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E Roig

Publications and source records attributed to E Roig.

At least 19 recordsLinked to original sources
PubMed2001

[Estradiol enhances endothelium-dependent vasodilation via a nitric oxide pathway].

BACKGROUND AND AIM: The mechanisms by which estradiol dilates arterial vessels are still unclear. Our aim was to study if estradiol enhances endothelium-dependent vasodilation in an experimental model of human arteries in vitro, and if this effect is nitric oxide mediated. METHODS: Using organ bath chambers, we studied 18 arterial rings obtained from left internal mammary arteries during coronary artery bypass grafting surgery. Response to acetylcholine was evaluated at baseline and after the addition of estradiol 10-6 mol/l to the medium, both in the presence or absence of a nitric oxide synthase inhibitor (L-NNA 10-4 mol/l). RESULTS: Estradiol significantly enhanced the relaxation of the arterial rings in response to acetylcholine (52 +/- 20% after estradiol versus 42 +/- 22% at baseline; n = 10; p = 0.02). However, endothelium-dependent vasodilation relaxation after estradiol addition was not enhanced in the presence of L-NNA (47 +/- 25% after estradiol versus 38 +/- 22% at baseline; n = 8; p = NS). CONCLUSIONS: Estradiol in vitro enhances endothelium-dependent vasodilation of internal human mammary artery rings; this effect is blunted after the addition to the medium of a nitric oxide inhibitor. Therefore, the vasodilator properties of estradiol at the studied dosage depend on the nitric oxide pathway.

Aged↗
PubMed2000

Mitochondrial function in heart muscle from patients with idiopathic dilated cardiomyopathy.

OBJECTIVE: To study the mitochondrial respiratory chain enzyme activities in patients with idiopathic dilated cardiomyopathy (IDC). METHODS: Mitochondrial respiratory chain enzyme activities were assessed spectrophotometrically in left ventricular tissue of 17 patients with IDC undergoing cardiac transplantation, as well as in two groups of controls: a group of six patients suffering from ischemic dilated cardiomyopathy (IC) also undergoing cardiac transplantation, and a group of 17 organ donors considered normal from a cardiac point of view. Cytochrome b gene from three IDC patients whose complex III activity was particularly low and from three controls was also sequenced. RESULTS: We found that complex III enzymatic activity was lower not only in IDC but also in IC patients when compared with normal controls. When analysing cytochrome b gene we only found neutral polymorphisms previously described. CONCLUSIONS: In view of such results, we believe that the decrease of respiratory chain complex III activity found in some cases of IDC is a secondary phenomenon, and not due to a primary mitochondrial disease.

Adult↗
PubMed2000

[Effect of cyclooxygenase inhibition on the adaptation of coronary blood flow to tachycardia].

BACKGROUND: The role of different endothelium-derived vasoactive substances in the regulation of coronary circulation during tachycardia is not well defined. In order to elucidate the contribution of prostacyclin to the adaptation of coronary blood flow to tachycardia, the effect of meclofenamate, a cyclooxygenase inhibitor on the coronary blood flow response to rapid atrial pacing was analyzed in a porcine model. METHODS: A group of seventeen pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing. Heart rate was increased by 20 beats every 5 minutes. Coronary blood flow and aortic pressure were measured, and coronary resistance calculated, basally and at each pacing interval, before and after saline serum (n = 6), meclofenamate 5 mg/kg, i.v. (n = 7) or meclofenamate 35 mg/kg, i.v. (n = 4). RESULTS: Neither saline nor meclofenamate modified the normal increase of coronary blood flow provoked by rapid atrial pacing (163 +/- 28% increase before versus 172 +/- 29% after saline; 159 +/- 21% increase before versus 161 +/- 22% after meclofenamate low doses and 201 +/- 39% before vs 172 +/- 36 after meclofenamate high doses). There were no differences in the response of coronary vascular resistance to tachycardia before and after meclofenamate (44% reduction vs 40% respectively). CONCLUSION: Cyclooxygenase blockade does not modify the response of coronary circulation to rapid atrial pacing, suggesting that prostacyclin does not play a limiting role in the regulation of coronary blood flow during tachycardia in this model.

