肝素对内皮细胞增殖和收缩因子释放的影响

目的 观察肝素对内皮细胞增殖与内皮源性收缩因子释放的影响,方法（１）采用人脐静脉ＥＣ的覆盖率,（３）采用人脐静脉ＥＣ培养技术,绘制ＥＣ生长曲线;（２）用扫描电镜观察大鼠颈总动脉血管吻合口ＥＣ的覆盖率;（３４）采用牛主动脉ＥＣ培养及离体血管舒缩功能实验技术,观察肝素对血管的直接解痉作用及培养ＥＣ释放收缩因子的影响。结果 （１）即使浓度高达５００μｇ／ｍｌ的肝素对培养ＥＣ的增殖也无作用,但能明显增强内     

吸烟对血管损伤机制的研究

目的探讨因吸烟致移植或再植组织发生血循环危象的机制。方法（１）对因吸烟而致血循环危象的７例断指再植、组织移植病例进行总结分析。（２）对大鼠进行被动吸烟实验，分成术前被动吸烟组、术后被动吸烟组及正常对照组。应用检测离体血管舒缩功能的方法及扫描电镜技术，观察吸烟对大鼠血管吻合口内皮细胞的愈合过程；尼古丁对离体动脉的舒缩功能及血管内膜完整性的影响。结果临床７例各自在术后不同时间吸烟１次后，３例移植组织和４例再植组织发生血循环危象。实验结果表明：（１）血管吻合后１０天，吸烟组血管吻合口内皮细胞覆盖率为２８％～３２％，而对照组达８５％。（２）尼古丁能使血管环产生浓度依赖性收缩，并且造成血管内皮结构的严重破坏。结论吸烟能延缓内皮细胞愈合、血管收缩与损伤血管内膜，是形成移植与再植组织血循环危象的主要因素之一     

茉莉花提取物的舒血管作用

目的 观察中药茉莉花提取物（EJs）对大鼠离体胸主动脉环的舒血管作用并探讨其作用机制。 方法 采用离体血管环灌流装置,观察EJs对苯肾上腺素（PE）或氯化钾（KCl）预收缩血管的影响。检测左旋硝基精氨酸甲酯（L-NAME）和氯化钡（BaCl2）,格列本脲（Gli）对0.5,1,2,4,8 g.L-1EJs舒血管作用的影响;观察EJs对氯化钙（CaCl2）及PE在无钙液中收缩影响;激光扫描共聚焦显微镜技术检测血管平滑肌细胞内钙浓度。结果 在内皮完整血管上,EJs依赖性地降低PE或KCl预收缩血管的张力,最大舒张幅度分别为（105.0±3.2）%,（78.0±6.5）%; L-NAME明显削弱对EJs的舒血管作用（P<0.01）,最大舒张幅度为（58.0±6.9）%;BaCl2,Gli均能明显削弱EJs的舒血管作用（P <0.01）,最大舒张幅度分别为（37.0±5.2）%,（78.0±10.0）%;在无钙环境下,EJs能抑制PE引起去内皮主动脉环短暂收缩（P <0.01）,最大收缩幅度（70.0±6.3）%,EJs能抑制0.5～8 mmol.L-1CaCl2引起的收缩（P <0.01）,血管收缩幅度降低（65.0±3.2）%。4,8 g.L-1Ejs钙Fmax/F0分别为（2.0±0.2）和（1.5±0.2）。结论 EJs 能够浓度依赖性舒张大鼠胸主动脉,其作用机制可能与促进一氧化氮释放、激活多个K＋通道,减少细胞内钙离子浓度有关。     

一氧化碳合成酶抑制剂对缺氧性肺血管收缩反应的影响

目的 观察内皮及内源性一氧化碳（CO）合成酶抑制剂（血红素氧化酶抑制剂ZnppIX)对大鼠缺氧性肺血管收缩反应的影响，探讨内源性CO在缺氧性肺血管收缩反应中的作用。方法 制备Wistar大鼠动脉环，观察内皮与缺氧性肺血管收缩反应的关系；并以一氧化氮合成酶抑制剂L－NAME为对照，观察ZnppIX对缺氧性肺血管收缩反应的影响。结果 缺氧可使去氧肾上腺素顶收缩的肺动脉环出现明显的收缩反应，去除内皮或血管环用L－NAME孵育后，缺氧性肺血管收缩反应受抑，而用ZnppIX及L－NAME共同孵育后，缺氧性肺血管收缩反应明显抑制或消除，与L－NAME组相比有显著性差异（P＜0．01）。L－NAME组的缺氧张力变化率与未孵育前相比也有显著性差异（P＜0．01）。结论 缺氧性肺血管收缩反应是内皮依赖性的，ZnppIX可抑制大鼠氧性肺血管收缩反应，内源性CO与NO一样参与了缺氧性血管收缩反应。     

