Quantification of low-gradient severe aortic stenosis using a hybrid approach combining Doppler echocardiography and thermodilution.

BACKGROUND AND AIM OF THE STUDY: Estimation of stroke volume in the left ventricular outflow tract (LVOT) is a main limitation to aortic valve area (AVA) calculation by echocardiography when using the continuity equation. In this study, the hypothesis was tested that a hybrid method using thermodilution-derived cardiac output measurement and simultaneous Doppler estimation of the systolic ejection period and transvalvular aortic velocities could be used to accurately assess AVA in patients with low-gradient severe aortic stenosis (AS). METHODS: Eighteen patients with low mean gradient (< 40 mmHg) and nine patients with conventionally defined (> or = 40 mmHg) severe AS (< 1 cm2), as assessed by the echocardiographic continuity equation (baseline echocardiography), underwent catheterization and simultaneous Doppler recording of trans-aortic velocities. RESULTS: The mean pressure gradient was slightly lower by Doppler in the catheterization laboratory (35.8 +/-15.7 mmHg) compared to baseline echocardiography (37.4 +/- 15.2 mmHg) and invasive (38.5 +/- 16.6 mmHg) measurements (both p < 0.05). The AVA values were 0.72 +/- 0.12 cm2 during baseline echocardiography, 0.74 +/- 0.14 cm2 by catheterization, and 0.71 +/- 0.14 cm2 by the hybrid method (bias -0.01 +/- 0.11 cm2 and -0.02 +/- 0.08 cm2, versus echocardiography and catheterization, respectively; both p = NS). CONCLUSION: The hybrid method is reasonably accurate in assessing AVA in patients with low-gradient severe AS. Although the continuity equation should be used in routine clinical practice in most patients, this method could serve as an alternative when the LVOT diameter and/or velocities seem questionable.

Pulmonary vasoreactivity in spontaneously hypertensive rats--effects of endothelin-1 and leptin.

BACKGROUND: Systemic hypertension may be associated with an increased pulmonary vascular resistance, which we hypothesized could be, at least in part, mediated by increased leptin. METHODS: Vascular reactivity to phenylephrine (1 µmol/L), endothelin-1 (10 nmol/L) and leptin (0.001-100 nmol/L) was evaluated in endothelium-intact and -denuded isolated thoracic aorta and pulmonary arteries from spontaneously hypertensive versus control Wistar rats. Arteries were sampled for pathobiological evaluation and lung tissue for morphometric evaluation. RESULTS: In control rats, endothelin-1 induced a higher level of contraction in the pulmonary artery than in the aorta. After phenylephrine or endothelin-1 precontraction, leptin relaxed intact pulmonary artery and aortic rings, while no response was observed in denuded arteries. Spontaneously hypertensive rats presented with increased reactivity to phenylephrine and endothelin-1 in endothelium-intact pulmonary arteries. After endothelin-1 precontraction, endothelium-dependent relaxation to leptin was impaired in pulmonary arteries from hypertensive rats. In both strains of rats, aortic segments were more responsive to leptin than pulmonary artery. In hypertensive rats, pulmonary arteries exhibited increased pulmonary artery medial thickness, associated with increased expressions of preproendothelin-1, endothelin-1 receptors type A and B, inducible nitric oxide synthase and decreased endothelial nitric oxide synthase, together with decreased leptin receptor and increased suppressor of cytokine signaling 3 expressions. CONCLUSIONS: Altered pulmonary vascular reactivity in hypertension may be related to a loss of endothelial buffering of vasoconstriction and decreased leptin-induced vasodilation in conditions of increased endothelin-1.

Revascularization versus medical treatments in stable coronary artery disease: predicting the future of novel drug therapies for stable angina.