Animals↗
PubMed2000

Prognostic value of serum cytokines in patients with congestive heart failure.

BACKGROUND: Increased levels of circulating cytokines have been previously reported in patients with congestive heart failure; however, whether they have prognostic implications is still unknown. The aim of this study was to assess the prognostic implications of elevated serum cytokines in patients with heart failure and to identify the predictors of cytokine activation. METHODS AND RESULTS: We assessed neurohormonal determinations, circulating cytokines, ejection fraction (EF) and end-diastolic and end-systolic left ventricular lengths in 87 patients (aged 57 +/- 9 years) with left ventricular dysfunction (EF 24% +/- 6%). In 48 patients, we also assessed cytokine receptors. During follow-up (mean, 14 +/- 9 months), 8 patients died and 12 had new heart failure episodes that required hospital admission, 5 of whom underwent heart transplantation. The univariate predictors of these events were serum interleukin-6 (IL-6) (p = 0.00001), New York Heart Association (NYHA) functional class (p = 0.0004), tumor necrosis factor-soluble receptor I (p = 0. 001), atrial natriuretic peptide (p = 0.002), tumor necrosis factor-soluble receptor II (p = 0.004), angiotensin II (p = 0.006), serum interleukin-1 beta (p = 0.01), and plasma renin activity (p = 0.02). Increased serum interleukin-6 (>10 pg/ml) was a significant predictor of death or new heart failure episodes according to the Kaplan-Meier survival method by log-rank test (p = 0.004). By Cox regression analysis, serum IL-6 (p = 0.0005) and the NYHA functional class (p = 0.005) were identified as independent predictors of prognosis. CONCLUSIONS: In patients with congestive heart failure, increased serum IL-6 was identified as a powerful independent predictor of the combined end point: death, new heart failure episodes, and need for heart transplantation.

Adult↗
PubMed2000

Nitric oxide synthase II mRNA expression in cardiac tissue of patients with heart failure undergoing cardiac transplantation.

OBJECTIVES: To examine whether inducible nitric oxide synthase is expressed in myocardial tissue of patients with heart failure. BACKGROUND: There is increasing evidence that alterations in nitric oxide synthesis are of pathophysiologic importance in heart failure. Nitric oxide (NO) can exert negative inotropic and cytotoxic effects on cardiomyocytes. A number of studies have shown altered nitric oxide production by the endothelial constitutive isoform of nitric oxide synthase (NOS III), but there is little information on the role of NOS II. Expression of NOS II could lead to excessive production of NO in the myocardium and affect cardiac contractility. METHODS: NOS II mRNA expression in myocardial tissue of 18 patients with idiopathic dilated cardiomyopathy (DCM), 7 patients with ischemic cardiopathy and severe ventricular dysfunction (ISCH), 4 patients with acute myocardial infarction (AMI) and 11 controls. Serum concentration of NO2-/NO3- (NOx) was also measured. RESULTS: NOS II gene expression occurred in all the patients with DCM, in 1 out of the 7 ISCH patients, in 2 out of the 4 patients with AMI and in none of the controls. Moreover, DCM patients showed a significant 6-fold increase in NOx concentration (253+/-47 nm/ml) as compared to controls (40+/-2 nm/ml) P < 0.001, a phenomenon not observed in ISCH patients (56+/-3 nm/ml). CONCLUSIONS: NOS II expression occurs in failing human cardiac myocytes and can play an specific role in the pathogenesis of DCM.

Cardiomyopathy, Dilated↗
PubMed2000

Nitric oxide inhibition intensifies the depressant effect of cocaine on the left ventricular function in anaesthetized pigs.

