Biomedical subjects

Nicolás Nin

Publications and source records attributed to Nicolás Nin.

6 recordsLinked to original sources

PubMed2006

The role of bundles in sepsis care.

The understanding of the pathogenesis of sepsis has substantially changed in past years and continues to improve. New therapeutic options are being developed and incorporated into clinical practice. There are different specific interventions and therapies that benefit patients' outcome. As demonstrated by the early goal-directed therapy strategy, the success of the resuscitation treatment is strongly time dependent. The recognition of severe sepsis should be accompanied without delay by very well defined therapeutic measures. In 2002 the Surviving Sepsis Campaign was introduced with the overall goal of increasing clinicians' awareness and improving outcome in severe sepsis and septic shock.

Anti-Bacterial Agents↗

PubMed2006

Ventilation-induced lung injury in rats is associated with organ injury and systemic inflammation that is attenuated by dexamethasone.

OBJECTIVE: To determine whether mechanical ventilation using high tidal volume is associated with nonpulmonary organ dysfunction that can be attenuated by dexamethasone. DESIGN: Prospective randomized animal intervention study. SETTING: Animal care facility in a university hospital. SUBJECTS: Sedated and tracheostomized male Sprague-Dawley rats. INTERVENTIONS: Three groups of rats were ventilated with different strategies: tidal volume = 9 mL/kg, positive end-expiratory pressure = 8 cm H(2)O, control group (C); tidal volume = 35 mL/kg, positive end-expiratory pressure = 0 cm H(2)O, overventilated group (OV); and tidal volume = 35 mL/kg, positive end-expiratory pressure = 0 cm H(2)O, plus administration of 6 mg/kg dexamethasone intraperitoneally (OV + dexamethasone). All rats were ventilated for 75 mins with respiratory rate = 70 breaths/min, FIO(2) = 0.35, and plateau time = 0. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and peak airway pressure were monitored. We measured arterial blood gases, aspartate aminotransferase, alanine aminotransferase, lactate, nitrates and nitrites, tumor necrosis factor-alpha, and interleukin-6 serum concentration. Lung slices were prepared for blind histologic examination. Heart tissue was analyzed for cyclooxygenase-1 and -2 expression (reverse transcription-polymerase chain reaction). Compared with the C group, the OV group showed hypotension; worsened gas exchange; increased aspartate aminotransferase, lactate, nitrates and nitrites, and interleukin-6 serum concentrations; and hyaline membrane formation in the lungs, as well as increased cyclooxygenase-1 and cyclooxygenase-2 expression in the heart. Dexamethasone prevented the pulmonary and cardiovascular injury and attenuated the increase in aspartate aminotransferase, nitrates and nitrites, interleukin-6, and cyclooxygenase-1 and cyclooxygenase-2 expression. CONCLUSIONS: High tidal volume ventilation induces cardiovascular, pulmonary, and liver injury as well as a systemic proinflammatory response. These changes are attenuated by dexamethasone, suggesting that inflammatory rather than purely hemodynamic mechanisms are involved in the changes induced by high tidal volume ventilation.

Animals↗

PubMed2005

Large tidal volume mechanical ventilation induces vascular dysfunction in rats.

BACKGROUND: Experimental studies have shown that mechanical ventilation using high tidal volumes (V(T)) damages the lungs, causing pulmonary edema. We tested the hypothesis that high V(T) ventilation in rats induces major vascular dysfunction. METHODS: Healthy Sprague-Dawley rats, weighing (mean +/- SD) 340 +/- 15 g, were ventilated with either V(T) = 9 mL/kg and positive end-expiratory pressure (PEEP) = 8 (n = 8) or V(T) = 35 mL/kg and PEEP = 0 (n = 8). The high V(T) used in the injurious ventilation group is in the V(T) range used in other studies to induce lung damage in a short period of time in rats. Lungs were removed for examination under light microscopy and vascular rings from the thoracic aorta were studied for isometric tension recording. RESULTS: Relaxations to acetylcholine (p < 0.001) and sodium nitroprusside (p < 0.05) and contractions to norepinephrine were markedly decreased (p < 0.001) in the high V(T) group, as compared with the low V(T) group. CONCLUSION: Injurious mechanical ventilation in normal rats is associated with vascular dysfunction characterized by decreased relaxation to an endothelium-dependent vasodilator and to a nitrous oxide donor and by decreased response to norepinephrine.

