PubMed Health⌕ Search

Biomedical subjects

R Corbalán

Publications and source records attributed to R Corbalán.

At least 19 recordsLinked to original sources
PubMed2003

Cavity solitons in two-level lasers with dense amplifying medium.

Local-field effects are known to induce bistability in dense optical media. We examine theoretically whether this property is preserved in broad-area cavities, and show that bistability between the homogeneous lasing and nonlasing states of the system persists provided a Fourier filtering technique is used to prevent off-axis emission. The resulting bistability gives rise to spatial light localization in the form of cavity solitons, which exhibit a particularly large degree of plasticity as a function of the characteristics of the addressing beam. This is the simplest laser able to sustain cavity solitons.

Journal Article↗
PubMed2002

Phase scaling properties of perturbation-induced multistability in a driven nonlinear system.

Phase scaling relations for the onsets of both saddle-node bifurcations and boundary crises induced by resonant periodic perturbations at subharmonic frequencies are found in a period-doubled system from the results of numerical simulation. These phase dependences determine the domains of existence of induced attractors in (bifurcation parameter, perturbation phase) parameter space. The overlapping of these domains leads to the formation of zones with different numbers of coexisting attractors. The numerical evidence was obtained on the basis of single-mode rate equations of a laser with parameters corresponding to a realistic loss-modulated CO2 laser.

Journal Article↗
PubMed2002

Altered modulation of soluble guanylate cyclase by nitric oxide in patients with liver disease.

The glutamate-nitric oxide-cGMP pathway is impaired in brain in vivo in animal models of chronic moderate hyperammonemia either with or without liver failure. The impairment occurs at the level of activation of soluble guanylate cyclase by nitric oxide (NO). It has been suggested that the impairment of this pathway may be responsible for some of the neurological alterations found in hyperammonemia and hepatic encephalopathy. Soluble guanylate cyclase is also present in lymphocytes. Activation of guanylate cyclase by NO is also altered in lymphocytes from hyperammonemic rats or from rats with portacaval anastomosis. We assessed whether soluble guanylate cyclase activation was also altered in human patients with liver disease. We studied activation of soluble guanylate cyclase in lymphocytes from 77 patients with liver disease and 17 controls. The basal content of cGMP in lymphocytes was decreased both in patients with liver cirrhosis and in patients with chronic hepatitis. In contrast, cGMP concentration was increased in plasma from patients with liver disease. Activation of guanylate cyclase by NO was also altered in liver disease and was higher in lymphocytes from patients with cirrhosis or hepatitis than that in lymphocytes from controls. Successful treatment with interferon of patients with hepatitis C reversed all the above alterations. Altered modulation of soluble guanylate cyclase by NO in liver disease may play a role in the neurological and hemodynamic alterations in these patients.

Animals↗
PubMed2001

Association of noninvasive markers of coronary artery reperfusion to assess microvascular obstruction in patients with acute myocardial infarction treated with primary angioplasty.

Early restoration of coronary artery patency through primary angioplasty limits infarct size and improves survival. Increasing evidence, however, suggests that microvascular obstruction is often present despite coronary artery recanalization. This may limit the benefits of reperfusion therapy. We studied the use of noninvasive markers of coronary artery reperfusion as indicators of microvascular obstruction and determinants of prognosis in 98 patients with acute myocardial infarction (AMI) who were successfully treated with primary angioplasty (Thrombolysis In Myocardial Infarction grade 3 flow and residual stenosis <30%). Plasma creatine kinase (CK) levels and 12-lead electrocardiograms were performed on admission, at 90 minutes, and at 6, 12, and 24 hours after treatment. We defined: (1) reperfusion as resolution of ST-segment elevation >50% at 90 minutes, with peak CK levels within 12 hours, and T-wave inversion within 24 hours; and (2) failed reperfusion, as the absence of these parameters. Of the 98 patients studied, 87 (88.8%) had reperfusion and 11 (11.2%) had failed reperfusion. Infarct location was anterior (versus inferior) in 9 patients in the failed reperfusion group (81.8%) compared with 41 patients in the reperfusion group (47.1%) (p <0.01). Congestive heart failure >24 hours after presentation or in-hospital death occurred in 11 patients (12.6%) in the reperfusion group versus 5 (45.5%) in the failed reperfusion group (p <0.01). One-year survival was 96.1% for the reperfusion group and 60.6% for the failed reperfusion group (p <0.0001). We conclude that the association of noninvasive markers of reperfusion better identifies patients with microvascular obstruction among those who had a "successful" primary angioplasty. Evidence of impaired microvascular reperfusion is associated with a poor in-hospital and 1-year outcome.