Myocardial ischaemia and left ventricular dysfunction have been described in cocaine users. Whether nitric oxide (NO) inhibition may potentiate the effects of cocaine on coronary circulation and ventricular function is still unknown. In order to test this hypothesis, 38 pentobarbital-anaesthetized pigs were instrumented for systolic blood pressure, coronary blood flow, left ventricular dp/dt, cardiac output, left ventricular end-diastolic and end-systolic lengths and shortening fraction. The pigs were randomized into three groups: control group: i.v. saline (n = 5); group 1: i.v. cocaine, 10 mg kg-1 over 20 min (n = 17); group 2: the same doses of cocaine 30 min after i.c. L-NAME 20 microg/kg min-1 infusion (n = 16). In order to know whether the observed effects were specific of NO inhibition, in five pigs i.c. L-arginine was simultaneously infused with L-NAME, in five pigs i.c. NTG, an endothelial-independent vasodilator, was simultaneously infused with L-NAME before cocaine was administered, and in nine additional pigs the proximal left anterior descending (LAD) flow was reduced to around 20% of the basal value by means of a mechanical occluder before cocaine was administered. Cocaine i.v did not change the coronary blood flow, while it induced a significant reduction in cardiac output, left ventricular dp/dt and shortening fraction (15 +/- 4-8 +/- 4%, P < 0.05). When cocaine was administered after L-NAME infused i.c. during 30 min, a significantly more severe reduction of the shortening fraction (12 +/- 3-4 +/- 2%, P < 0.0001) was induced; this effect was abolished by simultaneous perfusion of L-arginine i.c. NTG. The results when cocaine was administered after the 20% LAD flow reduction by mechanical occluder did not differ from those of cocaine alone. NO inhibition intensifies the cocaine-induced left ventricular dysfunction.

Anesthesia↗
PubMed2000

Identification of the Escherichia coli K-12 Nramp orthologue (MntH) as a selective divalent metal ion transporter.

The Escherichia coli mntH (formerly yfeP) gene encodes a putative membrane protein (MntH) highly similar to members of the eukaryotic Nramp family of divalent metal ion transporters. To determine the function of E. coli MntH, a null mutant was created and MntH was overexpressed both in wild-type E. coli and in the metal-dependent mutant hflB1(Ts). At the restrictive temperature 42 degrees C, the mntH null mutation reduces the suppression of hflB1(Ts) thermosensitivity by exogenous divalent metals. Conversely, overexpression of MntH restores growth at 42 degrees C, increases suppression of the ts phenotype by Fe(II) and Ni(II) and renders hflB1(Ts) cells hypersensitive to Mn(II). Transport studies in intact cells show that MntH selectively facilitates uptake of 54Mn(II) and 55Fe(II) in a temperature-, time- and proton-dependent manner. Competition studies in uptake assays and growth inhibition experiments in hflB1(Ts) mutants together indicate that MntH is a divalent metal cation transporter of broad substrate specificity. The functional characteristics of MntH suggest that it corresponds to the previously described manganese transporter of E. coli. This study indicates that proton-dependent divalent metal ion uptake has been preserved in the Nramp family from bacteria to humans.

Base Sequence↗
PubMed2000

Clinical implications of increased plasma angiotensin II despite ACE inhibitor therapy in patients with congestive heart failure.

AIMS: The aim of the study was to assess the incidence and clinical implications of increased plasma angiotensin II despite chronic ACE inhibitor therapy in patients with heart failure. METHODS AND RESULTS: The studied population consisted of 70 patients (mean age 59+/-9 years). Plasma renin activity and plasma concentration of aldosterone, norepinephrine, atrial natriuretic peptide, angiotensin II, tumour necrosis factor, interleukin-6 and interleukin-1B were assessed at 6 months of ACE inhibitor therapy. Mean left ventricular ejection fraction was 24+/-5% and the end-systolic and end-diastolic diameters were 59+/-9 and 71+/-8 mm, respectively. Despite chronic enalapril or captopril therapy, 35 patients (50%) had increased plasma angiotensin II (median 33 pg. ml(-1), range 17-84), while it was in the normal range in the remaining 35 patients (median 10 pg. ml(-1), range 5-15). Plasma renin activity (P=0.005), interleukin-6 (P=0.004), New York Heart Association functional class III-IV (P=0. 006), furosemide dose (P=0.01), lack of beta-blocker therapy (P=0. 04) and norepinephrine (P=0.04) were univariately associated with increased angiotensin II. Multivariate regression analysis identified the plasma renin activity (0.0004), norepinephrine (0.02) and interleukin-6 (0.03) as independent predictors of plasma angiotensin II. During follow-up (35+/-29 months), nine (12.8%) patients died and 13 had new heart failure episodes. Increased plasma angiotensin II, despite ACE inhibitor therapy, was a significant predictor of death or heart failure according to the Kaplan-Meier survival method by log rank test (P=0.002). CONCLUSION: Fifty per cent of patients with heart failure, ha increased plasma angiotension II despite chronic ACE inhibitor therapy. These patients had higher neurohormonal activation and poor prognosis.

