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Gilbert Blaise

Publications and source records attributed to Gilbert Blaise.

7 recordsLinked to original sources
PubMed2005

Effects of inhaled nitric oxide on inflammation and apoptosis after cardiopulmonary bypass.

BACKGROUND: Cardiopulmonary bypass (CPB), a procedure often used during cardiac surgery, is associated with an inflammatory process that leads to lung injury. We hypothesized that inhaled nitric oxide (INO), which has anti-inflammatory properties, possesses the ability to modulate lung cell apoptosis and prevent CPB-induced inflammation. METHODS: Twenty male pigs were randomly classified into four groups: sham, sham plus INO, CPB, and CPB plus INO. INO (20 ppm) was administered for 24 h after anesthesia. CPB was performed 90 min into INO treatment. BAL fluid and blood were collected at time 0 (before CPB), at 4 h after beginning CPB, and 24 h after beginning CPB (T24). RESULTS: At T(24), BAL interleukin (IL)-8 levels and neutrophil percentages were elevated significantly in the CPB group. At T(24), INO reduced IL-8 concentrations and attenuated the increase of neutrophil percentage in the CPB-plus-INO group. Nitrite-plus-nitrate (NOx) concentrations were decreased significantly in groups without INO. Moreover, animals treated with INO showed higher rates of pulmonary apoptosis compared to their respective control groups except for the sham-plus-INO group, in which they were diminished. CONCLUSION: These results demonstrate that NOx production is reduced after CPB, and that INO acts as an anti-inflammatory agent by decreasing neutrophil numbers and their major chemoattractant, IL-8. INO also increases cell apoptosis in the lungs during inflammatory conditions, which may explain, in part, how it resolves pulmonary inflammation.

Administration, Inhalation↗
PubMed2005

Postoperative cognitive dysfunction after cardiac surgery.

Prolonged postoperative cognitive dysfunction (POCD) is reported to occur frequently after cardiac surgery. However, it is rarely assessed in routine clinical practice and receives little attention. Although the cerebral consequences of cardiopulmonary bypass have been measured clinically, insights into the resulting molecular and pathologic events within the brain have only begun to be investigated. POCD is likely to impair quality of life and constitutes a large burden on society when elderly patients prematurely lose their independence. Numerous studies have reported that neurocognitive deficit is associated with heightened mortality, increased length of hospital stay, and discharge to a nursing home. This is linked with a tremendous demand for health-care resources. Because of the magnitude of the clinical problem, serious consideration must be directed toward understanding its etiology and the development of neuroprotective strategies. Clearly identifying the mechanisms of POCD is challenging. The purpose of this review is to discuss recent developments in our understanding of the pathophysiologic mechanisms, prevention, and treatments that have been designed to ameliorate brain dysfunction after cardiac surgery.

Alzheimer Disease↗
PubMed2004

Ventilation prevents pulmonary endothelial dysfunction and improves oxygenation after cardiopulmonary bypass without aortic cross-clamping.

OBJECTIVE: Endothelial dysfunction of the pulmonary arterial tree occurring after cardiopulmonary bypass (CPB) contributes to pulmonary hypertension and respiratory failure in the postoperative period. The goal of the present study was to characterize the alterations of endothelial cell signal transduction pathways in pulmonary arteries following CPB, the effect of ventilation and nitric oxide (NO) inhalation on endothelium-dependent relaxations and the alterations in hemodynamics and oxygenation. METHODS: Six groups of Landrace swine were compared: control, sham without CPB, CPB 150min+no reperfusion, CPB 150min+reperfusion 60 min, CPB 150min+ventilation (tidal volume 12 ml/kg)+reperfusion 60 min, and CPB 150min+NO inhalation (with ventilation, NO 40 ppm)+60 min of reperfusion. No cross-clamping was applied, the heart was left beating, empty. Pulmonary artery reactivity was evaluated in organ chambers to assess the endothelium-dependent relaxations. RESULTS: CPB alone did not alter endothelial function. CPB and pulmonary reperfusion induced a statistically significant decrease in endothelium-dependent relaxations to acetylcholine. Mechanical ventilation during CPB prevented the reduction of relaxations to acetylcholine. Ventilation and NO inhalation during CPB did not differ from ventilation alone in terms of endothelium-dependent relaxations. There were no differences between groups for relaxations to bradykinin. There was a significant increase in arterial oxygen tension in the ventilated group compared to the non-ventilated group. CONCLUSION: Pulmonary reperfusion after CPB causes a selective dysfunction of Gi-protein-mediated relaxations. Mechanical ventilation prevents the pulmonary endothelial dysfunction due to reperfusion after CPB. Ventilation also improves oxygenation after CPB. Mechanical ventilation could be used as a preventive approach for patients undergoing cardiac surgery with extracorporeal circulation.