Over the past 2 decades, drug therapy of patients with stable angina pectoris has improved, with a marked impact on the hard clinical outcomes of mortality and myocardial infarction. In contrast, recent trials have not demonstrated beneficial effects of revascularization on mortality. However, in the large trials that compared medical treatment with percutaneous coronary intervention (PCI) or surgery, high-risk patients, such as those with severe 3-vessel disease with or without left ventricular dysfunction, were excluded. In the COURAGE and FAME 2 trials, the only difference between the PCI and medical therapy groups was a higher rate of revascularization in the latter. Similar findings were made in studies comparing medical treatment with coronary surgery. New pharmacological approaches are being developed to further delay the progression of atherosclerosis. These include new lipid-lowering drugs acting in concert with statins (cholesteryl ester transfer protein inhibitors, proprotein convertase subtilisin/kexin type 9 inhibitors), aldosterone antagonists, colchicine, methotrexate, and interleukin-1 inhibitors. In conclusion, from the available data, PCI and coronary surgery have not been shown to improve hard end points and routine use of invasive revascularization should be avoided in patients with chronic stable angina. Evidence-based secondary prevention remains the most important approach.

Predictors, cost, and outcomes of patients with acute coronary syndrome who receive optimal secondary prevention therapy: results from the antiplatelet treatment observational registries (APTOR).

BACKGROUND: We sought to evaluate outcomes, costs of care, quality of life and predictors at 12 months in patients with an acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) and evaluated use of optimal secondary prevention therapy, defined as use of aspirin and clopidogrel along with ≥ 3 of the following 4 therapies at both hospital discharge and at one-year post-PCI: statins, beta-blockers, ARB/ACE-inhibitors, and exercise or diet. METHODS: Data were from the prospective, observational APTOR study of 14 European countries from 2007 to 2009 (n=4184 patients). RESULTS: Optimal therapy was received in 43% of patients. Use of optimal therapy varied significantly by country. Diet or exercise at 1 year was more likely prescribed to the optimal cohort (34% vs 16%) as was dual antiplatelet therapy (99% vs 49%). Rates of CV event (3.1% vs 3.5%), bleeding (2.9% vs 2.8%) and mortality (0.9% vs 1.3%) at 1 year were similar between the optimal and non-optimal cohorts, respectively. Total costs were similar for both cohorts, but differences in post-discharge costs were observed (optimal: £1760 [£1682-£1844]; non-optimal: £1492 [£1434-£1554]), primarily due to post-discharge medication and resource use. CONCLUSIONS: In conclusion, in this contemporary, European ACS-PCI registry, optimal therapy was low (<50%) overall, particularly for diet or exercise and dual antiplatelet therapy, highlighting a considerable gap between evidence-based guidelines and implementation of such treatments. Whether this gap reflects a missed opportunity to improve patient outcomes or whether it reflects appropriate deviation from guidelines by front-line clinicians requires further investigation.

Acute exposure to diesel exhaust impairs nitric oxide-mediated endothelial vasomotor function by increasing endothelial oxidative stress.

Exposure to diesel exhaust was recently identified as an important cardiovascular risk factor, but whether it impairs nitric oxide (NO)-mediated endothelial function and increases production of reactive oxygen species (ROS) in endothelial cells is not known. We tested these hypotheses in a randomized, controlled, crossover study in healthy male volunteers exposed to ambient and polluted air (n=12). The effects of skin microvascular hyperemic provocative tests, including local heating and iontophoresis of acetylcholine and sodium nitroprusside, were assessed using a laser Doppler imager. Before local heating, skin was pretreated by iontophoresis of either a specific NO-synthase inhibitor (L-N-arginine-methyl-ester) or a saline solution (Control). ROS production was measured by chemiluminescence using the lucigenin technique in human umbilical vein endothelial cells preincubated with serum from 5 of the subjects. Exposure to diesel exhaust reduced acetylcholine-induced vasodilation (P<0.01) but did not affect vasodilation with sodium nitroprusside. Moreover, the acetylcholine/sodium nitroprusside vasodilation ratio decreased from 1.51 ± 0.1 to 1.06 ± 0.07 (P<0.01) and was correlated to inhaled particulate matter 2.5 (r=-0.55; P<0.01). NO-mediated skin thermal vasodilatation decreased from 466 ± 264% to 29 ± 123% (P<0.05). ROS production was increased after polluted air exposure (P<0.01) and was correlated with the total amount of inhaled particulate matter <2.5 µm (PM2.5). In healthy subjects, acute experimental exposure to diesel exhaust impaired NO-mediated endothelial vasomotor function and promoted ROS generation in endothelial cells. Increased PM2.5 inhalation enhances microvascular dysfunction and ROS production.

