The effects of inhaled nitric oxide on the levels of cGMP plasma and lung tissue in a canine model of smoke inhalation injury.

[1]  R. Maier,et al.  Current clinical options for the treatment and management of acute respiratory distress syndrome. , 2000, The Journal of trauma.

[2]  Rodgers,et al.  Immunosuppressive effects of factor IX products: an in vitro study , 1999, Haemophilia : the official journal of the World Federation of Hemophilia.

[3]  R. Cohen,et al.  Ca2+-dependent Cl- channels in mouse and rabbit aortic smooth muscle cells: regulation by intracellular Ca2+ and NO. , 1999, American journal of physiology. Heart and circulatory physiology.

[4]  G. Iotti,et al.  Acute effects of inhaled nitric oxide in adult respiratory distress syndrome. , 1998, The European respiratory journal.

[5]  M. Haller,et al.  Response to inhaled nitric oxide (NO) is not associated with changes of plasma cGMP levels in patients with acute lung injury. , 1998, European journal of medical research.

[6]  E. Troncy,et al.  Inhaled nitric oxide in acute respiratory distress syndrome: a pilot randomized controlled study. , 1998, American journal of respiratory and critical care medicine.

[7]  C. Bode,et al.  Inhaled nitric oxide inhibits human platelet aggregation, P-selectin expression, and fibrinogen binding in vitro and in vivo. , 1998, Circulation.

[8]  I. Kim,et al.  Enhanced expression of cytokine genes in spleen macrophages during acute infection with infectious bursal disease virus in chickens. , 1998, Veterinary immunology and immunopathology.

[9]  J. Gordon,et al.  Relative Effects of Cyclooxygenase and Nitric Oxide Synthase Inhibition on Vascular Resistances in Neonatal Lamb Lungs , 1997, Pediatric Research.

[10]  Frostell Cg.  Update on clinical trials with inhaled nitric oxide. , 1997 .

[11]  M. Blaustein,et al.  NO hyperpolarizes pulmonary artery smooth muscle cells and decreases the intracellular Ca2+ concentration by activating voltage-gated K+ channels. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[12]  B. Markewitz,et al.  Endothelins and the lung. , 1996, American journal of respiratory and critical care medicine.

[13]  A. Mason,et al.  The effect of inhaled nitric oxide on pulmonary ventilation-perfusion matching following smoke inhalation injury. , 1994, The Journal of trauma.

[14]  R. Cohen,et al.  Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle , 1994, Nature.

[15]  Cioffi,et al.  The effect of inhaled nitric oxide on smoke inhalation injury in an ovine model. , 1993, The Journal of trauma.

[16]  S. Moncada,et al.  Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor , 1987, Nature.

[17]  J. Saffle,et al.  Effect of inhalation injury on fluid resuscitation requirements after thermal injury , 1985 .

[18]  C. Yowler,et al.  Current status of burn resuscitation. , 2000, Clinics in plastic surgery.

[19]  I. Chaudry,et al.  L-arginine: a unique amino acid for restoring the depressed macrophage functions after trauma-hemorrhage. , 1999, The Journal of trauma.

[20]  T. Saich.  The People’s Liberation Army , 1981 .