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Biomedical subjects

A H Chester

Publications and source records attributed to A H Chester.

At least 19 recordsLinked to original sources
PubMed2001

The effects of diaspirin cross-linked hemoglobin on the tone of human saphenous vein.

Diaspirin cross-linked hemoglobin (DCL-Hb), when infused into animals, causes vasoconstriction thought to be caused by nitric oxide (NO) binding by the hemoglobin molecule. The purpose of this study was to ascertain whether DCL-Hb causes vasoconstriction in human saphenous vein taken from patients undergoing myocardial revascularization and whether NO scavenging is the mechanism. The direct effect of DCL-Hb on saphenous vein tone was tested by adding increasing concentrations (10(-8) to 10(-5)M) of the drug. In an additional series of experiments, the influence of DCL-Hb on the dilator response to endothelial dependent and independent vasodilators was tested. This was achieved by attempting either to reverse the effects of acetylcholine, sodium nitroprusside, or S-nitrosylglutathione with prior incubation with DCL-Hb or to inhibit the dilator response in vessels preconstricted with 10(-6)M norepinephrine. There was no effect of DCL-Hb alone on saphenous vein tone. DCL-Hb significantly reduced vasodilatation with all vasodilators (P < 0.05). After maximal relaxation with sodium nitroprusside and s-nitrosylglutathione, there was significant vasoconstriction with DCL-Hb at concentrations larger than 10(-6)M, (P < 0.05). The authors conclude that DCL-Hb does not constrict human saphenous vein but can affect vessel tone by reversal of the effect of endogenously or exogenously released NO.

Acetylcholine↗
PubMed2001

Influence of 5-hydroxytryptamine on aortic valve competence in vitro.

BACKGROUND AND AIM OF THE STUDY: The contraction of cusp tissue has been implicated to play a role in aortic valve function. The effect of the contractile agent 5-hydroxytryptamine (5-HT) on the competence of isolated aortic roots has been assessed, and the vasomotor properties of 5-HT on aortic root tissue examined. METHODS: Isolated porcine aortic roots were pressurized with Kreb's solution through the aortic arch. 5-HT was added in increasing concentrations (10(-7) to 10(-5) M) and the degree of leakage measured over time. In additional experiments, portions of sinotubular junction, sinus, annular and cusp tissue were set up in organ baths, placed under tension, and challenged with 5-HT (10(-9) to 10(-5) M). Viability of each valve structure was assessed by addition of KCl (90 mM). RESULTS: The rate of leakage from intact aortic roots increased when 10(-6) and 10(-5) M 5-HT was added. The maximum effect, observed at 10(-5) M 5-HT, was equal to an increase of 61.8+/-23.0% above control (p <0.05). The perfusion pressure at each concentration of 5-HT was unchanged. This response was inhibited by the 5-HT2A receptor antagonist ketanserin. Addition of KCl to isolated valve structures gave a mean contractile response of 0.8+/-0.1mN for cusp, 19+/-11.0 mN for annular, 29+/-8.0 mN for sinus, and 23+/-8.0 mN for sinotubular junction tissue (each n = 4). Only cusp tissue contracted when treated with 5-HT, with a maximum 105.5+/-17.2% (n = 4) of the response to KCl. The response to 5-HT was blocked by the 5-HT2A-receptor antagonist ketanserin at 10(-6) M (n = 4). None of the other aortic root structures responded to 5-HT. CONCLUSION: These results show that 5-HT influences the competence of isolated porcine aortic valves. This effect is contributed by contraction of the cusp tissue, and is mediated by 5-HT2A receptors. These effects may contribute to the association between valve dysfunction, 5-HT and certain appetite suppressants.

Animals↗
PubMed2000

Expression and function of angiotensin converting enzyme, chymase, and angiotensin II in the human radial artery and internal thoracic artery.