Aged↗
PubMed2001

Aluminium impairs the glutamate-nitric oxide-cGMP pathway in cultured neurons and in rat brain in vivo: molecular mechanisms and implications for neuropathology.

Aluminium (Al) is a neurotoxicant and appears as a possible etiological factor in Alzheimer's disease and other neurological disorders. The mechanisms of Al neurotoxicity are presently unclear but evidence has emerged suggesting that Al accumulation in the brain can alter neuronal signal transduction pathways associated with glutamate receptors. In cerebellar neurons in culture, long term-exposure to Al added 'in vitro' impaired the glutamate-nitric oxide (NO)-cyclic GMP (cGMP) pathway, reducing glutamate-induced activation of NO synthase and NO-induced activation of the cGMP generating enzyme, guanylate cyclase. Prenatal exposure to Al also affected strongly the function of the glutamate-NO-cGMP pathway. In cultured neurons from rats prenatally exposed to Al, we found reduced content of NO synthase and of guanylate cyclase, and a dramatic decrease in the ability of glutamate to increase cGMP formation. Activation of the glutamate-NO-cGMP pathway was also strongly impaired in cerebellum of rats chronically treated with Al, as assessed by in vivo brain microdialysis in freely moving rats. These findings suggest that the impairment of the Glu-NO-cGMP pathway in the brain may be responsible for some of the neurological alterations induced by Al.

Aluminum↗
PubMed2001

Altered content and modulation of soluble guanylate cyclase in the cerebellum of rats with portacaval anastomosis.

It is shown that the glutamate-NO-cGMP pathway is impaired in cerebellum of rats with portacaval anastomosis in vivo as assessed by in vivo brain microdialysis in freely moving rats. NMDA-induced increase in extracellular cGMP in the cerebellum was significantly reduced (by 27%) in rats with portacaval anastomosis. Activation of soluble guanylate cyclase by the NO-generating agent S-nitroso-N-acetyl-penicillamine and by the NO-independent activator YC-1 was also significantly reduced (by 35-40%), indicating that portacaval anastomosis leads to remarkable alterations in the modulation of guanylate cyclase in cerebellum. Moreover, the content of soluble guanylate cyclase was increased ca. two-fold in the cerebellum of rats with portacaval anastomosis. Activation of soluble guanylate cyclase by NO was higher in lymphocytes isolated from rats with portacaval anastomosis (3.3-fold) than in lymphocytes from control rats (2.1-fold). The results reported show that the content and modulation of soluble guanylate cyclase are altered in brain of rats with hepatic failure, resulting in altered function of the glutamate-NO-cGMP pathway in the rat in vivo. This may lead to alterations in cerebral processes such as intercellular communication, circadian rhythms, including the sleep-waking cycle, long-term potentiation, and some forms of learning and memory.

Animals↗
PubMed2001

Variation in patient management and outcomes for acute coronary syndromes in Latin America and North America: results from the Platelet IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial.