山莨菪碱对离体大鼠腹主动脉舒缩张力的作用及其机制

目的 观察山莨菪碱对离体大鼠腹主动脉舒缩张力的作用,探讨其作用机制.方法 采用Wistar大鼠离体腹主动脉环(长4～5 mm的血管)灌流技术,观察山莨菪碱累积浓度(每5 min加入山莨菪碱,使营养液中山莨菪碱浓度分别达3×10-6,10-5,3×10-5,10-4,3×10-4 mol/L)对单剂量苯肾上腺素(PE)(10-5 mol/L)预处理的血管舒张作用的影响,及不同浓度山莨菪碱(10-6,10-5,10-4 mol/L)预孵对累积浓度PE(每5 min加入PE,使营养液中PE浓度分别达10-8,3×10-8,10-7,3×10-7,10-6,3×10-6 mol/L)收缩血管作用的影响,分别运用一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(L-NAME)(100 μmol/L)(对照组加入等容积的蒸馏水)和KATP通道阻断剂格列苯脲(Gly)(100 μmol/L)(两对照组分别加入等容积的蒸馏水及溶剂二甲基亚砜DMSO)处理血管环,观察对山莨菪碱舒张血管的抑制作用.结果 山莨菪碱累积浓度对单剂量PE预收缩内皮完整及去内皮血管环均有舒张作用,最大舒张分别为(78.6±6.9)%和(65.76±11.39)%.程度相似,差异无统计学意义(P＞0.05).不同浓度山莨菪碱预孵对累积浓度PE收缩血管环作用呈浓度依赖性抑制,浓度越大,抑制作用越明显.用阻断剂L-NAME及Gly处理后,L-NAME可阻断山莨菪碱的舒张血管(内皮完整)作用(P＜0.05),而Gly对去内皮血管具阻断作用,但只在2 min时与对照组差异有统计学意义(P＜0.05).结论 山莨菪碱具有内皮及平滑肌依赖性舒张血管作用,即通过内皮上一氧化氮-环鸟苷酸(NO-cGMP)及平滑肌上α受体发挥作用.山莨菪碱抑制血管收缩主要通过ATP依赖性K+通道发挥作用.     

脓毒症患者病情恶化与血浆内皮素-1浓度升高相关

内皮素是新近发现的一种强有力的血管收缩肽,近来已从人和猪的内皮细胞培养液中分离得到。内皮素对各种血管床具有强烈的血管收缩作用,并导致前列环素和内皮衍化松弛因子的释放。实验证实,羊内毒素血症时,其血浆和肺淋巴中内皮素-1样免疫活性物质(内皮素-1-LI)浓度增加,而正常羊则无此现象,其原因可能系内毒素诱导内皮细胞受损所致。有迹象表明,内皮素参与了急性心肌梗塞、尿毒症的发病机理,本文测定了脓毒症患者血浆内皮     

离体大鼠颈总动脉的内皮依赖性舒张反应

研究内皮细胞在药物舒张离体大鼠颈总动脉中的作用。方法；鼠血管环被悬挂在含２０ｍｌ Ｋｒｅｂｓ液的浴槽中，测定血管环对药物反应的等长收缩张力。结果：实验显示乙酰胆硷，三磷酸腺苷，硝普钠和酚妥拉明使内皮完整的颈总动脉产生浓度依赖性舒张反应。     

内皮素 - 1对离体动脉的收缩作用及舒张药物的对抗效应

目的　研究内皮素-1（Endothelin-1,ET-1）收缩血管的特性及显微血管外科常用舒张药物的对抗效应。方法　采用离体血管舒缩功能的实验技术比较ET-1与去甲肾上腺素（noradrenaline,NE）对离体动脉张力的影响,同时检测舒张药物对ET-1收缩血管的拮抗作用。结果　ET-1使离体大鼠颈总动脉环产生浓度依赖性的恒定收缩,ET-1与NE的半数有效浓度(medianeffectiveconcentration,EC     