BACKGROUND: The potential role of the local renin-angiotensin system to differentially affect radial artery and internal thoracic artery graft performance has not been examined. METHODS: Contractile responses to angiotensin I and II in the radial artery and the internal thoracic artery were examined in vitro. The expression function, and localization of angiotensin receptors, angiotensin converting enzyme, and chymase were studied in radial artery and internal thoracic artery segments. RESULTS: Angiotensin I and II contractions were significantly greater (p < 0.05) in the radial artery compared to the internal thoracic artery. In both arteries, angiotensin II responses were mediated via the AT1 receptor. Messenger RNA transcripts for angiotensin-converting enzyme and chymase were detected in both arteries. Angiotensin-converting enzyme was localized to luminal and vaso vasorum endothelial cells and smooth muscle cells in both vessels, while chymase was colocalized with mast cells in adventitial and medial layers. An angiotensin converting enzyme or a chymase inhibitor singularly had no effect on angiotensin I contractions, however, when combined, a marked inhibition of the angiotensin I response was observed in both vessels. CONCLUSIONS: Our results illustrate the complexities which exist within the local renin angiotensin system and suggest that clinical trials which may modulate the system are warranted.

Aged↗
PubMed2000

Transplant atherosclerosis: role of phenotypic modulation of vascular smooth muscle by nitric oxide.

Occlusive accelerated atherosclerosis of coronary grafts is the predominant factor that limits longevity of heart transplant recipients. This form of vascular disease affects both the large epicardial and the smaller intramyocardial vessels, leading to characteristic clinical presentation that necessitates the use of sophisticated techniques for their accurate detection. Accelerated atherosclerosis after transplantation is a multifactorial disease with many events contributing to its progression. The initial vascular injury associated with ischemia-reperfusion appears to aggravate preexisting conditions in the donor vasculature in addition to activation of new immunological and nonimmunological mechanisms. Throughout these events, the endothelium remains a primary target of cell- and humoral-mediated injury. Changes in the vascular intima leads to alterations in vascular smooth muscle cell (VSMC) physiology, resulting in VSMC phenotypic modulation with the orchestration of a broad spectrum of growth and inflammatory reactions, which might be a healing response to vascular injury. Endogenous nitric oxide (NO) pathways regulate a multiplicity of cellular mechanisms that play a major role in determining the structure and function of the vessel wall during normal conditions and during remodeling associated with accelerated atherosclerosis. Recently identified signaling pathways, including mitogen-activated protein kinase, cGMP-dependent protein kinase, phosphatidylinositol 3-kinase, and transcriptional events in which nuclear factor kappa B and activator protein 1 take part, can be associated with NO modulation of cell cycle perturbations and phenotypic alteration of VSMC during accelerated atherosclerosis. This article reviews recent progress covering the aforementioned matters. We start by summarizing the clincal aspects and pathogenesis of accelerated atherosclerosis associated with transplantation, including clinical presentation and detection. This summary is followed by a discussion of the multiple factors of the disease process, including immunological and nonimmunolgical contributions. The next section focuses on cellular responses of the VSMCs relevant to lesion formation, with special emphasis on classical and recent paradigms of phenotypic modulation of these cells. To examine the influence of NO on VSMC phenotypic modulation and consequent lesion development, we briefly overview characteristics of NO production in the normal coronary vascular bed and the changes in endogenous NO release and activity during atherosclerosis. This overview is followed by a section covering molecular mechanisms whereby NO regulates a range of signaling pathways, transcriptional events underlying cell cycle perturbation, and phenotypic alteration of VSMC in accelerated atherosclerosis.

Animals↗
PubMed2000

Interaction between thromboxane A2 and 5-hydroxytryptamine in the radial artery compared to the internal thoracic artery.

The aim of the present study was to investigate if the function of 5-hydroxytryptamine-1B/1D (5-HT1B/1D) receptors in human radial artery (RA) and internal thoracic artery (ITA) can be modified by thromboxane A2 (TXA2) released from the vessel wall in these two arteries that are commonly used in coronary artery bypass grafts. The 5-HT1B/1D agonist sumatriptan contracted the RA with a maximum response of 23.5+/-6.8 mN and a pD2 value of 6.6+/-0.1. The effect of sumatriptan was significantly reduced in the ITA with a maximum of 5.8+/-2.7 mN (P<.05) and a pD2 value of 6.4+/-0.2. The TXA2 receptor antagonist SQ30741 inhibited contractions to sumatriptan in the RA but not in the ITA. It is concluded that the effect mediated by 5-HT1B/1D is augmented by endogenous TXA2 in the RA.

Aged↗
PubMed2000

A redox-based mechanism for nitric oxide-induced inhibition of DNA synthesis in human vascular smooth muscle cells.