Vasorelaxant and antihypertensive effects of methanolic extracts from Hymenocardia acida Tul.

ETHNOPHARMACOLOGICAL RELEVANCE: In Congolese traditional medicine, decoctions of Hymenocardia acida root bark (HaRB) and trunk bark (HaTrB) are used for the treatment of conditions assumed to be hypertension. In this work, we propose to study the vasorelaxant effect of HaRB and HaTrB methanolic extracts on isolated rat thoracic aorta, to characterize the group of molecules responsible for the observed vasorelaxant activity, to evaluate the in vitro antioxidant activity of these extracts and to determine the antihypertensive activity of the HaRB extract on spontaneously hypertensive rats (SHR). MATERIALS AND METHODS: The vasorelaxant effect of the HaRB and HaTrB methanolic extracts was studied on endothelium-intact aortic rings pre-contracted with phenylephrine (PE, 1µM). The mechanism of this vasorelaxant effect was investigated on endothelium-denuded vessels and on endothelium-intact aortic rings in the presence of three inhibitors: l-N(G)-nitroarginine methyl ester (100µM), indomethacin (10µM) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10µM). To determine the nature of the compounds responsible for the vasorelaxant activity, we carried out a fractionation of the extracts and a thiolysis of the most active fraction followed by a liquid chromatography/electrospray ionization mass spectrometry (LC/ESI-MS) analysis. The extracts antioxidant activity was determined by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) colorimetric assay. In vivo anti-hypertensive activity of the HaRB extract was conducted on SHR. RESULTS: HaRB and HaTrB methanolic extracts produced a concentration-dependent vasorelaxation on intact aortic rings pre-contracted with PE (1µM). The vasorelaxant responses obtained were 95.3±1.5% (5µg/ml) and 100.6±3.0% (1µg/ml), respectively. The effect was markedly attenuated by removal of endothelium or pretreatment of aortic rings with all inhibitors except indomethacin. The LC/ESI-MS analysis of the thiolysis products indicated that the fraction which caused the most important vasorelaxation (97.9±2.5% at 3µg/ml) was a mixture of procyanidins and prodelphinidins, with a predominance of procyanidins. Both extracts and all fractions from HaRB extract showed a DPPH scavenging activity, ranging from 0.4 to 0.8 quercetin-equivalents. The HaRB methanolic extract reduced the systolic blood pressure in SHR (from 214±3mmHg to 194±4mmHg) after a 5-week treatment. CONCLUSIONS: The methanolic extracts of Hymenocardia acida root and trunk bark have vasorelaxant activity. The vasorelaxant effect observed is endothelium-dependent and seems mainly mediated through the NO-cGMP pathway. The COX pathway is not involved. The vasorelaxant activity appears to be due to polymeric procyanidins and prodelphinidins. These extracts also have an antioxidant effect. The extract of Hymenocardia acida root bark shows a significant but weak antihypertensive activity in SHR.

L-NAME iontophoresis: a tool to assess NO-mediated vasoreactivity during thermal hyperemic vasodilation in humans.

BACKGROUND: Decreased endothelial Nitric oxide (NO) bioavailability is one of the earliest events of endothelial dysfunction. Assessment of microvascular blood flow using a Laser Doppler Imager during local noninvasive administration of L-N-Arginine-Methyl-Ester (L-NAME) by skin iontophoresis may help discriminate the relative contributions of NO and non-NO pathways during a skin thermal hyperemic test. METHODS: In healthy nonsmokers, the effects of thermal vasodilation and sodium nitroprusside-mediated vasodilation were tested on skin pretreated with 0.9% saline solution, 2% L-NAME iontophoresis (n = 12), or intradermal injection of 25 nmol L-NAME (n = 10). The effects of L-NAME iontophoresis were also measured in a group of smokers (n = 10). RESULTS: L-NAME iontophoresis and intradermal injection of L-NAME decreased the skin response to local heating to a similar degree (-41% ± 4% vs. -44% ± 6%). L-NAME iontophoresis site-to-site and day-to-day coefficients of correlation were 0.83 and 0.76, respectively (P < 0.01). The site-to-site and day-to-day coefficients of correlation of L-NAME injection were lower than those of iontophoresis at 0.66 (P < 0.05) and 0.12, respectively (P = not significant). Sodium nitroprusside-induced skin hyperemia was not affected by L-NAME administration. L-NAME iontophoresis-mediated inhibition of skin thermal hyperemia was greater in smokers than in nonsmokers (P < 0.05). CONCLUSIONS: Laser Doppler Imager assessment of skin thermal hyperemia after L-NAME iontophoresis provides a reproducible and selective bedside method of qualitatively analyzing the contribution of the NO pathway to microvascular vasomotor function.