静脉麻醉药对去甲肾上腺素累积剂量致兔肺动脉环收缩量-效关系的影响

目的:通过硫喷妥钠、异丙酚、氯胺酮对去甲肾上腺素(NE)收缩肺动脉量-效关系的影响,了解三种药物对肺血管平滑肌的直接作用,以及内皮细胞完整性对其作用的影响。方法:制备兔离体肺动脉环,应用DC-001型离体器官测定仪,观察三种药物(1mM)对NE累积剂量量-效曲线的影响。结果:与NE对照组比较,完整内皮时,硫喷妥钠可加强肺动脉环对低浓度NE(10~(-10)M)的收缩反应,高剂量NE(10~(-3)、10~(-4)M)时收缩幅度低于对照组(P<0.05);异丙酚、氯胺酮均使NE累积剂量量-效曲线呈非平行性右移,表现为非竞争性抑制。去内皮时,硫喷妥钠组高剂量NE时收缩幅度与完整内皮时比较有所降低(P<0.05);异丙酚、氯胺酮组高剂量NE时收缩幅度与完整内皮时比较明显增加(P<0.05)。结论:硫喷妥钠增强了NE对肺动脉的收缩作用;异丙酚和氯胺酮均可抑制NE的肺动脉收缩作用,且异丙酚的作用呈内皮依赖性。     

犬呼吸窘迫综合征血浆内皮素和一氧化氮的变化

犬呼吸窘迫综合征血浆内皮素和一氧化氮的变化蹇华胜毕敏樊贵升作者单位：６３００３８重庆市，第三军医大学西南医院急症科一氧化氮和内皮素（ＥＴ１）是一对较强的血管舒缩因子，ＥＴ１除了可引起血管收缩外，还可引起气管、支气管平滑肌的收缩。肺内皮细胞具有释放和清...     

Contraction coupled endothelial nitric oxide release: a new paradigm for local vascular control?

INTRODUCTION: Nitric oxide (NO), a potent vasodilator, is presumed to be constitutively released in most mammalian blood vessels. In isolated rat thoracic aorta, however, hemoglobin (Hb), a nitric oxide scavenger, elicited contraction only when the vessels were precontracted with an alpha adrenergic agonist. Does vascular contraction induce endothelial NO release? METHODS: Thoracic aortic rings from male Sprague-Dawley rats were prepared with or without the endothelium. Vessel rings were contracted with several distinct types of contractile agonists and NO release was probed using a Hb contraction assay in the presence and absence of nitro-l-arginine methyl ester (NAME), a NO synthase inhibitor. RESULTS: In vessel rings precontracted with norepinephrine, potassium chloride, arginine vasopressin, prostaglandin F(2alpha), or serotonin, Hb elicited significant additional contractions. In contrast, Hb failed to elicit significant contractions in vessel rings without the functional endothelium or vessels pretreated with NAME. The Hb mediated additional contraction was not inhibited by calmidazolium, a calmodulin antagonist, and protein kinase inhibitors staurosporine and 2,5-dihydromethylcinnamate. Intercellular gap junction inhibitor 2,3-butanedione monoxime at a low dose (<2 mM) significantly attenuated the NE/Hb mediated contractions but at a high dose (>15 mM) completely prevented both contractions. The contraction coupled NO release may be mediated through a mechanism distinct from the Ca(2+)-calmodulin-dependent endothelial NOS pathway. CONCLUSIONS: In the isolated rat thoracic aorta, endothelial NO release may be coupled to contractile stimulus. This vascular property appears to render a unique local control mechanism independent of baroreflex and other central mechanisms.     