BACKGROUND: Although more than 9500 patients have been enrolled in major clinical trials in Latin America, practice patterns in this region have rarely been examined. We sought to compare characteristics, resource utilization, and outcomes of patients treated for acute coronary syndromes in Latin America with those in North America. METHODS: The Platelet IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Theraphy Trial (PURSUIT) enrolled 10,948 patients with non-ST-segment elevation acute coronary syndromes, including 585 in Latin America and 4358 in North America. We analyzed regional differences in patient groups, treatment patterns, and outcomes and used logistic regression analysis to identify association of enrollment region and survival. RESULTS: For patients in Latin America, the length of hospital stay was significantly longer (10 [7, 15] days vs 6 [4, 9], P <.001). Angiograms, angioplasty, and bypass surgery were significantly less common in Latin America (46.2%, 17.6%, and 11.3% vs 79.4%, 33.6%, and 19.4%, P <.001). Thirty-day death/myocardial infarction was not significantly higher, although mortality alone was significantly higher (6.8% vs 3.1%, P <.001). After adjustment for baseline characteristics, enrollment in Latin America remained an independent predictor for death at 30 days (odds ratio [OR] [95% confidence interval (CI)] 2.42 [1.60-3.67]) and persisted at 6 months (OR [95% CI] 2.5 [1.8-3.4]). CONCLUSIONS: Latin American patients treated for acute coronary syndromes were managed less invasively and were twice as likely as their North American counterparts to die within 6 months. This mortality difference was not explained by imbalances in baseline risk.

Angina, Unstable↗
PubMed2001

[Selective training of respiratory muscles in patients with chronic heart failure].

BACKGROUND: Patients with chronic heart failure have a lower inspiratory muscle strength and fatigue endurance. AIM: To assess the effects of selective training of respiratory muscles in patients with heart failure. PATIENTS AND METHODS: Twenty patients with stable chronic heart failure, aged 58.3 +/- 3 years with an ejection fraction of 28 +/- 9%, were subjected to respiratory muscle training with threshold valves. The load was fixed in 30% of maximal inspiratory pressure (PImax) in 11 and in 10% of PImax in nine. Two sessions of 15 minutes, 6 days per week, during 6 weeks were done. Degree of dyspnea (Mahler score), maximal oxygen uptake, distance walked in 6 minutes, respiratory muscle function and left ventricular ejection fraction were measured before and after training. RESULTS: Both training loads were associated to an improvement in dyspnea (+2.7 +/- 1.8 and +2.8 +/- 1.8 score points with 30% PImax and 10% PImax respectively), maximal oxygen uptake (from 19 +/- 3 to 21.6 +/- 5 and from 16 +/- 5 to 18.6 +/- 7 ml/kg/min with 30% PImax and 10% PImax respectively, p < 0.05), PImax (from 78 +/- 22 to 99 +/- 22 and from 72 +/- 34 to 82.3 cm H20 with 30% PImax and 10% PImax respectively), sustained PImax (from 63 +/- 18 to 90 +/- 22 and from 58 +/- 3 to 69 +/- 3 cm H20 with 30% PImax and 10% PImax respectively), and maximal sustained load (from 120 +/- 67 to 195 +/- 47 and from 139 +/- 120 to 192 +/- 154 g with 30% PImax and 10% PImax respectively). The distance walked in 6 min only increased in subjects trained at 30% PImax (from 451 +/- 78 to 486 +/- 68 m). CONCLUSIONS: Selective training of respiratory muscles results in a functional improvement of patients with chronic heart failure.

Breathing Exercises↗
PubMed2001

[Changes in the patterns of drug prescription for acute myocardial infarct. Comparison of 2 periods].

