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PubMed2006

Circulating markers of endothelial function in cardiovascular disease.

Endothelial dysfunction is a key event in cardiovascular disease. Measurement of endothelial dysfunction in vivo presents a major challenge, but has important implications since it may identify the clinical need for therapeutic intervention, specifically in primary prevention. Several biological markers have been used as indicators of endothelial dysfunction. The soluble adhesion molecules sICAM-1 and sVCAM-1 lack specificity and are increased in inflammatory processes. Both markers are increased in coronary artery disease. sICAM-1 level predicts the risk for cardiovascular disease or diabetes mellitus in healthy individuals. sE-selectin is specific for the endothelium and is increased in coronary artery disease and diabetes mellitus. sE-selectin is also associated with diabetic risk. The endothelium-specific marker, soluble thrombomodulin, is associated with severity of coronary artery disease, stroke or peripheral occlusive arterial disease and is not increased in healthy or asymptomatic subjects. Interestingly, thrombomodulin decreases during treatment of hypercholesterolemia or hyperhomocysteinemia. In contrast, von Willebrand factor is the best endothelial biomarker and predicts risk for ischemic heart disease or stroke.

Animals↗

PubMed2002

Vesicle formation and trafficking in endothelial cells and regulation of endothelial barrier function.

Endothelial barrier function is regulated in part by the transcellular transport of albumin and other macromolecules via endothelial caveolae (i.e., this process is defined as transcytosis). Using pulmonary microvascular endothelial cells, we have identified the specific interactions between a cell surface albumin-docking protein gp60 and caveolin-1 as well as components of the signaling machinery, heterotrimeric G protein (G(i))- and Src-family tyrosine kinase. Ligation of gp60 on the apical membrane induces the release of caveolae from the apical membrane and activation of endocytosis. The formed vesicles contain the gp60-bound albumin and also albumin and other solutes present in the fluid phase. Vesicles are transported in a polarized manner to the basolateral membrane, releasing their contents by exocytosis into the subendothelial space. The signaling functions of G(i) and Src are important in the release of caveolae from the plasma membrane. The Src-induced phosphorylation of caveolin-1 is crucial in regulating interactions of caveolin-1 with other components of the signaling machinery such as G(i), and key signaling entry of caveolae into the cytoplasm and endocytosis of albumin and other solutes. This review addresses the basis of transcytosis in endothelial cells, its central role as a determinant of endothelial barrier function, and signaling mechanisms involved in regulating fission of caveolae and trafficking of the formed vesicles from the luminal to abluminal side of the endothelial barrier.

Animals↗

PubMed1991

Endothelial function and contractility of human vena saphena magna prepared for aortocoronary bypass grafting.

The aim of this study was to examine whether contractility and endothelial function of the human saphenous vein prepared for aortocoronary bypass grafting are altered by the surgical technique, e.g. cannulation and gentle distension of the vessel. Two segments (2 cm length each) of native vena saphena magna and 2 segments (2 cm length each) of the same vessel prepared for coronary bypass grafting were taken for further experimentation. After ligation of all side branches the segments were cannulated and arranged in two systems (with two segments each) in a serial manner (system I: prepared vessel followed by a native segment; system II: native vessel followed by a prepared segment) and perfused with Tyrode's solution at a constant flow rate of 20 ml/min (PO2 = 45 mmHg). Pressure gradient was measured continuously over each segment as a function of the vessel's radius according to the Hagen-Poiseuille equation. Endothelial and smooth muscle function was checked by perfusion with increasing concentrations of acetylcholine (ACH) to provoke the release of endothelium-derived relaxing factor (EDRF) (ACH; 0.3, 1, 3, 10, 30 mumol/L) after precontraction of the vessels with 1 mumol/L norepinephrine (NE). This showed normal contractility and ACH-induced relaxation in the native vessels but a reduced contractile response and a total lack of ACH-EDRF-induced relaxation in the prepared vessels. Perfusion with 5-hydroxytrytamine (5-HT) (0.25, 0.5, 1, 10 mumol/L for 10 min each concentration) resulted in marked constriction of all vessels with preserved contractility which could be completely prevented by pretreatment with the 5-HT2-receptor antagonist ketanserine (20 mumol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed2007

Restoration of coronary endothelial function in obese Zucker rats by a low-carbohydrate diet.