1. The current study explored potential redox mechanisms of nitric oxide (NO)-induced inhibition of DNA synthesis in cultured human and rat aortic smooth muscle cells. 2. Exposure to S-nitrosothiols, DETA-NONOate and NO itself inhibited ongoing DNA synthesis and S phase progression in a concentration-dependent manner, as measured by thymidine incorporation and flow cytometry. Inhibition by NO donors occurred by release of NO, as detected by chemiluminescence and judged by the effects of NO scavengers, haemoglobin and cPTIO. 3. Co-incubation with redox compounds, N-acetyl-L-cysteine, glutathione and L-ascorbic acid prevented NO inhibition of DNA synthesis. These observations suggest that redox agents may alternatively attenuate NO bioactivity extracellularly, interfere with intracellular actions of NO on the DNA synthesis machinery or restore DNA synthesis after established inhibition by NO. 4. Recovery of DNA synthesis after inhibition by NO was similar with and without redox agents suggesting that augmented restoration of DNA synthesis is an unlikely mechanism to explain redox regulation. 5. Study of extracellula interactions revealed that all redox agents potentiated S-nitrosothiol decomposition and NO release. 6. Examination of intracellular NO bioactivity showed that as opposed to attenuation of NO inhibition of DNA synthesis by redox agents, there was no inhibition (potentiation in the presence of ascorbic acid) of soluble guanylate cyclase (sGC) activation judged by cyclic GMP accumulation in rat cells. 7. These data provide evidence that NO-induced inhibition of ongoing DNA synthesis is sensitive to redox environment. Redox processes might protect the DNA synthesis machinery from inhibition by NO, in the setting of augmented liberation of biologically active NO from NO donors.

Acetylcysteine↗
PubMed2000

The renin angiotensin system in bypass graft surgery.

The renin angiotensin system is implicated in the development of vein graft disease after coronary artery bypass surgery. Components of this system have been shown to play important roles in determining the short-term and long-term performance of coronary artery bypass grafts. Significant differences exist in the commonly used arterial and venous grafts in angiotensin converting enzyme activity and angiotensin responses. The existence of a dual enzyme pathway in angiotensin II formation has also been demonstrated. Such findings have implications for the use of AT1-receptor antagonists over enzyme inhibitors to improve graft performance and prevent the development of coronary artery bypass graft disease.

Angiotensin II↗
PubMed2000

Receptor-mediated contraction of aortic valve leaflets.

BACKGROUND AND AIM OF THE STUDY: The mechanisms that regulate the function of the aortic valve are not fully understood. Cusp tissue has been shown to have contractile properties, but little is known as to which receptors mediate these effects. METHODS: We have examined, using isolated organ baths, the response of porcine aortic valve leaflets to a range of vasoactive agents including endothelin-1, noradrenaline, adrenaline, the thromboxane (TX) A2 mimetic U46619, 5-hydroxytryptamine (5-HT), histamine and angiotensin II. The viability of each individual leaflet was tested by the addition of 90 mM KCl. RESULTS: All agents tested, with the exception of angiotensin II, were capable of inducing concentration-dependent contractions of the valve leaflets. The responses to endothelin-1 and U46619 were significantly greater than those of all the other agents tested. Responses to endothelin-1 could be inhibited by 10(-5) M of the mixed ET(A/B) receptor antagonist bosantan. The response to both catecholamines was blocked by 10(-6) M yohimbine, but not by 3 x 10(-7) M prazosin, indicating the presence of alpha2-adrenoceptors. The response to histamine was mediated exclusively by H1-receptors, as judged by the antagonistic effect of 10(-6) M of the H1-receptor antagonist mepyramine. The response to 5-HT could be blocked by 10(-6) M of the 5-HT2A-receptor antagonist ketanserin, and that of U46619 by 10(-6) M of the TXA2-receptor antagonist SQ30741. CONCLUSION: These results demonstrate the range of receptor systems that can mediate contraction of aortic valve leaflets. Further studies are required to elucidate the role of these receptors in the physiology and pathophysiology of the aortic valve.

Animals↗
PubMed2000

Mitogenic and secretory responses of human valve interstitial cells to vasoactive agents.