Effect of mild hypothermia on the vascular actions of phenylephrine in rat aortic rings

Intraoperative mild hypothermia is common. We have investigated the effects of mild hypothermia (34 vs 38 degrees C) on phenylephrine--(10(- 8) to 10(-5) mol litre-1) induced contractions of rat aortic rings mounted for isometric tension recordings. A marked decrease in Emax (maximal tension) (P < 0.05) and significant increase in EC50 (phenylephrine concentration producing 50% of maximal tension) were observed at the lower temperature in endothelium intact rings, but there was no effect of temperature when the endothelium had been removed. The decreased contraction with hypothermia in the endothelium intact vessels was restored to 84% by administration of the nitric oxide synthase inhibitor L-NNA and a small additional amount of tone was restored in the presence of the cyclooxygenase inhibitor, indomethacin. We conclude that mild hypothermia markedly decreased phenylephrine-induced rat aortic contraction in vitro by endothelium dependent mechanisms, largely related to increased nitric oxide production or action.      

Endothelial cell preservation at 10 degrees C minimizes catalytic iron, oxidative stress, and cold-induced injury

There is growing evidence that oxidative stress plays an important role in mediating the injury induced by hypothermia during the preservation of cells and tissues for clinical or research use. In cardiovascular allografts, endothelial cell loss or injury may lead to impaired control of vascular permeability and tone, thrombosis, and inflammation. We hypothesized that hypothermia-induced damage to the endothelium is linked to increases in intracellular catalytic iron pools and oxidative stress. In this study, bovine aortic endothelial cells and cell culture methods were used to model the response of the endothelium of cardiovascular tissues to hypothermia. Confluent cells were stored at 0 degrees C to 25 degrees C and cell damage was measured by lipid peroxidation (LPO) and lactate dehydrogenase release. Varying the bleomycin-detectible iron (BDI) in cells modulated cold-induced LPO and cell injury. In untreated cells, injury was highest at 0 degrees C and a minimum at 10 degrees C. A similar temperature-dependent trend was found in BDI levels and cell plating efficiencies. Arrhenius plots of cell killing and iron accumulation rates showed biphasic temperature dependence, with minima at 10 degrees C and matching activation energies above and below 10 degrees C. These findings imply that the mechanisms underlying the hypothermic increase in catalytic iron, oxidative stress, and cell killing are the same and that preservation of the endothelium may be optimized at temperatures above those routinely used.     

Attenuation of endothelium-mediated vasodilation by halothane

To determine whether halothane alters endothelium-mediated vasodilation of vascular smooth muscle, isolated ring preparations of rabbit aorta and canine femoral and carotid arteries were suspended for isometric tension recordings in Krebs-Ringer bicarbonate solution at 37 degrees C. Acetylcholine and bradykinin have been shown to relax these norepinephrine contracted arteries via an endothelium-dependent process. In this study, these relaxations were reversibly and significantly attenuated by 2% halothane. However, halothane did not affect relaxations caused by nitroglycerin, which, in these vessels, acts by an endothelium independent mechanism. These results suggest that halothane is not interfering with cyclic guanylate-monophosphate mediated relaxation of vascular smooth muscle, but may interfere with the synthesis, release, or transport of the endothelium-derived relaxing factor. In addition, during contractions evoked by norepinephrine, halothane caused significant decreases in tension in both the canine carotid and rabbit aortic preparations, but increased tension in the femoral artery rings. These effects were not altered by mechanical removal of the endothelium. These results suggest a direct action of halothane on the vascular smooth muscle, which can result in either an increase or decrease in tension, depending on the specific vessel. In addition to its direct vascular effect, this study suggests a new action of halothane; it interferes with endothelium-derived relaxing factor-mediated relaxation of vascular smooth muscle. This action may contribute in part to the vascular alterations seen clinically during administration of halothane.     

Differential effect of hypothermia on the vascular tone and reactivity of the human coronary artery and graft vessels

Hypothermia may contribute to vascular spasm during bypass surgery. The effect of cooling on the reactivity of the human coronary artery (CA), saphenous vein (SV) and internal mammary artery (IMA) was studied in vitro. In CA and IMA cooling diminished the resting tension and the contraction to potassium, noradrenaline and 5-hydroxytryptamine. In contrast, in SV the contraction to noradrenaline and 5-hydroxytryptamine was augmented by cooling. The effect of cold was reversible. These results demonstrate different effects of hypothermia in CA and the graft vessels. Thus, hypothermia augments the receptor-mediated contraction in SV but depresses it in IMA which thereby resembles CA. The difference is most marked in the contractile response to 5-hydroxytryptamine, which may accumulate during surgery. This may contribute to spasm in the saphenous vein grafts and may be involved in the mechanisms responsible for the inferior patency of SV compared to IMA as a graft vessel.     