A popular diet used for weight reduction is the low-carbohydrate diet, which has most calories derived from fat and protein, but effects of this dietary regimen on coronary vascular function have not been identified. We tested the hypothesis that obesity-induced impairment in coronary endothelial function is reversed by a low-carbohydrate diet. We used four groups of male Zucker rats: lean and obese on normal and low-carbohydrate diets. Rats were fed ad libitum for 3 wk; total caloric intake and weight gain were similar in both diets. To assess endothelial and vascular function, coronary arterioles were cannulated and pressurized for diameter measurements during administration of acetylcholine or sodium nitroprusside or during flow. When compared with lean rats, endothelium-dependent acetylcholine-induced vasodilation was impaired by approximately 50% in obese rats (normal diet), but it was restored to normal by the low-carbohydrate diet. When the normal diet was fed, flow-induced dilation (FID) was impaired by >50% in obese compared with lean rats. Similar to acetylcholine, responses to FID were restored to normal by a low-carbohydrate diet. N(omega)-nitro-L-arginine methyl ester (10 microM), an inhibitor of nitric oxide (NO) synthase, inhibited acetylcholine- and flow-induced dilation in lean rats, but it had no effect on acetylcholine- or flow-induced vasodilation in obese rats on a low-carbohydrate diet. Tetraethylammonium, a nonspecific K(+) channel antagonist, blocked flow-dependent dilation in the obese rats, suggesting that the improvement in function was mediated by a hyperpolarizing factor independent of NO. In conclusion, obesity-induced impairment in endothelium-dependent vasodilation of coronary arterioles can be dramatically improved with a low-carbohydrate diet most likely through the production of a hyperpolarizing factor independent of NO.

Animals↗

PubMed1984

The effects of ouabain on endothelial function in human and rabbit corneas.

These experiments were undertaken to study the effects of ouabain on endothelial function in isolated perfused human and rabbit corneas. Both human and rabbit corneas swell at rates which are dose-dependent when perfused with ouabain (10(-8) to 10(-5) M). The human tissue, however, requires tenfold higher concentrations to achieve swelling rates comparable to rabbit. Dose-dependent ultrastructural changes are seen in ouabain-perfused endothelia progressing from moderate endothelial edema (7.5 X 10(-7) M) to marked edema with altered subcellular organelles and vacuolization (10(-5) M). Ouabain-perfused human corneas show marked endothelial edema even at the lowest concentrations of ouabain tested. Apical junctions remain intact, however, in both human and rabbit endothelia at all concentrations. These results suggest that endothelial Na/K ATPase is essential to pump function in both human and rabbit corneas.

Aged↗

PubMedDate not supplied

Amplified biochemical activation of endothelial function in hypertension associated with moderate to severe renal failure.

BACKGROUND: Arterial hypertension and endothelial dysfunction have a role in the development of athero-sclerosis. This study assessed autocrine-paracrine endothelial function in patients with hypertension associated with renal failure. METHODS: Angiotensin II (Ang II), endothelin-1 ( ET-1), basic fibroblast growth factor (bFGF), transforming growth factor-beta (TGF-beta), soluble forms of adhesion molecules (ICAM-1, VCAM-1), E-selectin, von Willebrand factor (vWf) and nitric oxide (NO) were measured in 26 patients with hypertension and chronic renal failure (CRF), in 19 essential hypertensives (EH) and in 28 normotensive healthy subjects. RESULTS: Plasma concentrations of Ang-II, ET-1, ICAM-1, VCAM-1, E-selectin, bFGF and TGF-beta all were significantly higher in patients than in healthy subjects and EH. Furthermore, in CRF, serum creatinine correlated negatively with NO plasma levels (r = - 0.51; p < 0.0) and this relationship held true after adjusting the data for potential confounders. Plasma NO was inversely related with ET-1 and bFGF (P < 0.01). CONCLUSION: Hypertension in CRF is characterized by biochemical evidence of marked endothelial dysfunction, apparently more pronounced than in patients with EH. Amplified endothelial activation in CRF probably contributes to the high rate of atherosclerotic complications in CRF.

Adult↗

PubMed2006

Corneal endothelial function after phacoemulsification using the fluid-based system compared to conventional ultrasound technique.