BACKGROUND: Pharmacotherapy of Chilean patients with acute myocardial infarction has been recorded in 37 hospitals since 1993. AIM: To compare pharmacotherapy for acute myocardial infarction in the period 1993 to 1995 with the period 1997-1998. PATIENTS AND METHODS: Drug prescription during hospital stay was recorded in 2957 patients admitted to Chilean hospitals with an acute myocardial infarction in the period 1993-1995 and compared with that of 1981 subjects admitted in the period 1997-1998. RESULTS: When compared with the former period, in the lapse 1997-1998 there was an increase in the frequency of prescription of aspirin (93 and 96.1% respectively) beta blockers (37 and 55.2% respectively) and angiotensin converting enzyme inhibitors (32 and 53%). The prescription of thrombolytic therapy did not change (33 and 33.7% respectively). There was a reduction in the prescription of calcium antagonists and antiarrhythmic drugs. CONCLUSIONS: During the period 1997-1998, the prescription of drugs with a potential to reduce the mortality of acute myocardial infarction, increased. The diffusion of guidelines for the management of this disease may have influenced this change.

Adrenergic beta-Antagonists↗
PubMed2001

[Hyperuricemia as a marker for anaerobic threshold in chronic cardiac failure].

BACKGROUND: Patients with chronic cardiac failure often have elevated plasma uric acid levels, that are associated to a dismal prognosis. AIM: To investigate possible metabolic mechanisms to explain elevated uric acid levels in these patients. PATIENTS AND METHODS: Eighteen patients with chronic cardiac failure aged 61 +/- 10 years old, without gout or renal failure and not using high doses of diuretics (equal or less than 80 mg/day furosemide or 50 mg/day hydrochlorothiazide) were studied. Plasma uric acid levels were correlated with anaerobic threshold, maximal oxygen uptake, plasma noradrenaline and creatinine and left ventricular ejection fraction, measured radioisotopically. RESULTS: Mean maximal oxygen uptake was 16.6 +/- 4.2 ml/kg/min. There was a negative correlation between uric acid levels and maximal oxygen uptake or maximal oxygen uptake/body surface area (r = 0.521 and -0.533 respectively, p < 0.05). Patients with uric acid levels over 7 mg/dl had a lower anaerobic threshold than patients with lower levels (9.81 +/- 2.41 and 13.08 +/- 3.28 ml/kg/min respectively, p < 0.05). No significant differences in maximal oxygen uptake were observed in these two groups of patients (15.5 +/- 4.24 and 18.08 +/- 3.86 ml/kg/min respectively). Uric acid levels did not correlate with plasma noradrenaline, creatinine or left ventricular ejection fraction. CONCLUSIONS: These results suggest that a defect in cellular oxygenation contributes to the elevation of plasma uric acid levels in patients with chronic cardiac failure.

Aged↗
PubMed2000

Association between minor elevations of creatine kinase-MB level and mortality in patients with acute coronary syndromes without ST-segment elevation. PURSUIT Steering Committee. Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy.

CONTEXT: Controversy surrounds the diagnostic and prognostic importance of slightly elevated cardiac markers in patients with acute coronary syndromes without ST-segment elevation. OBJECTIVES: To investigate the relationship between peak creatine kinase (CK)-MB level and outcome and to determine whether a threshold CK-MB level exists below which risk is not increased. DESIGN AND SETTING: Retrospective observational analysis of data from the international Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial, conducted from November 1995 to January 1997. PATIENTS: A total of 8250 patients with acute coronary syndromes without ST-segment elevation who had at least 1 CK-MB sample collected during their index hospitalization. MAIN OUTCOME MEASURE: Mortality at 30 days and 6 months, was assessed by category of index-hospitalization peak CK-MB level (0-1, >1-2, >2-3, >3-5, >5-10, or >10 times the upper limit of normal). Multivariable logistic regression was used to determine the independent prognostic significance of peak CK-MB level after adjustment for baseline predictors of 30-day and 6-month mortality. RESULTS: Mortality at 30 days and 6 months increased from 1.8% and 4.0%, respectively, in patients with normal peak CK-MB levels, to 3.3% and 6.2 % at peak CK-MB levels 1 to 2 times normal, to 5.1% and 7.5% at peak CK-MB levels 3 to 5 times normal, and to 8.3% and 11.0% at peak CK-MB levels greater than 10 times normal. Log-transformed peak CK-MB levels were predictive of adjusted 30-day and 6-month mortality (P<.001 for both). CONCLUSIONS: Our data show that elevation of CK-MB level is strongly related to mortality in patients with acute coronary syndromes without ST-segment elevation, and that the increased risk begins with CK-MB levels just above normal. In the appropriate clinical context, even minor CK-MB elevations should be considered indicative of myocardial infarction.