Differences in the use of guideline-recommended therapies among 14 European countries in patients with acute coronary syndromes undergoing PCI.

AIMS: Despite common European Society of Cardiology recommendations, adherence to guideline therapy varies, both temporally and geographically. We sought to examine current differences in the use of guideline-recommended therapies among 14 European countries in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: Data were obtained from the Antiplatelet Therapy Observational Registry (APTOR), a non-interventional, prospective observational cohort study enrolling patients with ACS undergoing PCI. Medication data were captured through 1 year. The large majority of patients in the APTOR registry received statins at hospital discharge (89%) and remained on statins at 1 year (87%), a finding that was consistent across countries. Likewise, beta-blocker use was similar at discharge and 1 year (83 and 81%, respectively). There was large disparity in aspirin loading dose between countries, but the discharge maintenance dose was more consistent, with most receiving ≤ 100 mg (87%). While 95% of patients were discharged on dual antiplatelet therapy, 71% remained on both treatments by 1 year, with wide variation by country in 1-year use. CONCLUSIONS: These data from the APTOR study provide key information on current European ACS patient care management from hospitalization through 1 year. Even with European Society of Cardiology (ESC) guidelines, variations in practice patterns exist among ACS patients treated with PCI between the 14 European countries studied, including the use of proven therapies, as well as appropriate duration and dosing of antiplatelet regimens. Efforts are needed to further explain why such variation exists and to continue to improve adherence to ESC guidelines to improve patient care.

Vascular oxidative stress induced by diesel exhaust microparticles: synergism with hypertension.

BACKGROUND: Epidemiological and clinical studies have shown that traffic-related air pollution and, particularly, diesel exhaust particles (DEP) are strongly linked to cardiovascular mortality. METHODS: Vascular toxicity was studied by assessing vasomotor responses of aortas isolated from normotensive Wistar rats exposed in vitro to DEP (DEP suspension and aqueous DEP extract). In vivo experiments were performed on Wistar rats and spontaneously hypertensive rats (SHRs) exposed for 4 weeks via intratracheal instillation to either DEP or saline vehicle. After killing, vascular responses to acetylcholine (ACh) or sodium nitroprusside were assessed in vitro and the expression of p22phox, a major nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit, was studied by real-time quantitative polymerase chain reaction. RESULTS: In aortas from Wistar rats, in vitro DEP incubation (both preparations) markedly inhibited the relaxations to ACh and slightly to sodium nitroprusside; this effect was reversed in the presence of superoxide dismutase. In contrast, in aortas from in vivo-exposed animals, ACh-induced relaxations were only significantly impaired in the SHR group, accompanied with a significant upregulation of p22phox and no change in systolic blood pressure. CONCLUSIONS: Although in vitro exposure to DEP produces a vascular oxidative stress, repeated in vivo exposures to DEP only impair vascular function in SHR, via an upregulation of p22phox. This suggests a synergistic effect on endothelial dysfunction between particulate air pollution and hypertension.

Vascular effects and antioxidant activity of two Combretum species from Democratic Republic of Congo.

