The Experts below are selected from a list of 279288 Experts worldwide ranked by ideXlab platform
Warren M Zapol - One of the best experts on this subject based on the ideXlab platform.
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inhaled Nitric Oxide for the adult respiratory distress syndrome
The New England Journal of Medicine, 1993Co-Authors: Rolf Rossaint, Konrad J Falke, Frank Lopez, K Slama, U Pison, Warren M ZapolAbstract:Background The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling Nitric Oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange. Methods Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled Nitric Oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during Nitric Oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of Nitric Oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days. Results Inhalation of Nitric Oxide in a concentration of 18 ppm reduced the mean (±SE) pulmonary-artery pressure from 37 ±3 mm Hg to 30 ±2...
Michael D Schreiber - One of the best experts on this subject based on the ideXlab platform.
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inhaled Nitric Oxide in premature infants with the respiratory distress syndrome
The New England Journal of Medicine, 2003Co-Authors: Michael D Schreiber, Karen Ginmestan, Jeremy D Marks, Dezheng Huo, Grace M Lee, Pimol SrisuparpAbstract:background Inhaled Nitric Oxide improves gas exchange, decreases pulmonary vascular lability, and reduces pulmonary inflammation. We hypothesized that the use of inhaled Nitric Oxide would decrease the incidence of chronic lung disease and death in premature infants with the respiratory distress syndrome. methods We conducted a randomized, double-blind, placebo-controlled study of the effect of inhaled Nitric Oxide during the first week of life on the incidence of chronic lung disease and death in premature infants (less than 34 weeks’ gestation) who were undergoing mechanical ventilation for the respiratory distress syndrome. Infants were randomly assigned to receive inhaled Nitric Oxide (10 ppm on day 1, followed by 5 ppm for six days) or inhaled oxygen placebo for seven days. We further randomly assigned the infants in each group to receive intermittent mandatory or high-frequency oscillatory ventilation. results A total of 207 premature infants were enrolled. In the group given inhaled Nitric Oxide, 51 infants (48.6 percent) died or had chronic lung disease, as compared with 65 infants (63.7 percent) in the placebo group (relative risk, 0.76; 95 percent confidence interval, 0.60 to 0.97; P=0.03). There was no significant difference between the Nitric Oxide and placebo groups in the overall incidence of intraventricular hemorrhage and periventricular leukomalacia (33.3 percent and 38.2 percent, respectively), but the group given inhaled Nitric Oxide had a lower incidence of severe intraventricular hemorrhage and periventricular leukomalacia (12.4 percent vs. 23.5 percent; relative risk, 0.53; 95 percent confidence interval, 0.28 to 0.98; P = 0.04). The type of ventilation had no significant effect on the outcome. conclusions The use of inhaled Nitric Oxide in premature infants with the respiratory distress syndrome decreases the incidence of chronic lung disease and death.
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inhaled Nitric Oxide and persistent pulmonary hypertension of the newborn
The New England Journal of Medicine, 1997Co-Authors: Jesse D. Roberts, Jeffrey R Fineman, Frederick C Morin, Philip W Shaul, Stephen Rimar, Michael D Schreiber, Maurice S Zwass, Michael M Zayek, Richard A. Polin, Ian GrossAbstract:Background Persistent pulmonary hypertension of the newborn causes systemic arterial hypoxemia because of increased pulmonary vascular resistance and right-to-left shunting of deoxygenated blood. Inhaled Nitric Oxide decreases pulmonary vascular resistance in newborns. We studied whether inhaled Nitric Oxide decreases severe hypoxemia in infants with persistent pulmonary hypertension. Methods In a prospective, multicenter study, 58 full-term infants with severe hypoxemia and persistent pulmonary hypertension were randomly assigned to breathe either a control gas (nitrogen) or Nitric Oxide (80 parts per million), mixed with oxygen from a ventilator. If oxygenation increased after 20 minutes and systemic blood pressure did not decrease, the treatment was considered successful and was continued at lower concentrations. Otherwise, it was discontinued and alternative therapies, including extracorporeal membrane oxygenation, were used. Results Inhaled Nitric Oxide successfully doubled systemic oxygenation in 16 of 30 infants (53 percent), whereas conventional therapy without inhaled Nitric Oxide increased oxygenation in only 2 of 28 infants (7 percent). Long-term therapy with inhaled Nitric Oxide sustained systemic oxygenation in 75 percent of the infants who had initial improvement. Extracorporeal membrane oxygenation was required in 71 percent of the control group and 40 percent of the Nitric Oxide group (P=0.02). The number of deaths was similar in the two groups. Inhaled Nitric Oxide did not cause systemic hypotension or increase methemoglobin levels. Conclusions Inhaled Nitric Oxide improves systemic oxygenation in infants with persistent pulmonary hypertension and may reduce the need for more invasive treatments.