Analysis of Variance↗

PubMed2004

Septic diaphragmatic dysfunction is prevented by Mn(III)porphyrin therapy and inducible nitric oxide synthase inhibition.

OBJECTIVE: Decreased diaphragmatic contractility and organ failure observed during sepsis is mediated by an overproduction of nitric oxide ((.)NO)-derived species, mitochondria being a major target of oxidative and nitrative stress. We tested the potential protective effects of (a) a novel synthetic antioxidant, the manganese(III) 5,10,15,20-tetrakis(N-ethylpyridinium-2-yl) porphyrin (MnTE-2-PyP(5+)) and (b) the inducible (.)NO synthase inhibitor aminoguanidine (AG) on a rat model of sepsis. SETTING: University research laboratories. SUBJECTS AND INTERVENTIONS: Sepsis was induced by cecal ligation and perforation in rats. MEASUREMENTS AND RESULTS: Systemic hemodynamics, pulmonary gas exchange, in vitro diaphragmatic function and mitochondrial respiration were evaluated. Moreover, plasma and mitochondrial oxidative and nitrative stress parameters were investigated. Sepsis determined diaphragmatic dysfunction and a significant decrease in mitochondrial coupling and respiration. Oxidative stress was evidenced by decreased plasma antioxidants and increased lipid oxidation. Tyrosine nitration was increased in the plasma and mitochondria of the septic animals. These alterations were ameliorated or prevented by either MnTE-2-PyP(5+) or AG. CONCLUSIONS: Our results demonstrate that overproduction of (.)NO and (.)NO-derived reactive species play a critical role in mitochondrial impairment and diaphragmatic function during sepsis. More importantly, AG but mainly the novel metalloporphyrin MnTE-2-PyP(5+) were able to ameliorate diaphragmatic and mitochondrial dysfunction and could contribute to preventing organ failure during severe sepsis.

Animals↗

PubMed2004

Epidemiology of acute lung injury and acute respiratory distress syndrome.

PURPOSE OF REVIEW: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are diseases with a significant influence in the public health. A better knowledge of their epidemiology could help to improve the outcome of these diseases. RECENT FINDINGS: Although the clinical criteria of the American-European Consensus Conference definitions for ALI and ARDS are simple, there is a risk of misclassification due to a poor reliability. Except for new emerging infectious diseases, such as severe acute respiratory syndrome, the etiology of ALI/ARDS has remained the same for several years. The only recent innovation is the hypothesis that pulmonary ARDS and extrapulmonary ARDS could be different clinical entities. In recent years, there has been a special interest in the study of genetic predisposition to development ALI/ARDS. Recent studies have estimated the incidence of these diseases to be between 15 and 34 cases per 100,000 inhabitants per year. This wide range could stem from differences in the methodology used to calculate the incidence or could be a true variation due to regional differences. Mortality rate of ALI/ARDS have remained steady for several years. Respiratory failure is the cause of the death in less than 20% of the patients. SUMMARY: The epidemiology of ALI and ARDS has some issues to improve, such as the accuracy of the clinical criteria of ALI/ARDS. Future research must to include study of genetic polymorphisms of the mediators involve in the development of ALI/ARDS. Studies to define better the population at risk are necessary to estimate better their true incidence.

Acute Disease↗

PubMed2004

Calcium citrate ameliorates the progression of chronic renal injury.

BACKGROUND: Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation. METHODS: Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, alpha-smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks. RESULTS: The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P < 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P < 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P < 0.05). Inulin clearances were higher (P < 0.05), and urine protein excretion rates were lower (P < 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group. CONCLUSION: Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.

Alkalies↗