Vascular effects of poly-N-acetylglucosamine in isolated rat aortic rings.

BAACKGROUND: Poly-N-acetylglucosamine (p-GlcNAc) is a secretion of marine diatoms that is known to be useful in controlling bleeding. As a component of promoting hemostasis, p-GlcNAc is thought to exert vasoconstrictor effects in arteries. The present study was undertaken to determine whether p-GlcNAc induced a significant vasoconstrictor effect and, if so, what the mechanism of this effect might be. MATERIALS AND METHODS: We examined vascular effects of p-GlcNAc on isolated aortic rings obtained from Sprague-Dawley rats. The rings were suspended in organ baths and precontracted with U46619, a thromboxane A2 mimetic. RESULTS: p-GlcNAc produced a concentration-dependent vasoconstriction over the range of 14 to 100 microg/ml. At a concentration of 100 microg/ml, p-GlcNAc significantly contracted aortic rings by 133 +/- 20 mg of developed force (P < 0.01). Neither a deacetylated derivative of p-GlcNAc nor a structurally related macromolecule, chitin, contracted rat aortic rings, indicating a specificity for p-GlcNAc. The vasoconstriction to p-GlcNAc was totally abolished in deendothelialized rat aortic rings, suggesting that an endothelial component is essential to the vasoconstriction. Pretreatment with the endothelin ET(A) receptor antagonist, JKC-301 (0.5 and 1 microM), significantly diminished p-GlcNAc-induced vasoconstriction by 57 to 61% (P < 0.01). However, p-GlcNAc did not significantly diminish nitric oxide release from rat aortic endothelium. CONCLUSION: These results provide evidence that p-GlcNAc significantly contracts isolated rat aortic rings via an endothelium-dependent mechanism, partly via enhancement of endothelin-1 release from endothelial cells.     

Cerebral vascular responsiveness after experimental traumatic brain injury: the beneficial effects of delayed hypothermia combined with superoxide dismutase administration

OBJECT: Traumatic brain injury (TBI) induces cerebral vascular dysfunction reflected in altered responses to vasodilators such as acetylcholine and hypercapnia. It has been demonstrated that the use of either posttraumatic hypothermia or free radical scavengers offered vascular protection when those treatments were delivered early after the injury, losing efficacy when the initiation of either treatment was delayed. Because immediate posttraumatic treatment is not realistic in the clinical setting, the authors undertook this study to investigate whether the combination of delayed hypothermia and the delayed administration of the free radical scavenger superoxide dismutase (SOD) could result in improved vascular protection. METHODS: Male Sprague-Dawley rats were anesthetized and subjected to either an impact-acceleration or sham injury. Animals were treated either with hypothermia (32 degrees C) initiated 60 minutes after TBI, delayed SOD (60 U/ml) applied 90 minutes after TBI, or a combination of delayed hypothermia (32 degrees C) and delayed SOD (60 U/ml) applied 15 minutes prior to the cessation of hypothermia. In this investigation, the diameter of cerebral pial arterioles was measured at rest and then challenged with vasodilator acetylcholine and hypercapnia. Four vessels were assessed per animal prior to injury and then again up to 6 hours after injury. RESULTS: Delayed SOD treatment did not enhance vascular function, while delayed hypothermia treatment only partially preserved pial vascular function. However, the combination of delayed hypothermia and delayed SOD significantly preserved vascular function after the injury. CONCLUSIONS: The results of these studies demonstrate that delayed hypothermia partially preserves vascular function after TBI, while expanding the therapeutic window over which agents such as SOD can now provide enhanced protection.     

Cold storage sensitizes rat femoral artery to an endotoxin-induced decrease in endothelium-dependent relaxation