AIM: To quantitatively assess corneal endothelial changes after phacoemulsification with the fluid-based system compared to conventional ultrasound technique. METHODS: This prospective, randomized clinical study included patients with cataract who were randomly assigned either to have phacoemulsification with the fluid-based system (30 eyes of 30 patients--Group 1) or with traditional ultrasound (30 eyes of 30 patients--Group 2). Patients who were available at each follow-up visit (25 eyes in both groups) were enrolled in the statistical analysis. Endothelial function was evaluated by measuring central corneal thickness, central endothelial cell density (ECD), mean cell size, and coefficient of variation in cell size preoperatively, 10 days, 1 and 3 months, and 1 year after surgery. Statistical analyses were performed using two-way repeated measure ANOVA. RESULTS: An acute, reversible increase of central corneal thickness (CCT) was found 10 days after surgery, which was similar in both groups (P=0.35). ECD decreased, whereas mean cell size increased significantly immediately after surgery. However, the impairments were finished after 1 month. The alterations were similar in both groups (ECD: P=0.99; mean cell size: P=0.85). The coefficient of variation in cell size remained stable after surgery (P=0.08), and significant difference was not found between groups (P=0.99). The endothelial cell loss (ECL) was 6.5+/-8.4% in Group 1 and 6.5+/-11.7% in Group 2 (P=0.69). CONCLUSIONS: Corneal endothelial changes were similar using the fluid-based system compared to the traditional ultrasound technique. The fluid-based method proved to be as safe as conventional ultrasound in cataract surgery.

Aged↗

PubMed2004

Vascular endothelial function and plasma homocysteine levels in Behcet's disease.

The purpose of the present study was to test endothelial function and to determine if plasma homocysteine levels are associated with endothelial injury in patients with Behcet's disease (BD). Flow-mediated dilation in patients with BD was smaller than that of control subjects (p = 0.001), and mean plasma homocysteine levels in patients with BD were significantly higher (p = 0.0001). On regression analysis, only mean plasma homocysteine concentration was independently related to flow-mediated dilation (F = 5.7, p = 0.001).

Adult↗

PubMed2002

High-density lipoprotein restores endothelial function in hypercholesterolemic men.

BACKGROUND: Hypercholesterolemia is a risk factor for atherosclerosis-causing endothelial dysfunction, an early event in the disease process. In contrast, high-density lipoprotein (HDL) cholesterol inversely correlates with morbidity and mortality representing a protective effect. Therefore, we investigated the effects of reconstituted HDL on endothelial function in hypercholesterolemic men. METHODS AND RESULTS: Endothelium-dependent and -independent vasodilation to intraarterial acetylcholine and sodium nitroprusside (SNP), respectively, was measured by forearm venous occlusion plethysmography in healthy normo- and hypercholesterolemic men. In hypercholesterolemics, the effects of reconstituted HDL (rHDL; 80 mg/kg IV over 4 hours) on acetylcholine- and SNP-induced changes in forearm blood flow were assessed in the presence or absence of the nitric oxide (NO) synthase inhibitor L-NMMA. Hypercholesterolemics showed reduced vasodilation to acetylcholine but not to SNP compared with normocholesterolemics (P<0.0001). rHDL infusion increased plasma HDL cholesterol from 1.3+/-0.1 to 2.2+/-0.1 mmol/L (P<0.0001, n=18) and significantly enhanced the acetylcholine-induced increase in forearm blood flow without affecting that induced by SNP. rHDL infusion also improved flow-mediated dilation of the brachial artery (to 4.5+/-0.9% from 2.7+/-0.6%, P=0.02). NO synthase inhibition prevented the improvement in acetylcholine-induced vasodilation while leaving the response to SNP unchanged. Albumin infusion in an equivalent protein dose had no effect on vasomotion or lipid levels. CONCLUSIONS: In hypercholesterolemic patients, intravenous rHDL infusion rapidly normalizes endothelium-dependent vasodilation by increasing NO bioavailability. This may in part explain the protective effect of HDL from coronary heart disease and illustrates the potential therapeutic benefit of increasing HDL in patients at risk from atherosclerosis.

Acetylcholine↗

PubMed2003

[Effect of radiofrequency ablation on endothelial function and platelet activation].

