shown to improve coronary endothelial dysfunction in patients with coronary artery disease. The effectiveness of different vasoactive agents to improve human endothelial function is unknown. METHODS High resolution ultrasound was used to assess endothelium-dependent brachial artery flow-mediated vasodilation (FMD) in patients with coronary disease. We studied 80 patients (mean age 58 +/- 0.9 years) in a partial-block, cross-over design trial. Patients were randomized to one of four different drug sequences to receive quinapril 20 mg, enalapril 10 mg, losartan 50 mg or amlodipine 5 mg daily. Each patient received three drugs with a two-week washout period between treatments. The primary end point was the absolute difference in FMD after eight weeks of each study drug compared with their respective baselines analyzed in a blinded fashion. RESULTS There was mild impairment of FMD at baseline (7.3 +/- 0.6%). The change in FMD from baseline was significant only for quinapril (1.8 +/- 1%, p < 0.02). No change was seen with losartan (0.8 +/- 1.1%, p = 0.57), amlodipine (0.3 +/- 0.9%, p = 0.97) or enalapril (-0.2 +/- 0.8%, p = 0.84). No significant change in nitroglycerin-induced dilation occurred with drug therapy. The improvement in quinapril response was not seen in those with the DD ACE genotype (0.5 +/- 2.1%) but was seen in those with the ID and II genotype (3.3 +/- 1.2 and 3.2 +/- 1.9%, respectively, p = 0.03). CONCLUSION Only quinapril was associated with significant improvement in FMD, and this response is related to the presence of the insertion allele of the ACE genotype. (C) 1999 by the American College of Cardiology.

关键词：氨氯地平/投药和剂量氨氯地平/副作用血管紧张素Ⅱ/投药和剂量血管紧张素Ⅱ/生理学血管紧张素转换酶抑制药/投药和剂量血管紧张素转换酶抑制药/副作用血流速度/药物作用血流速度/生理学钙通道阻滞药/投药和剂量钙通道阻滞药/副作用冠状动脉循环/药物作用冠状动脉循环/生理学冠心病/药物疗法冠心病/病理生理学药物疗法联合依那普利/投药和剂量依那普利/副作用内皮血管/药物作用内皮血管/病理生理学异喹啉类/投药和剂量异喹啉类/副作用洛沙坦/投药和剂量洛沙坦/副作用四氢异喹啉类血管舒张/药物作用血管舒张/生理学老年人女(雌)性人类男(雄)性中年人

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Vitamin E supplementation improves endothelial function in type I diabetes mellitus: A randomized, placebo-controlled study

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第1期36卷 94-102页

作者： Skyrme-Jones, RAP O'Brien, RC Berry, KL Meredith, IT Monash Med Ctr Ctr Heart & Chest Res Melbourne Vic Australia Monash Med Ctr Dept Med Melbourne Vic Australia Monash Univ Ctr Heart & Chest Res Melbourne Vic 3168 Australia Monash Univ Dept Med Melbourne Vic 3168 Australia

OBJECTIVE We sought to determine, in a double-blind, placebo-controlled, randomized study, whether vitamin E supplementation (1,000 IU for three months) would improve impaired conduit and resistance vessel endothelial vasodilator function (EVF) and systemic arterial compliance (SAC) in type I diabetes mellitus (DM). BACKGROUND Oxidative stress is thought to be important in the pathogenesis of impaired EVF. Consistent with this hypothesis, we have recently shown that impaired EVF is related to low density lipoprotein (LDL) vitamin E content (VEC) in young subjects with type 1 DM. METHODS We assessed EVF in the brachial artery (using noninvasive ultrasound, flow-mediated vasodilation [FMD];n = 41) and in the forearm resistance vessels (by flow responses to intrabrachial acetylcholine [ACh];n = 21) and measured SAC (simultaneous aortic blood flow and carotid pressure measurements;n = 41) before and after active or placebo therapy. RESULTS The LDL VEC was increased by 127% after supplementation, resulting in a significant reduction in the oxidative susceptibility of LDL. There was no time-dependent change in FMD or in the response to ACh or SAC in the placebo group. A significant improvement in FMD (2.6 +/- 0.6% to 7.0 +/- 0.7%, p < 0.005) and the dose response to ACh (p < 0.05) were observed in those randomized to vitamin E therapy. Systemic arterial compliance was not affected by vitamin E (0.41 +/- 0.03 vs. 0.49 +/- 0.06 arbitrary compliance units, p = NS). The change in FMD was related to the change in LDL VEC (r = 0.42, p < 0.05) and the change in the oxidative susceptibility of LDL (r = 0.64, p < 0.0001). CONCLUSION Short-term daily oral supplementation with vitamin E improves EVF in both the conduit and resistance vessels of young subjects with type I DM. (J Am Cell Cardiol 2000;36:44-102) (C) 2000 by the American College of Cardiology.