BACKGROUND AND AIM OF THE STUDY: The vasoactive agent 5-hydroxytryptamine (5-HT) has been implicated in valve disease due to possible trophic effects on valve interstitial cells (IC). The present study was aimed at characterizing the responses of cultured human heart valve IC to 5-HT in terms of intracellular calcium concentration ([Ca2+]i), mitogenesis and collagen synthesis. The effects of angiotensin II (Ang II) were also studied in parallel. METHODS: IC were obtained by collagenase digestion of valve leaflets isolated from transplant recipient hearts. Changes in [Ca2+]i were measured from fluorescence of the ratiometric calcium dye, fura 2. Mitogenic and collagen synthetic responses of valve IC were measured by 3H-thymidine incorporation (DNA synthesis) and 3H-proline incorporation assays respectively, in quiescent cells. RESULTS: Human valve IC responded to 5-HT and Ang II with mean maximal increases in [Ca2+]i of 249 +/- 47 nM and 397 +/- 159 nM, respectively. 5-HT stimulated DNA synthesis in quiescent IC, although to varying degrees among different isolations, with a maximum 43.4 +/- 20.1% increase by 10(-7) M 5-HT (p <0.05). Ang II did not stimulate IC DNA synthesis. Valve IC also responded to 5-HT with a maximum increase in collagen synthesis of 15.7 +/- 2.0% by 10(-6) M 5-HT (p <0.05). Ang II provoked a more powerful collagen synthesis response (maximum 50.5 +/- 15.1% increase by 10(-5) M Ang II; p <0.05). CONCLUSION: We have shown that 5-HT and Ang II promote the prolonged processes of growth and collagen synthesis in cultured human valve IC. Thus, these vasoactive agents may play a role in the development of heart valve disease.

Angiotensin II↗
PubMed1999

Endothelin-1 stimulates proliferation of human coronary smooth muscle cells via the ET(A) receptor and is co-mitogenic with growth factors.

We investigated the effects of endothelin-1 (ET-1) on growth of cultured human coronary artery smooth muscle cells (cSMC). ET-1 alone stimulated DNA synthesis in growth-arrested cSMC as measured by [3H]thymidine incorporation, with a maximum 63 +/- 23% increase above control by 10(-7) M (P < 0.05). ET-1 (10(-7) M) also stimulated increases in cyclin D1 protein levels after 24 h, and in absolute cell number after 4 days. Furthermore, ET-1 stimulated protein synthesis (maximum 73 +/- 32% increase in [3H]leucine incorporation by 10(-7) M (P < 0.05)), as well as triggering intracellular calcium transients in human cSMC, as visualised under fura-2 fluorescence microscopy. The selective ET(A) receptor antagonist BQ123 inhibited the increases in DNA synthesis, cell number, protein synthesis and intracellular calcium concentration in response to ET-1, whereas the ET(B) receptor antagonist BQ788 had no such effects. Furthermore, the ET(B) agonist sarafotoxin 6c had no effect on cSMC DNA synthesis. In addition, co-incubation of ET-1 with threshold concentrations of the growth factors, platelet-derived growth factor-BB (PDGF-BB), basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF), resulted in pronounced synergistic increases in DNA synthesis over that observed with the factors alone. In conclusion, we have shown that ET-1 stimulates proliferation of human cSMC via the ET(A) receptor and is also a co-mitogen with the growth factors tested. These findings indicate a role for ET-1 in the development of coronary intimal hyperplasia in man.

Becaplermin↗
PubMed1999

Inhibition of human cardiac fibroblast mitogenesis by blockade of mitogen-activated protein kinase and phosphatidylinositol 3-kinase.

1. Interstitial fibroblast proliferation is an elemental feature in the development of cardiac fibrosis. The effects of inhibitors of the intracellular signalling proteins, MEK, a kinase involved in the mitogen-activated protein kinase (MAPK) pathway and phosphatidylinositol 3-kinase (PI3-K), were tested on growth of cultured human cardiac fibroblasts. 2. Cardiac fibroblasts were isolated from transplant recipient myocardium and made quiescent by serum deprivation for 48 h. Cells were incubated for 24 h with the inhibitors PD 098059 (0.3-30 mumol/L) and LY294002 (1-25 mumol/L) in the presence and absence of platelet-derived growth factor-AB (PDGF-AB, 10 ng/mL). DNA synthesis was measured by [3H]-thymidine incorporation assay (20-24 h). 3. Both compounds markedly inhibited both basal and PDGF-stimulated increases in DNA synthesis in a concentration-dependent manner. Cardiac fibroblast DNA synthesis was reduced to near control levels by PD 098059, while it was inhibited completely by LY294002. 4. These results implicate the importance of MAPK and PI3-K activation in the signal transduction pathways necessary for cardiac fibroblast replication.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1999

Characterisation of constrictor endothelin receptors in the human internal thoracic artery and saphenous vein.