Acute Disease↗
PubMed2000

[Infective endocarditis: short and long-term results in 261 cases managed by a multidisciplinary approach].

BACKGROUND: Early diagnosis, an effective treatment and prompt recognition of complications are essential to improve the prognosis of infective endocarditis (IE). AIM: To report the results of a multidisciplinary approach to diagnosis and management of patients with IE at the Universidad Católica de Chile Hospital. PATIENTS AND METHODS: The clinical history, diagnosis, treatment and outcome of 261 episodes (Duke criteria) of IE admitted between January 1980 and January 1999 were analyzed. These included 185 episodes of native, 73 of prosthetic valve and 3 of nonvalvular IE. RESULTS: Sixty nine percent of patients were men and the mean age was 49 +/- 16 years. Seventy five percent had a definite diagnosis of IE (Duke). S. viridans, staphylococci and enterococci together constituted 85% of the isolated bacterial strains. Twenty seven had culture-negative IE, related to a high incidence of antibiotic therapy prior to diagnosis. Transesophageal echocardiography was performed in 102 cases and it detected vegetations in 91% of aortic and 96% of mitral IE, rupture or prosthesis dehiscence in 67% of aortic and 52% of mitral IE and abscesses in 51% of aortic and 15% of mitral IE. Fifty one percent developed heart failure and 34% had embolic events. S. aureus IE was associated to a higher incidence of embolic events, complications which contraindicated surgery and increased mortality rate (27%). Of all patients, 40% were treated exclusively with antibiotics, 52% were operated on and 8% had surgical indication but were nonoperable because of serious complications. The overall mortality was 16.3%: 13% in the medical, 9% in the surgical and 81% in the non-operable groups. The type of treatment and mortality rates did not differ between IE of native valves and prosthetic valves. Long term follow up showed survival rates of 73% at 5 years and 66% at 10 years. CONCLUSION: A multidisciplinary approach may be very helpful to improve the prognosis of IE.

Adolescent↗
PubMed1999

Chronic hyperammonemia in rats impairs activation of soluble guanylate cyclase in neurons and in lymphocytes: a putative peripheral marker for neurological alterations.

Chronic hyperammonemia impairs the glutamate-nitric oxide-cGMP pathway in rat brain in vivo. The aims of this work were to assess whether hyperammonemia impairs modulation of soluble guanylate cyclase, and to look for a peripheral marker for impairment of this pathway in brain. We activated the pathway at different steps using glutamate, SNAP, or YC-1. In control neurons these compounds increased cGMP by 7.4-, 9.7- and 7.2-fold, respectively. In ammonia-treated neurons formation of cGMP induced by glutamate, SNAP, and YC-1 was reduced by 50%, 56%, and 52%, respectively, indicating that hyperammonemia impairs activation of guanylate cyclase. This enzyme is also present in lymphocytes. Activation of guanylate cyclase by SNAP or YC-1 was impaired in lymphocytes from hyperammonemic rats. These results suggest that determination of the activation of soluble guanylate cyclase in lymphocytes could serve as a peripheral marker for impairment of the neuronal glutamate-nitric oxide-cGMP pathway in brain.

Ammonia↗
PubMed1999

Bedside markers of coronary artery patency and short-term prognosis of patients with acute myocardial infarction and thrombolysis.