ETHNOPHARMACOLOGICAL RELEVANCE: Combretum racemosum P. Beauv (Combretaceae) leaves (CrLv) and root bark (CrRB) and Combretum celastroides subsp. laxiflorum Welw (Combretaceae) leaves (ClLv) are used in Congolese traditional medicine for several therapeutic purposes, notably for the treatment of conditions consistent with hypertension. The present study aims to investigate the vasorelaxant and in vitro antioxidant activities of these plants polar extracts and to examine the in vivo antihypertensive effect of the extract which displays the most potent vasorelaxant effect. MATERIAL AND METHODS: The vasorelaxant effect of CrLv, CrRB and ClLv methanolic extracts was studied on rat aorta rings pre-contracted with phenylephrine (PE, 1 µM) in the presence or absence of the endothelium. In some experiments, prior to the addition of the extract, rings were incubated for 30 min with either L-N(G)-nitroarginine methyl ester (L-NAME; 100 µM), a nitric oxide synthase (NOS) inhibitor, indomethacin (10 µM), a cyclooxygenase inhibitor, or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 µM), a guanylate cyclase inhibitor. The antioxidant activity was determined by the measurement of the scavenging ability of extracts towards the stable free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH). Blood pressure was measured on normotensive Wistar rats and spontaneously hypertensive rats (SHR) treated orally with a daily dose (40 mg/kg) of the CILv extract for 5 weeks. Tested extracts have been characterised by TLC profiles targeted at flavonoids. RESULTS: All tested extracts showed an important DPPH scavenging activity, ranging from 0.6 to 1.1 quercetin-equivalents. They caused a concentration-dependent vasorelaxation on intact aortic rings pre-contracted with PE (1 µM). The responses to CrRB and CrLv methanolic extracts reached 74.0±5.1% and 62.2±8.6% at a cumulative concentration of 50 µg/ml, respectively. The ClLv (10 µg/ml) extract was more active and, in the same conditions, relaxed aortic rings by 90.3±5.8%. The vasorelaxant activity of all extracts disappeared or was significantly attenuated by removal of the endothelium or after pretreatment with L-NAME or ODQ. Indomethacin only inhibited the activity of CrLv and CrRB extracts. The ClLv extract was able to lower the systolic blood pressure in SHR rats by 7% after a 5-week treatment. CONCLUSIONS: The present study shows that methanolic extracts from ClLv, CrRB and CrLv have an antioxidant activity and an endothelium-dependent vasorelaxant effect. ClLv induces the vasorelaxant effect through the NO-cGMP pathway while CrLv and CrRB extracts also act via a prostanoid pathway. ClLv extract demonstrated a modest but significant antihypertensive activity in SHR rats.

Vitamin D deficiency-induced hypertension is associated with vascular oxidative stress and altered heart gene expression.

Vitamin D deficiency (VDD) is associated with an increased cardiovascular risk. We investigated the effect of VDD on the cardiovascular system of growing male rats fed with a vitamin D-deficient diet. Using isolated rat aorta, we assessed both superoxide anion and endothelial-dependent relaxations. Microarray technology was used to identify changes induced by VDD in cardiac gene expression. Compared with control, VDD increased systolic blood pressure (P < 0.05) and superoxide anion production in the aortic wall (P < 0.05) and tended to increase serum levels of angiotensin II and atrial natriuretic peptide (P < 0.15). However, VDD slightly improved maximal relaxation to acetylcholine from 75 % ± 3% to 83% ± 2% (P < 0.05). Incubation of aortic rings either with nitro-l-arginine methyl ester (l-NAME) or catalase did not eliminate the enhancement of endothelial-mediated relaxation observed in vitamin D-deficient rats. Only incubation with indometacin or calcium-activated potassium channels blockers suppressed this difference. Compared with control, the expression of 51 genes showed different expression, including several genes involved in the regulation of oxidative stress and myocardial hypertrophy. In conclusion, VDD in early life increases arterial blood pressure, promotes vascular oxidative stress, and induces changes in cardiac gene expression. However, the endothelial-mediated regulation of vasomotor tone is maintained throughout the enhancement of an NO-independent compensatory pathway.

Myocardial homing and coronary endothelial function after autologous blood CD34+ progenitor cells intracoronary injection in the chronic phase of myocardial infarction.