关键词：投药口服血流速度/药物作用血压肱动脉/诊断显像肱动脉/药物作用肱动脉/代谢顺应性/药物作用糖尿病 1型/血液糖尿病 1型/药物疗法糖尿病 1型/病理生理学营养保健品双盲法内皮血管/药物作用内皮血管/代谢内皮血管/病理生理学脂蛋白类 LDL/血液氧化性应激/药物作用体积描记术治疗结果超声检查血管阻力/药物作用血管阻力/生理学血管舒张/药物作用血管舒张/生理学维生素E/投药和剂量成年人女(雌)性人类男(雄)性

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Role of nitric oxide in the pathogenesis of chronic pulmonary hypertension

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PHYSIOLOGICAL REVIEWS 2000年第4期80卷 1337-1372页

作者： Hampl, V Herget, J Charles Univ Prague Sch Med 2 Dept Physiol Prague 15000 5 Motol Czech Republic

Chronic pulmonary hypertension is a serious complication of a number of chronic lung and heart diseases. In addition to vasoconstriction, its pathogenesis includes injury to the peripheral pulmonary arteries leading to their structural remodeling. Increased pulmonary vascular synthesis of an endogenous vasodilator, nitric oxide (NO), opposes excessive increases of intravascular pressure during acute pulmonary vasoconstriction and chronic pulmonary hypertension, although evidence for reduced NO activity in pulmonary hypertension has also been presented. NO can modulate the degree of vascular injury and subsequent fibroproduction, which both underlie the development of chronic pulmonary hypertension. On one hand, NO can interrupt vascular wall injury by oxygen radicals produced in increased amounts in pulmonary hypertension. NO can also inhibit pulmonary vascular smooth muscle and fibroblast proliferative response to the injury. On the other hand, NO may combine with oxygen radicals to yield peroxynitrite and other related, highly reactive compounds. The oxidants formed in this manner may exert cytotoxic and collagenolytic effects and, therefore, promote the process of reparative vascular remodeling. The balance between the protective and adverse effects of NO is determined by the relative amounts of NO and reactive oxygen species. We speculate that this balance may be shifted toward more severe injury especially during exacerbations of chronic diseases associated with pulmonary hypertension. Targeting these adverse effects of NO-derived radicals on vascular structure represents a potential novel therapeutic approach to pulmonary hypertension in chronic lung diseases.

关键词：慢性病内皮血管/药物作用内皮血管/代谢酶抑制剂/药理学自由基/代谢自由基/药理学高血压肺性/病因学高血压肺性/代谢肺/血液供给肺/药物作用肺/胚胎学一氧化氮/代谢一氧化氮/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Ⅱ型一氧化氮合酶Ⅲ型肺循环/药物作用肺循环/生理学血管阻力/药物作用血管阻力/生理学血管收缩/药物作用血管收缩/生理学血管舒张/药物作用血管舒张/生理学成年人动物人类婴儿新生

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Pharmacological examination of the neurokinin-1 receptor mediating relaxation of human intralobar pulmonary artery