OBJECTIVE: To investigate the effect of radiofrequency catheter ablation on endothelial function and platelet activation. METHODS: With radioimmunoassay, enzyme linked immunosorbent assay, cell labeling with monoclonal antibody and flow cytometry technique, thirty-one consecutive patients were checked for levels of plasma endothelin (ET), von willebrand's factor (vWF) and expression of platelet alpha-granule membrane glucoprotein (CD(62P)), platelet lysosome membrane glucoprotein (CD(63)) before, immediately and 47 - 115 hours after radiofrequency catheter ablation. RESULTS: There was no significant difference in the levels of plasma ET and vWF before and after catheter ablation; The rate of CD(62P) and CD(63) expression rate on platelets was (4.75 +/- 2.32)% and (9.62 +/- 4.08)% before catheter ablation, and it significantly increased to (7.64 +/- 5.25)% (t = 3.05, P < 0.01) and (12.23 +/- 5.70)% (t = 2.10, P < 0.05) immediately after catheter ablation and then returned to baseline levels 47 - 115 hours after catheter ablation. There was a positive correlation between the change of CD(62P) expression and total energy dose of radiofrequency (r = 0.30, P < 0.05). CONCLUSIONS: Radiofrequency catheter ablation did not bring about significant damage to endothelium but can increase expression of platelet membrane CD(62P), CD(63) and promote platelet activation, total energy dose of radiofrequency is one of important influencing factor.

Adolescent↗

PubMed1993

[Effect of different solutions of preservatives on the endothelial function of coronary arteries in rats].

The effects of cold storage and type of preservation solution on coronary endothelial function are not well established. Experiments were designed to evaluate coronary endothelial-dependent relaxation after a 4-hour cold (4 degrees C) storage in different preservation solutions. Rat hearts, mounted in the Langendorff apparatus, were arrested with a 10-minute perfusion of 4 degrees C crystalloid hyperkaliemic cardioplegic solution (CHCS) (KCl 24 mEq/l) and stored for 4 hours in the following preservation solutions: CHCS (n = 6), Krebs-Ringer solution (KR) (n = 6), 0.9% NaCl (NS) (n = 6) and the University of Wisconsin solution (UW) (n = 6). A fifth group (n = 6) was perfused and stored in UW solution. Endothelium-dependent and independent coronary artery vasorelaxations were respectively tested by infusing 5-hydroxytryptamine (5-HT) (10(-6) mol/l) and sodium nitroprusside (SNP) (10(-5) mol/l) before and after the storage period. In hearts stored with CHCS or KR, coronary artery flow increase to 5-HT and SNP infusions were not significantly affected. However, in hearts preserved with NS or UW solutions, 5-HT coronary response was significantly decreased, indicating endothelial dysfunction. In addition to these findings, coronary flow increase to SNP infusion was decreased in the group perfused and stored with UW, suggesting smooth muscle dysfunction. These experiments suggest that 4-hour cold storage in NS or UW impairs endothelial-dependent coronary relaxation in the isolated rat heart model.

Adenosine↗

PubMed1998

Does lipoprotein(a) impair endothelial function?

OBJECTIVES: This study was undertaken to test the hypothesis that lipoprotein(a) [Lp(a)] impairs endothelial function. BACKGROUND: Elevated Lp(a) plasma levels have been demonstrated to be associated with an increased risk of coronary heart disease. In atherosclerosis, endothelial dysfunction is known to be an early indicator of vascular changes. However, the effect of Lp(a) on nitric oxide (NO)-dependent vasodilator response has not yet been determined. We therefore examined the influence of Lp(a) on basal and stimulated NO-mediated vasodilator response in the forearm vascular bed. METHODS: Strain gauge plethysmography was used to measure changes in forearm blood flow produced by intraarterial infusion of increasing doses of acetylcholine (3, 12, 24 and 48 microg/min), sodium nitroprusside (200, 800 and 3,200 ng/min) and N-monomethyl L-arginine (L-NMMA) (1, 2 and 4 micromol/min) in 57 white subjects (mean age +/- SD 37 +/- 14 years). Lp(a) plasma concentrations were determined by rocket immunoelectrophoresis. RESULTS: Endothelium-dependent vasodilation tested by intraarterial acetylcholine and endothelium-independent vascular relaxation tested by intraarterial sodium nitroprusside were not correlated with Lp(a). Similarly, no significant differences in forearm blood flow changes were observed when patients were classified into tertiles according to their individual Lp(a) concentration. In contrast, changes in forearm blood flow after intraarterial L-NMMA indicating basal production and release of NO differed significantly among tertiles. Patients in the highest Lp(a) tertile (49.2 +/- 20.3 mg/dl) had a much greater vasoconstrictive response to L-NMMA than patients in the lowest Lp(a) tertile (4.8 +/- 2.5 mg/dl): 2 micromol/min of L-NMMA, -23.6 +/- 22.5% vs. -10.4 +/- 9.1% (p < 0.02); 4 micromol/min of L-NMMA, -27.8 +/- 10.3% vs. -17.6 +/- 9.9% (p < 0.03). Lp(a) plasma level consistently correlated negatively with the forearm blood flow responses to 4 micromol/min of intraarterial L-NMMA (r = -0.38, p < 0.01). Multiple stepwise regression analysis of variables, including total and high and low density lipoprotein cholesterol, further confirmed that plasma Lp(a) remained a significant independent determinant of forearm blood flow changes in response to L-NMMA (p < 0.02). CONCLUSIONS: The endothelium-dependent vasoconstrictive response to L-NMMA was enhanced in subjects with relatively high Lp(a) plasma levels, suggesting an increased basal production and release of NO. This response seemed to reflect a compensatory mechanism of the endothelium to yet unknown Lp(a)-induced atherosclerotic effects.