Transcoronary transplantation of progenitor cells has been proposed as a novel therapy for ischemic heart failure. The primary aims were to assess the feasibility of obtaining CD34+ cells from blood without mobilization in chronic conditions and to compare homing with results reported in acute conditions. We also evaluated the effect of CD34+ on endothelial function. In 7 patients with a history of an anterior myocardial infarction (20 +/- 2 months), a large amount of CD34 (18.2 +/- 3.0 x 10(6)) were obtained and an intracoronary infusion into the left anterior descending artery via an over-the-wire balloon catheter was performed. Myocardial homing involved 3.2% +/- 0.6% of injected cells. Endothelial function studied with increasing doses of bradykinin was not significantly modified after 3 months. In the treated group, compared with 5 nonrandomized control patients with a similar clinical history, the only echocardiographic significant change (2-way analysis of variance) was a decrease in end-systolic volume (P < 0.03). In conclusion, large amounts of CD34+ cells can be obtained from blood, without mobilization, in the chronic phase of myocardial infarction. As reported in the acute situation 1 hour after treatment, intracoronary infusion of CD34+ cells results in myocardial homing of a few percents of the cells. In this small group of patients, no effect of this therapy is detected on the endothelial function and only marginal changes are observed on echocardiographic parameters.

Oxidative stress produced by circulating microparticles in on-pump but not in off-pump coronary surgery.

OBJECTIVE: This study was undertaken to assess whether plasmas isolated during off-pump coronary surgery trigger less oxidative stress than those isolated during on-pump surgery. METHODS AND RESULTS: Plasmas were sampled from patients before (TO), just after (TI) and 24 hours after (T2) cardiac surgery (n=24 on-pump and n=10 off-pump). Rings of rat thoracic aortas were incubated for 20 hours with these different plasmas (100 microl + 4 ml medium) or saline (control). Thereafter, superoxide anion production was assessed by chemiluminescence and the mean signal was expressed as percent of that in the control ring. In rat aorta exposed to plasmas from on-pump CABG patients (n=6), the signal was enhanced by 210 +/- 29% at T1 (P < 0.05) and by 174 +/- 29% at T2 (P < 0.05) versus 53 +/- 12% at T0. Moreover, at T1 and T2, there was an upregulation of p22(phox), the key subunit of NADPH oxidase, the main enzyme involved in oxidative stress of the vascular wall. In contrast, off-pump plasmas did not induce this superoxide production. Incubation with microparticles obtained by ultracentrifugation also markedly enhanced the signal at T1 and T2 (vs. T0) in the on-pump group (but not in the off-pump group). Selective removal of CD34, CD105, CD59, CD146, CD42 microparticles using flow cytometry did not abolish the signal. CRP and SAA plasma levels were enhanced only at T2 in both groups. CONCLUSIONS: Plasmas isolated after on-pump but not off-pump coronary bypass surgery can induce superoxide generation by the vascular wall which seems related to circulating microparticles remaining present at least 24 hours after the procedure that might be of endothelial origin.

Acute effects of passive smoking on peripheral vascular function.

Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (P=0.01) and after (P<0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (r=0.84; P<0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (n=14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (P=0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (P<0.001), but only ETS reduced the late rise in skin blood flow in response to heating (P=0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels.

Protection of aortic endothelial function in both normal and diabetic rats by intravenous bolus injection of a medium-chain triglyceride: fish oil emulsion.

The bolus intravenous injection of a novel medium-chain triglyceride:fish oil emulsion (MCT:FO) was recently proposed as a tool to provoke a rapid and sustained increase of cell phospholipid content in long-chain polyunsaturated omega3 fatty acids, for instance in selected subjects prior to anesthesia and surgery. In this study, therefore, the possible protective effect of MCT:FO upon aortic endothelial function was investigated in both normal and diabetic rats. The animals were injected intravenously 20 h before sacrifice with 1.0 ml of either saline, MCT:FO or a control medium-chain triglyceride:long-chain triglyceride emulsion. The vasomotor response of isolated aortic rings was then explored by assessing the relaxation provoked by increasing concentrations of acetylcholine in rings contracted with phenylephrine. Such measurements were performed before and after exposure of the aortic rings to suitable concentrations of oxidized LDL. In both normal and diabetic rats, the prior injection of the MCT:FO emulsion protected the aortic rings against the deleterious effect of oxidized LDL. In the diabetic rats, a beneficial effect of the MCT:FO emulsion was even observed prior to exposure of the aortic rings to oxidized LDL. These findings support the view that this novel procedure is indeed appropriate to protect endothelial function against oxidative stress.