Angiotensin II↗
PubMed2000

A reply

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Journal Article↗
PubMed2000

Changes in the cooling rate and medium improve the vascular function in cryopreserved porcine femoral arteries.

PURPOSE: The purpose of this study was to design an adequate technique with which to cryopreserve pig femoral arteries and to assess the influence of storage times in vascular function. METHODS: Fifty-two femoral arteries were distributed in seven groups. In group A (control), 10 arteries were studied after harvest; in groups B1 and B2, 19 arteries were suspended in RPMI 1640 plus fetal calf serum plus dimethylsulfoxide and were cryopreserved at 1 degrees C per minute or 0.3 degrees C per minute, respectively. In groups C1 to C4, 23 arteries were suspended in modified Krebs-Henseleit plus dimethylsulfoxide plus sucrose, cryopreserved at 0.7 degrees C per minute, and kept frozen for 1, 15, 60, or 180 days, respectively. After being thawed, arteries were examined for contraction and endothelial-dependent vasodilation (organ bath studies), antithrombotic properties of the endothelial layer(perfusion studies), and vessel structure (electron microscopy). RESULTS: Endothelial cells were present in both cryopreserved and control arteries. The control vessels showed a mean contraction to norepinephrine (10(-7) mol/L) of 13010 +/- 3181 mg. Arteries in groups B1 and B2 did not respond to norepinephrine. Contraction in groups C1 to C4 was as follows: C1, 5354 +/- 1222 mg; C2, 5187 +/- 2672 mg; C3, 6867 +/- 2292 mg; C4, 7000 +/- 2858 mg, which represent 50% of the control values (P <.001). Vasodilation was similar in control (99% +/- 3%) and cryopreserved arteries (C1, 90% +/- 13%; C2, 93% +/- 12%; C3, 89% +/- 15%; C4, 88% +/- 22%). Storage time did not influence vascular function. Platelet interaction was almost absent and similar in all groups. CONCLUSION: A modified cryopreservation technique preserves endothelial function independently of the storage time up to 6 months.

Acetylcholine↗
PubMed1999

Captopril administration reduces thrombus formation and surface expression of platelet glycoprotein IIb/IIa in early postmyocardial infarction stage.

Long-term administration of the angiotensin-converting enzyme inhibitor captopril in survivors of myocardial infarction (MI) reduces the risk of cardiovascular death, recurrence of MI, and unstable angina, suggesting that captopril may possess antithrombotic properties that have not been clearly elucidated. We assessed the short-term antithrombotic effects of captopril on platelet aggregation, platelet-subendothelium interaction, and the expression of major glycoproteins on platelet surface. A double-blind study was carried out in 25 patients with MI. Blood samples were taken before (baseline) and 12 days after treatment in both the control and captopril groups. Platelet aggregation was tested by conventional aggregometry using common activating agents. Platelet interaction with deeply damaged subendothelial surface was evaluated in a perfusion model, with blood maintained under flow conditions. Deposition of platelets was quantified by using computer-assisted morphometric techniques on histological sections, and it was expressed as a percentage of total vessel surface covered by platelets (CS) and as a ratio between large aggregates (T) and surface covered by platelets (100XT/CS). Glycoprotein expression was measured using flow cytometric techniques. Aggregometric responses showed no significant variations; however, in the captopril group, 100XT/CS decreased after 12 days of treatment (100XT/CS: 36+/-12.1% captopril versus 64+/-8.0% baseline; P=0.005). This parameter was also significantly decreased from that found in control group patients (100XT/CS:67=/-4.5%, P=0.008). Flow cytometry showed a 30% reduction in glycoprotein IIb/IIIa expression (P=0.02). Captopril reduced the formation of large aggregates in a perfusion system, which might be related to a down-regulation of glycoprotein IIb/IIIa complex on the platelet surface. These results suggest that captopril exerts an antiplatelet effect that may contribute to its beneficial action in MI.