We studied the endothelin receptors mediating contraction in the human saphenous vein (SV) and internal thoracic artery (ITA). In the SV, the ET(A)-receptor antagonist BQ123 (1 microM) did not significantly shift the ET-1 concentration-response curve but did cause a parallel shift in the ITA. In the SV, the ET(A)-receptor agonist sarafotoxin 6b (S6b) produced a monophasic concentration-response curve that was antagonised biphasically by BQ123 (0.1-1 microM). In the ITA, S6b was an ineffective agonist with contractions seen only at 3 x 10(-9) M upward. The ET(B)-receptor agonist sarafotoxin 6c (S6c) caused constrictions in only 74% of SV rings and 42% of ITA rings. In the tissues that did respond, S6c caused a monophasic concentration-response curve with a lower maximal response than ET-1. The ET(B) antagonist BQ788 did not antagonise the responses to ET-1 in either the SV or the ITA but did antagonise the responses to S6c in the SV. The results from this study suggest that mainly ET(A) receptors mediate the contractile responses in the human SV and ITA. There is also evidence for an ET(B)-mediated response, although the contractions were much smaller than those elicited by ET-1. We also conclude that the ET(A) receptors mediating responses in these human vessels are atypical because of the different effects of BQ123 on the two vessels.

Adult↗
PubMed1999

Differential regulation of DNA synthesis by nitric oxide and hydroxyurea in vascular smooth muscle cells.

We investigated the influence of nitrovasodilators on DNA synthesis in cultured human aortic smooth muscle cells and explored the hypothesis that nitric oxide (NO) is directly involved in mediating the inhibitory effects of hydroxyurea on DNA synthesis. Both NO and hydroxyurea inhibited ongoing DNA synthesis and S phase progression in our cells. Exogenous deoxynucleosides partially reversed this inhibition, suggesting that ribonucleotide reductase is a primary target for both NO and hydroxyurea. Nitrovasodilators inhibited DNA synthesis by releasing NO, as detected by chemiluminescence and as shown by the reversal of DNA synthesis inhibition by NO scavengers. This inhibition appears to occur via a cGMP-independent mechanism. In contrast, hydroxyurea did not produce a detectable NO signal, and NO scavengers had no influence on its inhibition of DNA synthesis, suggesting that NO does not mediate the inhibitory action of hydroxyurea in our system. Furthermore, the action of nitrovasodilators and hydroxyurea on DNA synthesis differed according to redox sensitivity. The redox agents N-acetyl-L-cysteine and ascorbate reversed NO inhibition of DNA synthesis and had no effect on DNA synthesis inhibition caused by hydroxyurea.

Antioxidants↗
PubMed1999

Role of oxidant stress in cytokine-induced activation of NF-kappaB in human aortic smooth muscle cells.

The transcription factor nuclear factor-kappaB (NF-kappaB) has been implicated in inflammatory and proliferative vascular mechanisms. Activated NF-kappaB has been documented in human atherosclerotic lesions, and its activation in human vascular smooth muscle cells (SMC) by cytokines has been reported. However, intracellular mechanisms mediating NF-kappaB activation in human SMC are poorly understood. The aim of this study was to explore the potential role of reactive oxygen species and oxidant stress as signaling events in cytokine-induced NF-kappaB activation. Western blot analysis revealed the presence of inhibitory protein I-kappaBalpha in resting human aortic SMC, which was rapidly phosphorylated and degraded on exposure to interleukin-1beta (IL-1beta) followed by NF-kappaB translocation to the nucleus. IL-1beta had no effect on two measures of intracellular oxidant stress, fluorescence generated by the oxidation of 2',7'-dichlorodihydrofluorescin to dichlorofluorescein (DCF) or changes in intracellular sulfhydryl content. N-acetylcysteine (NAC) a membrane-permeant antioxidant, which augmented intracellular sulfhydryl content and inhibited H(2)O(2)-induced DCF fluorescence, had no effect on cytokine-induced NF-kappaB activation. In contrast to NAC, the metal chelators pyrrolidine dithiocarbamate and diethyldithiocarbamate attenuated IL-1beta-induced NF-kappaB activation but had no effect on intracellular sulfhydryl content. Treatment of the cells with the oxidant H(2)O(2) caused an increase in DCF fluorescence and decreased intracellular sulfhydryl content but had no effect on I-kappaBalpha or NF-kappaB. In conclusion, this study suggests that oxidant stress may not play a major role in cytokine-induced activation of NF-kappaB in human aortic SMC and that oxidants may not be primary activators of NF-kappaB in these cells.