Cold-stored arteries, tissues or organs are transferred in vascular, reconstructive and transplantation surgery. The function of transferred vessels and tissues diminishes when infection complicates transplantation, thereby contributing to morbidity. To evaluate the mechanisms involved, the effects of cold storage on basal vascular reactivity and the sensitivity to the vascular effects of endotoxin were tested in isolated rat femoral artery segments. A crossover design was followed, so that prior to cold storage 4 vessels were incubated for 2 h at 37 degrees C with endotoxin (Escherichia coli 0127:B8, 50 microg mL(-1)) in Krebs solution and 4 with Krebs solution only, while, after cold storage, segments from the former vessels were incubated with Krebs solution only and segments from the latter with endotoxin in Krebs solution. Vascular reactivity was tested in a wire myograph by the addition of depolarizing 125 mM KCl or norepinephrine (NE) as well as the endothelium-dependent vasodilator acetylcholine (ACh) and endothelium-independent vasodilator sodium nitroprusside (SNP). Cold storage did not affect vascular reactivity in the absence of endotoxin. Endotoxin decreased maximum response to NE prior to storage and sensitivity to SNP prior to and after cold storage. After cold storage, endotoxin decreased relaxation to ACh and increased vasoconstriction in response to KCl and NE (P < 0.05). We conclude that cold storage does not alter endothelial and smooth muscle function but sensitizes rat femoral artery to an endotoxin-induced decrease in endothelium-dependent relaxation and thereby to an increase in vasoconstrictor responses, whereas endotoxin alone only decreases receptor-dependent vasoconstrictor responses and sensitivity to NO donors. This may explain in part the detrimental effect of infection on function of cold-stored arterial grafts and tissue/organ transfers.     

Effect of ropivacaine on endothelium-dependent phenylephrine-induced contraction in guinea pig aorta

BACKGROUND: Previous studies have shown that ropivacaine has biphasic vascular effects, causing vasoconstriction at low concentrations and vasorelaxation at high concentrations. This study was designed to examine the role of the endothelium during accidental intravascular absorption of ropivacaine, and to elucidate the mechanisms responsible. METHODS: Isolated guinea pig aortic rings were suspended for isometric tension recording. The effects of ropivacaine on endothelium-intact and endothelium-denuded aortic rings were assessed. Endothelium-intact aortic rings were pre-contracted with phenylephrine before being exposed to ropivacaine and acetylcholine, in order to generate and compare concentration-response curves. In the absence and presence of yohimbine, propranolol, atropine, indometacin, N(G)-nitro-l-arginine methyl ester (l-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or methylene blue, the contractile response induced by ropivacaine was assessed on endothelium-intact aortic rings pre-contracted with phenylephrine. RESULTS: Ropivacaine (3 x 10(-4) to 10(-2) mol/l) produced vasoconstriction in endothelium-denuded aortic rings, whereas no such response was observed in aortic rings with intact endothelium. In phenylephrine pre-contracted intact aortic rings, ropivacaine induced a greater degree of vasorelaxation than did acetylcholine. Yohimbine, propranolol and atropine all failed to affect the relaxation responses induced by ropivacaine. However, pre-treatment with indometacin (cyclo-oxygenase inhibitor), l-NAME (nitric oxide synthase inhibitor), methylene blue (soluble guanylyl cyclase inhibitor) or ODQ (soluble guanylyl cyclase inhibitor), significantly decreased the ropivacaine-induced relaxation of endothelium-intact aortic rings (3 x 10(-4) to 10(-2) mol/l). CONCLUSIONS: Ropivacaine elicits an endothelium-dependent vasorelaxation in phenylephrine pre-contracted aortic rings via the nitric oxide-cyclic guanosine 3',5'-monophosphate pathway and the prostaglandin system.     

Mild hypothermia does not increase bacterial proliferation on implanted vascular grafts

BACKGROUND: Mild hypothermia may offer protection against spinal cord ischemia during aortic surgery. However, hypothermia also promotes postoperative infection via two mechanisms: peripheral vasoconstriction and impairment of various immune functions. If mild hypothermia aggravates graft infections, immune function impairment would presumably be the most important factor because thermoregulatory vasoconstriction does not appreciably reduce aortic blood flow. We therefore tested the hypothesis that resistance to vascular graft infection is not reduced by mild perioperative hypothermia in dogs. METHODS: After colonization with a solution of Staphylococcus epidermidis, prostheses were used to replace the infrarenal aorta in 20 dogs. During surgery, the dogs were randomly assigned to maintain of normothermia or passive cooling. Seven days later, grafts were recovered for bacteriologic study. RESULTS: Colony counts for the grafts removed from the normothermic and hypothermic dogs did not differ significantly. CONCLUSIONS: Mild perioperative hypothermia does not increase proliferation of S epidermidis on aortic vascular grafts.