Pimol Srisuparp - One of the best experts on this subject based on the ideXlab platform.
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inhaled Nitric Oxide in premature infants with the respiratory distress syndrome
The New England Journal of Medicine, 2003Co-Authors: Michael D Schreiber, Karen Ginmestan, Jeremy D Marks, Dezheng Huo, Grace M Lee, Pimol SrisuparpAbstract:background Inhaled Nitric Oxide improves gas exchange, decreases pulmonary vascular lability, and reduces pulmonary inflammation. We hypothesized that the use of inhaled Nitric Oxide would decrease the incidence of chronic lung disease and death in premature infants with the respiratory distress syndrome. methods We conducted a randomized, double-blind, placebo-controlled study of the effect of inhaled Nitric Oxide during the first week of life on the incidence of chronic lung disease and death in premature infants (less than 34 weeks’ gestation) who were undergoing mechanical ventilation for the respiratory distress syndrome. Infants were randomly assigned to receive inhaled Nitric Oxide (10 ppm on day 1, followed by 5 ppm for six days) or inhaled oxygen placebo for seven days. We further randomly assigned the infants in each group to receive intermittent mandatory or high-frequency oscillatory ventilation. results A total of 207 premature infants were enrolled. In the group given inhaled Nitric Oxide, 51 infants (48.6 percent) died or had chronic lung disease, as compared with 65 infants (63.7 percent) in the placebo group (relative risk, 0.76; 95 percent confidence interval, 0.60 to 0.97; P=0.03). There was no significant difference between the Nitric Oxide and placebo groups in the overall incidence of intraventricular hemorrhage and periventricular leukomalacia (33.3 percent and 38.2 percent, respectively), but the group given inhaled Nitric Oxide had a lower incidence of severe intraventricular hemorrhage and periventricular leukomalacia (12.4 percent vs. 23.5 percent; relative risk, 0.53; 95 percent confidence interval, 0.28 to 0.98; P = 0.04). The type of ventilation had no significant effect on the outcome. conclusions The use of inhaled Nitric Oxide in premature infants with the respiratory distress syndrome decreases the incidence of chronic lung disease and death.
Annie Higgs - One of the best experts on this subject based on the ideXlab platform.
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the l arginine Nitric Oxide pathway
The New England Journal of Medicine, 1993Co-Authors: Salvador Moncada, Annie HiggsAbstract:The discovery that mammalian cells generate Nitric Oxide, a gas previously considered to be merely an atmospheric pollutant, is providing important information about many biologic processes. Nitric Oxide is synthesized from the amino acid L-arginine by a family of enzymes, the Nitric Oxide synthases, through a hitherto unrecognized metabolic route -- namely, the L-arginine-Nitric Oxide pathway1–8. The synthesis of Nitric Oxide by vascular endothelium is responsible for the vasodilator tone that is essential for the regulation of blood pressure. In the central nervous system Nitric Oxide is a neurotransmitter that underpins several functions, including the formation of memory. . . .
Jose E Tanussantos - One of the best experts on this subject based on the ideXlab platform.
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endothelial Nitric Oxide synthase polymorphisms and haplotypes in amerindians
DNA and Cell Biology, 2009Co-Authors: Marcelo R Luizon, Tatiane C Izidorotoledo, Aguinaldo Luiz Simoes, Jose E TanussantosAbstract:Interethnic disparities in the distribution of endothelial Nitric Oxide synthase (eNOS) polymorphisms may affect Nitric Oxide (NO)-mediated effects of and responses to drugs. While there are differ...
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cell free hemoglobin limits Nitric Oxide bioavailability in sickle cell disease
Nature Medicine, 2002Co-Authors: Christopher D Reiter, Richard O Cannon, Jose E Tanussantos, Xunde Wang, Neil Hogg, Alan N Schechter, Mark T GladwinAbstract:Although the deleterious vasoconstrictive effects of cell-free, hemoglobin-based blood substitutes have been appreciated, the systemic effects of chronic hemolysis on Nitric Oxide bioavailability have not been considered or quantified. Central to this investigation is the understanding that Nitric Oxide reacts at least 1,000 times more rapidly with free hemoglobin solutions than with erythrocytes. We hypothesized that decompartmentalization of hemoglobin into plasma would divert Nitric Oxide from homeostatic vascular function. We demonstrate here that plasma from patients with sickle-cell disease contains cell-free ferrous hemoglobin, which stoichiometrically consumes micromolar quantities of Nitric Oxide and abrogates forearm blood flow responses to Nitric Oxide donor infusions. Therapies that inactivate plasma hemoglobin by oxidation or Nitric Oxide ligation restore Nitric Oxide bioavailability. Decompartmentalization of hemoglobin and subsequent dioxygenation of Nitric Oxide may explain the vascular complications shared by acute and chronic hemolytic disorders.