Aged↗
PubMed1998

Suppression of leukotriene B4 and tumour necrosis factor alpha release in acute inflammatory responses by novel prenylated hydroquinone derivatives.

A series of prenyl hydroquinone derivatives synthesized as structural analogs of marine products were tested for their effects on inflammatory responses in vitro and in vivo. 2-Prenyl-1,4-hydroquinone (H1), 2-diprenyl-1,4-hydroquinone (H2), 2-triprenyl-1,4-hydroquinone (H3) and 2-tetraprenyl-1,4-hydroquinone (H4) scavenged reactive oxygen species and inhibited 5-lipoxygenase (5-LO) activity in human neutrophils. The inhibition of 5-LO activity was demonstrated in vivo in the mouse air pouch injected with zymosan and arachidonic acid-induced ear inflammation. The four compounds suppressed the production of tumour necrosis factor alpha (TNFalpha) in J774 cells stimulated with lipopolysaccharide (LPS) and also in vivo in the mouse air pouch injected with zymosan. In addition, all prenyl-hydroquinones inhibited the release of nitrite and PGE2 in LPS-stimulated J774 cells, without direct effects on cyclo-oxygenase-1 (COX-1), cyclo-oxygenase-2 (COX-2) or inducible nitric oxide synthase (iNOS) activities in several cell-free systems. The reduction in the length of the lateral chain in prenyl-hydroquinones (1-4 isoprene units) with respect to their marine analogs (7-8 isoprene units) has improved the anti-inflammatory activity of this class of compounds. Marine natural products may be a model to design new anti-inflammatory agents.

Animals↗
PubMed1998

Short-term effects of transdermal estrogen replacement therapy on coronary vascular reactivity in postmenopausal women with angina pectoris and normal results on coronary angiograms.

OBJECTIVES: This study sought to analyze the effect of short-term transdermal estradiol treatment on in vivo coronary endothelial function in postmenopausal women with angina and normal results on coronary arteriograms. BACKGROUND: The incidence of coronary heart disease increases in women after menopause. Estrogen replacement therapy has been associated with a global reduction in cardiovascular disease incidence and mortality. In addition, coronary endothelial dysfunction has been demonstrated in a group of postmenopausal women. It has been shown that intravenous or intracoronary estrogens improve endothelial function in postmenopausal women with coronary atherosclerosis. However, the efficacy of this treatment is unknown in patients with angina and normal coronary arteries. METHODS: Endothelium-dependent coronary reactivity was analyzed in 15 postmenopausal women with angina and normal coronary arteries at baseline and after 24 h of estradiol transdermal administration (100 microg). RESULTS: Estradiol concentration increased from 22 +/- 8 pg/ml (mean +/- SEM) at baseline to 76 +/- 13 pg/ml (p < 0.01) at 24 h. At baseline, acetylcholine induced vasoconstriction, with a mean diameter reduction of -23 +/- 6% (p = 0.002). After estrogen treatment, there was no vasoconstriction with acetylcholine, with a mean diameter change of 0 +/- 4%, significantly different from the pretreatment diameter reduction observed (p = 0.003). Similarly, estimated coronary blood flow significantly increased in response to acetylcholine after estrogen treatment, with a mean change of 50 +/- 30% compared with 5 +/- 24% before estradiol administration (p = 0.04). CONCLUSIONS: Early after transdermal estrogen administration, endothelium-dependent coronary vasomotion is improved in postmenopausal women with angina and normal coronary arteries.

Aged↗
PubMed1997

Cocaine administration enhances platelet reactivity to subendothelial components: studies in a pig model.