Acetylcholine↗

PubMed2006

Pleiotrophin induces transdifferentiation of monocytes into functional endothelial cells.

OBJECTIVE: Pleiotrophin (PTN) is a cytokine that is expressed by monocytes/macrophages in ischemic tissues and that promotes neovascularization, presumably by stimulating proliferation of local endothelial cells. However, the effect of PTN on monocytes/macrophages remains unknown. We investigated the role of PTN in regulating the phenotype of monocytes/macrophages. METHODS AND RESULTS: RT-PCR, real-time PCR, and fluorescence-activated cell sorter analysis revealed that the expression of PTN by monocytic cells led to a downregulation of CD68, c-fms, and CD14 monocytic cell markers and an upregulation of FLK-1, Tie-2, vascular endothelial-cadherin, platelet endothelial cell adhesion molecule-1, endothelial NO synthase, von Willebrand factor, CD34, GATA-2, and GATA-3 endothelial cell markers. Fibrin gel assays showed that the treatment of mouse and human monocytic cells with PTN led to the formation of tube-like structures. In vivo studies showed that PTN-expressing monocytic cells incorporated into the blood vessels of the quail chorioallantoic membrane. The intracardial injection of PTN-expressing monocytic cells into chicken embryos showed that cells integrated only into the developing vasculature. Finally, the injection of PTN-expressing monocytes into a murine ischemic hindlimb model significantly improved perfusion of the ischemic tissue. CONCLUSIONS: PTN expression by monocytes/macrophages led to a downregulation of their monocytic cell markers and an upregulation of endothelial cell characteristics, thus inducing the transdifferentiation of monocytes into functional endothelial cells.

Animals↗

PubMed2001

Endothelial function and coronary artery disease.

The endothelium produces a number of vasodilator and vasoconstrictor substances that not only regulate vasomotor tone, but also the recruitment and activity of inflammatory cells and the propensity towards thrombosis. Endothelial vasomotor function is a convenient way to assess these other functions, and is related to the long-term risk of cardiovascular disease. Lipids (particularly low density lipoprotein cholesterol) and oxidant stress play a major role in impairing these functions, by reducing the bioavailability of nitric oxide and activating pro-inflammatory signalling pathways such as nuclear factor kappa B. Biomechanical forces on the endothelium, including low shear stress from disturbed blood flow, also activate the endothelium increasing vasomotor dysfunction and promoting inflammation by upregulating pro-atherogenic genes. In contrast, normal laminar shear stress promotes the expression of genes that may protect against atherosclerosis. The sub-cellular structure of endothelial cells includes caveolae that play an integral part in regulating the activity of endothelial nitric oxide synthase. Low density lipoprotein cholesterol and oxidant stress impair caveolae structure and function and adversely affect endothelial function. Lipid-independent pathways of endothelial cell activation are increasingly recognized, and may provide new therapeutic targets. Endothelial vasoconstrictors, such as endothelin, antagonize endothelium-derived vasodilators and contribute to endothelial dysfunction. Some but not all studies have linked certain genetic polymorphisms of the nitric oxide synthase enzyme to vascular disease and impaired endothelial function. Such genetic heterogeneity may nonetheless offer new insights into the variability of endothelial function.