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 319-325页

作者： Pedersen, KE Buckner, CK Meeker, SN Undem, BJ Johns Hopkins Univ Sch Med Johns Hopkins Asthma & Allergy Ctr Baltimore MD 21224 USA Univ Oklahoma Coll Pharm Oklahoma City OK USA

The effect of selective tachykinin receptor agonists and antagonists on human isolated intralobar pulmonary arterial rings was investigated. Neither Substance P (SP) nor neurokinin A (NKA) contracted the arteries. Both of these agonists, however, were potent and efficacious at relaxing the arteries that were precontracted with phenylephrine. The negative log (M) EC50 values for SP and NKA were 9.0 and 8.3, respectively. The neurokinin (NK)-3 selective agonist, senktide-analog, and the NK-2 receptor selective agonist, [beta-Ala(8)]NKA(4-10), caused neither contractions nor relaxations of the arteries, whereas the NK-1 receptor agonist Ac-[Arg6, Sar9, Met(O2)11] SP( 6-11) (ASM-SP) relaxed the tissue with a potency similar to SP. The relaxations to SP, NKA, and ASM-SP were competitively antagonized by the selective NK-1 receptor antagonist CP 99994, with a pK(b) in the nanomolar range. Antagonism of the ASM-SP-induced relaxations was also noted with FK 888, RP 67580, and L 732,138, although these antagonists were much less potent than CP 99994 in this regard. Another NK-1 receptor selective antagonist, SR 140333, caused an insurmountable antagonism of the SP-induced relaxations. The NK-1 receptor-mediated relaxations could be blocked by removing the endothelium, or by a combination of N- nitro-L-arginine and indomethacin. Measurement of prostanoid generation revealed that in endothelial-intact but not endothelial-denuded tissue, ASM-SP caused a selective increase in the production of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin. The results indicate that stimulation of NK-1 receptors leads to relaxation of human intralobar pulmonary arteries, which is mediated largely by nitric oxide and prostacyclin released from the endothelium of these vessels.

关键词：剂量效应关系药物药物相互作用内皮血管/生理学依前列醇/生理学依前列醇/分泌肺/生理学神经激肽A/药理学一氧化氮/生理学肽碎片/药理学苯福林/药理学肺动脉/生理学受体神经激肽1/生理学受体速激肽/激动剂受体速激肽/拮抗剂和抑制剂 P物质/类似物和衍生物 P物质/药理学血管收缩/药物作用血管舒张/生理学青少年成年人女(雌)性人类男(雄)性中年人

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Heterogeneity of endothelium-dependent vasodilation in pressurized cerebral and small mesenteric resistance arteries of the rat

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第2期290卷 832-839页

作者： Lagaud, GJL Skarsgard, PL Laher, I Van Breemen, C Univ British Columbia Fac Med Dept Pharmacol & Therapeut Vancouver BC V6T 1Z3 Canada St Pauls Hosp Vancouver Vasc Biol Res Ctr Vancouver BC V6Z 1Y6 Canada

We compared endothelial responses to calcium-mobilizing agents in mesenteric and cerebral resistance arteries of the rat. Middle cerebral and small mesenteric arteries were mounted in a pressure myograph, and myogenic responses were recorded. The effects of acetylcholine (ACh), bradykinin, substance P, histamine, A23187, cyclopiazonic acid (CPA), and sodium nitroprusside were investigated in both arteries with myogenic tone in the absence and presence of nitric oxide synthase and cyclooxygenase inhibitors. The effects of raised potassium, K+ channel blockers, and arachidonic metabolism inhibition were examined on the nitric oxide (NO) synthase/cyclooxygenase inhibitor-resistant dilation induced by ACh and CPA. Cerebral arteries display a high level of myogenic reactivity compared with mesenteric arteries. In cerebral arteries, only bradykinin and substance P induced endothelium-dependent dilation. The observed dilation was solely related to the activation of the NO pathway. However, in mesenteric arteries, all of the vasoactive agents induced endothelium-dependent dilation. A combination of NO, cyclooxygenase-devived prostanoids, and a factor with endothelium-derived hyperpolarizing factor-like properties was responsible for the observed vasodilation. NO and cyclooxygenase derivatives were able to compensate for each other in the CPA-induced endothelium-dependent: vasodilation when one of the two pathways was blocked. Moreover, small Ca2+-activated K+ channels and a combination of both large and small Ca2+-activated K+ channels were implicated in the endothelium-derived hyperpolarizing factor-like component of dilation to ACh and CPA, respectively. Finally, the results suggest that the pathway by which agonists raise intracellular calcium concentration may determine the nature of the endothelial secretory product.