BACKGROUND: In this study we have evaluated the prognostic power of noninvasive markers of coronary artery reperfusion in patients with acute myocardial infarction who were treated with intravenous streptokinase. METHODS: In 967 consecutive patients with acute myocardial infarction who were treated within 6 hours of symptoms, we analyzed the prognostic power of resolution of chest pain and ST-segment elevation >50% at 90 minutes, abrupt creatine kinase rise before 12 hours, and T-wave inversion in infarct-related electrocardiographic leads within the first 24 hours after thrombolysis. RESULTS: Global in-hospital mortality rate was 12.0%. Each reperfusion marker was associated with improved outcome. Multivariate logistic regression analysis showed that 3 of the 4 markers of coronary artery reperfusion were significantly and independently associated to low in-hospital mortality rate. The presence of early T-wave inversion was associated with the lowest in-hospital mortality rate (odds ratio 0.25, confidence interval 0. 10-0.56). When all markers of coronary artery reperfusion were included in the regression model, T-wave inversion (odds ratio 0.29, confidence interval 0.11-0.68) and abrupt creatine kinase rise (odds ratio 0.36, confidence interval 0.16-0.77) continued to be significantly associated with better outcome. CONCLUSION: A systemic analysis of noninvasive markers of coronary artery reperfusion can provide the clinician with an excellent tool to predict clinical outcomes when treating myocardial infarction.

Aged↗
PubMed1999

Role of cyclic GMP in glutamate neurotoxicity in primary cultures of cerebellar neurons.

The role of cGMP in the mediation of glutamate neurotoxicity remains controversial. Some reports indicate that cGMP mediates glutamate neurotoxicity while others indicate that cGMP is neuroprotective. We have studied the role of cGMP in the mediation of glutamate and nitric oxide neurotoxicity in primary cultures of cerebellar neurons. Inhibition of soluble guanylate cyclase prevents glutamate and nitric oxide neurotoxicity. There is a good correlation between inhibition of cGMP formation and neuroprotection. Moreover 8-Br-cGMP, a cell permeable analog of cGMP, induced neuronal death. These results indicate that increased intracellular cGMP is involved in the mechanism of neurotoxicity. Inhibitors of phosphodiesterase did not increase intracellular cGMP but increased the content of cGMP in the extracellular medium and prevented glutamate neurotoxicity. Moreover, addition of cGMP to the extracellular medium also prevented glutamate neurotoxicity in cerebellar neurons in culture. These results are compatible with a neurotoxic effect of increased intracellular cGMP and a neuroprotective effect of increased extracellular cGMP.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Prenatal exposure to aluminum reduces expression of neuronal nitric oxide synthase and of soluble guanylate cyclase and impairs glutamatergic neurotransmission in rat cerebellum.

Exposure to aluminum (Al) produces neurotoxic effects in humans. However, the molecular mechanism of Al neurotoxicity remains unknown. Al interferes with glutamatergic neurotransmission and impairs the neuronal glutamate-nitric oxide-cyclic GMP (cGMP) pathway, especially in rats prenatally exposed to Al. The aim of this work was to assess whether Al interferes with processes associated with activation of NMDA receptors and to study the molecular basis for the Al-induced impairment of the glutamate-nitric oxide-cGMP pathway. We used primary cultures of cerebellar neurons prepared from control rats or from rats prenatally exposed to Al. Prenatal exposure to Al prevented glutamate-induced proteolysis of the microtubule-associated protein-2, disaggregation of microtubules, and neuronal death, indicating an impairment of NMDA receptor-associated signal transduction pathways. Prenatal exposure to Al reduced significantly the content of nitric oxide synthase and guanylate cyclase and increased the content of calmodulin both in cultured neurons and in the whole cerebellum. This effect was selective for proteins of the glutamate-nitric oxide-cGMP pathway as the content of mitogen-activated protein kinase and the synthesis of most proteins were not affected by prenatal exposure to Al. The alterations in the expression of proteins of the glutamate-nitric oxide-cGMP pathway could be responsible for some of the neurotoxic effects of Al.

Aluminum↗