Animals↗

PubMed2003

Studies on effects of calcineurin inhibitor withdrawal on arterial distensibility and endothelial function in renal transplant recipients.

Whether withdrawal of calcineurin inhibitors has a beneficial effect on disturbed endothelial function and large artery distensibility in renal transplant recipients is not clear. We studied the effects of cyclosporine A (CsA) withdrawal on arterial compliance and endothelium-dependent flow-mediated vasodilatation (FMD) in a prospective, randomized trial; 24 renal transplant recipients receiving mycophenolate mofetil were randomized to withdrawal (n=12) or continuation of CsA (n=12). At baseline and after 6 months, carotid and brachial artery distensibility coefficients and brachial FMD were measured. Brachial distensibility coefficients increased in both groups (withdrawal: 11.1+/-1-14.9+/-2 10(-3)/kPa, continuation: 10.7+/-1-15.2+/-3 10(-3)/kPa, P<0.05, respectively). However, there was no significant effect of treatment on carotid artery distensibility coefficients, FMD, or graft function. Withdrawal of CsA failed to improve carotid artery distensibility or brachial FMD in patients after renal transplantation. Our data indicate that CsA treatment does not contribute significantly to endothelial dysfunction observed in renal transplant recipients.

Adolescent↗

PubMed2002

Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension.

BACKGROUND: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype. HYPOTHESIS: The study sought to determine whether treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery (LMCA) by cold pressor test in patients with essential hypertension, as shown by echocardiography. METHODS: The study population included 30 patients with mild to moderate essential hypertension and 30 matched healthy subjects. Measurements of the cold pressor test-induced and nitroglycerin-induced changes in LMCA diameter by echocardiography were performed at the end of the washout period and after 12 weeks of losartan administration. RESULTS: The percent change in LMCA diameter induced by the cold pressor test in hypertensive patients (-3.5 +/- 8.8%) was significantly lower than that in control subjects (10.2 +/- 3.7%, p<0.0001). After losartan treatment, the percent change (13.9 +/- 8.4%) was significantly higher than that before losartan treatment (-3.5 +/- 8.8%, p < 0.0001), but not significandy different between the 17 hypertensive patients with satisfactory control of blood pressure (13.8 +/- 9.1%) and the 13 hypertensive patients without satisfactory control of blood pressure (14.0 +/- 7.7%, p = 0.9). Losartan treatment in patients with essential hypertension did not modify the percent change in LMCA diameter caused by sublingual administration of nitroglycerin (23.2 +/- 14.0% vs. 27.3 +/- 13.7%, p = 0.2). CONCLUSIONS: This study demonstrates that treatment with losartan normalized response of the LMCA to the cold pressor test in patients with mild to moderate essential hypertension and that this effect is not dependent on the reduction of blood pressure.

Adult↗

PubMed2004

Comparison of endothelial function in young men and women with a family history of premature coronary artery disease.

Endothelial function was evaluated in 34 young men and women with a family history of premature coronary artery disease (CAD) and 28 control subjects. Men with a family history of CAD had significantly impaired flow-mediated, endothelium-dependent vasodilation of the brachial artery compared with controls; however, in women, there was no difference in flow-mediated vasodilation between subjects with a family history and controls.

Adult↗

PubMed2005

A novel method for assessing arterial endothelial function using phase contrast magnetic resonance imaging: vasoconstriction during reduced shear.

We investigated whether endothelial-dependent arterial constriction during reduced shear can be measured using phase contrast magnetic resonance imaging (PCMRI). A cross-section of the femoral artery was acquired during a 5-minute distal occlusion in 33 subjects. Systolic shear rate and radius were measured from the velocity profile via a best-fit parabola. Systolic shear rate decreased immediately after cuff inflation (404 +/- 78 to 233 +/- 75 sec(-1) p < .0001). Radius decreased at 2 min into inflation (3.52 +/- .41 to 3.43 +/- .42 mm, p < .0001). In conclusion, arterial constriction during reduced flow can be measured using PCMRI. This new method may add important information toward a comprehensive evaluation of endothelial function.

Adult↗