关键词：生物因子/生理学钙/代谢脑动脉/药物作用脑动脉/生理学环加氧酶抑制药/药理学内皮血管/药物作用内皮血管/生理学肠系膜动脉/药物作用肠系膜动脉/生理学肌张力/药物作用肌张力/生理学肌平滑血管/药物作用肌平滑血管/生理学一氧化氮合酶/拮抗剂和抑制剂钾通道/激动剂钾通道钙激活压力大鼠 Sprague-Dawley 信号传导/药物作用信号传导/生理学小电导钙激活钾通道血管阻力/药物作用血管阻力/生理学血管舒张/药物作用血管舒张/生理学动物男(雄)性大鼠

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Noninvasive determination of endothelium-mediated vasodilation as a screening test for coronary artery disease: Pilot study to assess the predictive value in comparison with angina pectoris, exercise electrocardiography, and myocardial perfusion imaging

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AMERICAN HEART JOURNAL 1999年第4期138卷 731-739页

作者： Schroeder, S Enderle, MD Ossen, R Meisner, C Baumbach, A Pfohl, M Herdeg, C Oberhoff, M Haering, HU Karsch, KR Univ Tubingen Dept Med Div Cardiol D-72076 Tubingen Germany Univ Tubingen Dept Med Inst Med Informat Proc Div Endocrinol D-72076 Tubingen Germany

Background Peripheral endothelial dysfunction (ED) quantified by the determination of flow-mediated dilation (FMD%) of the brachial artery with the use of high-resolution ultrasound is an early marker of atherosclerosis. Although a positive correlation with coronary artery disease (CAD) has been reported, the unanswered clinical question is the validity of FMD% as a screening test in patients with clinical suspicion of CAD. Thus the aim of this study was to determine the predictive value of FMD% compared with angina pectoris, exercise electrocardiography, and myocardial perfusion imaging. Methods and Results In this pilot study, we measured ED in 122 patients scheduled for coronary angiography by using high-resolution ultrasound (13 MHz). We defined ED as FMD% less than or equal to 4.5%. The presence of CAD was defined as angiographically detectable atherosclerotic vessel alterations of any degree. Exercise electrocardiography and myocardial perfusion imaging had been performed on an outpatient basis. Statistical analysis was conducted by analysis of variance and Mantel-Haenszel chi-square test. Patients with CAD (n = 101) had a significantly lower FMD% than patients without CAD (n = 21;3.7% +/- 4.1% vs 7.01% +/- 3.5%, P < .001). A sensitivity of 71%, a specificity of 81% with a positive predictive value of 0.95 (72 of 76), and a negative predictive value of 0.41 (17 of 46) was calculated. In comparison to angina pectoris (sensitivity 95%, specificity 47.6%), exercise electrocardiography (sensitivity 82.4%, specificity 57.1%) and myocardial perfusion imaging (sensitivity in our study group 100%) had the best specificity, and a high sensitivity for FMD% was found. Conclusions The determination of ED was found to be a sensitive and specific screening test to predict the presence of CAD. Because this is a noninvasive, nonradioactive, and cost-effective approach, ii warrants further evaluation to determine its value in daily clinical practice as an additional screening

关键词：心绞痛/诊断肱动脉/超声检查冠心病/诊断冠心病/流行病学心电描记术内皮血管/生理学运动试验心脏/放射性核素显像普查试点项目试验预期值前瞻性研究敏感性与特异性超声检查/方法血管舒张/生理学女(雌)性人类男(雄)性中年人

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