Administration, Inhalation↗
PubMed2003

Inhaled nitric oxide in 2003: a review of its mechanisms of action.

PURPOSE: To review the pulmonary and systemic effects of endogenous nitric oxide and inhaled nitric oxide administered to patients. SOURCE: A systematic search for experimental data, human case reports, and randomized clinical trials since 1980, the year of discovery of endothelium-derived relaxing factor. PRINCIPAL FINDINGS: Nitric oxide has pulmonary and systemic effects. Inhaled nitric oxide not only causes selective pulmonary vasodilation but also results in pulmonary vasoconstriction of the vessels perfusing non-ventilated alveolae. The systemic effects of inhaled nitric oxide, which include modulation of the distribution of systemic blood flow, increase in renal output, interaction with coagulation, fibrinolysis and platelet functions, alteration of the inflammatory response, are described and the mechanisms of nitric oxide transport are explained. The possible toxicity of inhaled nitric oxide is also discussed. CONCLUSION: The multiple effects of inhaled nitric oxide support its role as a pulmonary and extra-pulmonary medication.

Administration, Inhalation↗
PubMed2002

Nitric oxide-derived nitrate anion contributes to endotoxic shock and multiple organ injury/dysfunction.

OBJECTIVE: Because nitrate represents the major end-product of nitric oxide in vivo and can affect enzyme activity, cell electrophysiological functions, and cell membrane integrity, we hypothesized that overaccumulated nitric oxide-derived nitrate anion in tissues or organs in vivo may contribute to endotoxic shock and multiple organ injury/dysfunction during endotoxemia. DESIGN: Prospective, experimental animal study. SETTING: Laboratory at a university hospital. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Rats were injected intraperitoneally with 5, 10, or 20 mg/kg lipopolysaccharide or saline and were studied in groups at 0, 6, 12, and 24 hrs. MEASUREMENTS AND MAIN RESULTS: Significant differences were seen between nitrate concentrations in the heart, lung, kidney, liver, brain, aorta, diaphragm, spleen, thymus, testis or ovary, hind limb muscle, intestine, adipose tissue, bone, bladder, urine and plasma, which imply a nitrate gradient between intracellular and extracellular compartments. Lipopolysaccharide significantly increased nitrate concentration at 12 hrs in most tissues and organs, except in the brain, adipose tissue, and muscle. It increased more in plasma than in tissues. The lipopolysaccharide dose-dependent nitrate concentration was observed only in the aorta and lungs. The nitrate concentration change was paralleled by the systemic inflammatory response syndrome, as indicated by alterations of myeloperoxidase activity and by impaired histologic and cellular membrane integrity in tissues and organs. Mean arterial pressure was negatively correlated with nitrate concentration modifications in the aorta during 24 hrs of endotoxemia. CONCLUSIONS: These results collectively indicate that overaccumulated nitric oxide-derived nitrate anion in tissues or organs in vivo contributes to endotoxic shock and multiple organ injury/dysfunction during endotoxemia.

Analysis of Variance↗