Antioxidants↗
PubMed1998

Expression of functional angiotensin-converting enzyme and AT1 receptors in cultured human cardiac fibroblasts.

BACKGROUND: Angiotensin II (Ang II) has been implicated in the development of cardiac fibrosis. The aims of the present study were to examine expression and activity of ACE and of angiotensin receptors in human cardiac fibroblasts cultured from dilated cardiomyopathic and ischemic hearts. The effects of Ang II on fibroblasts were also investigated. METHODS AND RESULTS: Human cardiac fibroblasts were cultured from ventricular and atrial myocardium and characterized immunohistochemically. Expression of ACE and the angiotensin AT1 receptor was demonstrated in cardiac fibroblasts by reverse transcriptase-polymerase chain reaction and radioligand binding. Functional ACE activity, measured by radiolabeled substrate conversion assay, was detected in both ventricular (Vmax. Km-1. mg-1, 0.031+/-0.010; n=13) and atrial (0. 034+/-0.012; n=6) fibroblasts. Fibroblast ACE activity was increased after 48 hours of treatment with basic fibroblast growth factor, dexamethasone, and phorbol ester. Ang II did not affect DNA synthesis but stimulated [3H]proline incorporation in cardiac fibroblasts (20.0+/-4.0% increase above control by 10 micromol/L; P<0.05, n=7), which was abolished by losartan 10 micromol/L but not PD123319 1 micromol/L. Ang II also stimulated a rise in intracellular calcium (basal, 56+/-1 nmol/L; Ang II, 355+/-24 nmol/L) via the AT1 receptor, as shown by complete inhibition with losartan. CONCLUSIONS: We have demonstrated expression and activity of ACE and AT1 receptor in cultured human cardiac fibroblasts. In addition, cardiac fibroblasts respond to Ang II with AT1 receptor-mediated collagen synthesis. The presence of local ACE and AT1 receptors in human fibroblasts suggests their involvement in the development of cardiac fibrosis.

Calcium↗
PubMed1998

Role of vasoactive mediators in primary and secondary pulmonary hypertension.

The role of vasoactive mediators, such as endothelin-1, nitric oxide, prostacyclin, and thromboxane, in pulmonary hypertension remains undefined. This study investigated the circulating levels and transpulmonary gradients of these vasoactive mediators in patients with primary and secondary pulmonary hypertension to define whether there is increased production or decreased clearance of these substances in the lung vasculature.

Adult↗
PubMed1998

Expression of vascular adhesion molecules in saphenous vein coronary bypass grafts.

BACKGROUND: Adhesion of blood elements to the endothelium is an important step in the development of vein graft disease. This study examines the expression of vascular adhesion molecules on explanted saphenous vein bypass grafts. METHODS: Immunocytochemical staining was performed using explanted saphenous vein grafts from 28 patients. Antibodies against the endothelial markers CD31, von Willebrand factor, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin were used. RESULTS: Staining for CD31 and von Willebrand factor demonstrated the presence of endothelial cells in the lumen and the vasa vasorum. Expression of intercellular adhesion molecule-1 was variable between grafts, whereas vascular adhesion molecule-1 and E-selectin were almost always absent on the luminal endothelium. In contrast, the endothelium of the vasa vasorum stained positively for intercellular adhesion molecule-1 and vascular adhesion molecule-1, and was also seen on nonendothelial cells within the vessel wall. Expression of these adhesion molecules did not vary with the severity of vein graft disease. CONCLUSIONS: This study highlights the blood vessels in the adventitia as possible sites for the adhesion and migration of cells into the vessel wall.

Aged↗