Myocardial infarction in cocaine abusers may be related to a direct platelet-activating effect. We analysed this possibility in an experimental model. Studies were carried out in eight normal, anaesthetized pigs with a weight of 30.7 +/- 3.7 kg. Blood samples were withdrawn before and 20 min after i.v. administration of cocaine (10 mg kg-1; at 1 mg kg-1 every 2 min). Modifications in platelet responses to arachidonic acid (AA; 1.4 mmol L-1), ADP (1-4 microM), synthetic thromboxane endoperoxide analogue (U46619; 1 microM), collagen (2.5-5 micrograms mL-1), adrenaline (10 microM) and ristocetin (0.8-1 mg mL-1) were tested by conventional aggregometry. Changes in the capacity of platelets to form aggregates on damaged subendothelium were assessed by means of an ex vivo perfusion system in which blood was circulated for 10 min at 800 s-1, a shear rate similar to that found in normal coronary arteries. The interaction of platelets with perfused denuded arterial segments was morphometrically quantified and expressed as a percentage of damaged vessel surface covered by platelets (%CS). Cocaine administration did not influence platelet aggregation patterns in pigs. However, there was a significant increase in the interaction of pig platelets with subendothelial structures after cocaine infusion (%CS = 40 +/- 17% vs. 27 +/- 16% baseline; mean +/- SD; P < 0.01). Cocaine administration in this animal model increases the reactivity of platelets exposed to subendothelium. These results support the concept that the administration of cocaine to pigs has a prothrombotic effect by facilitating the interaction of platelets with damaged arteries.

Animals↗
PubMed1997

Anti-Candida albicans IgE and IgG subclasses in sera of patients with allergic bronchopulmonary aspergillosis (ABPA).

We performed immunoblotting experiments to determine specific IgE and IgG subclass responses to Candida albicans antigens in allergic bronchopulmonary aspergillosis (ABPA) patients. This is a first report describing C. albicans antigens recognized by serum IgE and IgG subclasses of ABPA patients sensitized to that yeast. Among the various antigens reacting with serum IgE, a 43-kDa component was recognized by all seven patients and can be considered a major antigen of C. albicans for this particular group of patients. By comparison, only 20% of a group of asthmatic atopics (25 patients) and 10% of a group of normal controls (10 subjects) were 43-kDa positive. Multiple banding patterns, revealing no major antigen, were observed for all four IgG subclasses except for IgG1 in one case. In particular, the 43-kDa component was not always recognized by all the patients. Furthermore, oral or inhaled steroid treatment appears to have no impact on the specific IgE immunopatterns obtained. Using immunoelectron-microscopy, we localized IgE-binding primarily in the mannoprotein-containing layers of the C. albicans cell wall. In conclusion, C. albicans-IgE and IgG subclasses may participate in the physiopathology of ABPA by exacerbating pulmonary infiltrates (IgE) and inducing eosinophil-mediated inflammatory reaction (IgG1, IgG3).

Adrenal Cortex Hormones↗
PubMed1996

Endothelial dysfunction of the non-infarct related, angiographically normal, coronary artery in patients with an acute myocardial infarction.

BACKGROUND: Patients with acute myocardial infarction and single-vessel disease may have early atherosclerosis in other angiographically normal coronary arteries. METHODS: Coronary endothelial responses were analysed in 20 non-diabetic patients with an acute myocardial infarction and one-vessel disease. In an angiographically normal, non-infarct related, coronary artery serial acetylcholine doses of 10(-7) M, 10(-6) M, 10(-5) M and 10(-4) M and nitroglycerin 40 micrograms were infused over 3 min. The responses of the coronary vessel were measured with quantitative angiography. Coronary blood flow was also measured with a Doppler catheter in 11 of the 20 patients. RESULTS: Four patients showed a trend towards vasodilation during acetylcholine infusion in the proximal and distal segments: from 2.49 +/- 0.23 mm to 2.95 +/- 0.42 mm and 2.43 +/- 0.56 mm to 2.81 +/- 0.66 mm, respectively. Coronary vascular resistance decreased to 57 +/- 4% (P = 0.03). The other 16 patients presented vasoconstriction in the proximal and distal segments: 2.61 +/- 0.75 mm to 2.03 +/- 0.65 mm (P = 0.0001), and 2.40 +/- 0.58 to 1.81 +/- 0.56 mm (P = 0.0036), respectively. Nitroglycerin caused vasodilation in the proximal (2.69 +/- 0.61 mm, P = 0.017, ANOVA) and distal segments (2.48 +/- 0.45 mm, P = 0.009, ANOVA). Coronary vascular resistance increased to 141 +/- 43% (P = 0.03) over the basal value in this group of patients. CONCLUSION: Endothelial dysfunction of the epicardial and resistance vessels was found in angiographically normal coronary arteries of patients with one-vessel disease in 75% of this population.

Adult↗