Role of inhaled nitric oxide as a selective pulmonary vasodilator in pediatric cardiac surgical practice

1999 ◽  
Vol 66 (3) ◽  
pp. 357-361 ◽  
Author(s):  
K. S. Murthy ◽  
Suresh G. Rao ◽  
K. Shiva Prakash ◽  
C. Robert ◽  
S. Dhinakar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inhaled Nitric Oxide ◽  
Surgical Practice ◽  
Pulmonary Vasodilator

Congenital NOS2 Deficiency Protects Mice from LPS-induced Hyporesponsiveness to Inhaled Nitric Oxide 

1999 ◽  
Vol 91 (6) ◽  
pp. 1744-1744 ◽  
Author(s):  
Jörg Weimann ◽  
Kenneth D. Bloch ◽  
Masao Takata ◽  
Wolfgang Steudel ◽  
Warren M. Zapol
Keyword(s):  
Nitric Oxide ◽  
Inhaled Nitric Oxide ◽  
Wild Type ◽  
Vasodilator Response ◽  
Pulmonary Vasodilator ◽  
Vascular Responsiveness ◽  
Deficient Mice ◽  
Inhaled No ◽  
Lipopolysaccharide Challenge

Background In animal models, endotoxin (lipopolysaccharide) challenge impairs the pulmonary vasodilator response to inhaled nitric oxide (NO). This impairment is prevented by treatment with inhibitors of NO synthase 2 (NOS2), including glucocorticoids and L-arginine analogs. However, because these inhibitors are not specific for NOS2, the role of this enzyme in the impairment of NO responsiveness by lipopolysaccharide remains incompletely defined. Methods To investigate the role of NOS2 in the development of lipopolysaccharide-induced impairment of NO responsiveness, the authors measured the vasodilator response to inhalation of 0.4, 4, and 40 ppm NO in isolated, perfused, and ventilated lungs obtained from lipopolysaccharide-pretreated (50 mg/kg intraperitoneally 16 h before lung perfusion) and untreated wild-type and NOS2-deficient mice. The authors also evaluated the effects of breathing NO for 16 h on pulmonary vascular responsiveness during subsequent ventilation with NO. Results In wild-type mice, lipopolysaccharide challenge impaired the pulmonary vasodilator response to 0.4 and 4 ppm NO (reduced 79% and 45%, respectively, P < 0.001), but not to 40 ppm. In contrast, lipopolysaccharide administration did not impair the vasodilator response to inhaled NO in NOS2-deficient mice. Breathing 20 ppm NO for 16 h decreased the vasodilator response to subsequent ventilation with NO in lipopolysaccharide-pretreated NOS2-deficient mice, but not in lipopolysaccharide-pretreated wild-type, untreated NOS2-deficient or untreated wild-type mice. Conclusions In response to endotoxin challenge, NO, either endogenously produced by NOS2 in wild-type mice or added to the air inhaled by NOS2-deficient mice, is necessary to impair vascular responsiveness to inhaled NO. Prolonged NO breathing, without endotoxin, does not impair vasodilation in response to subsequent NO inhalation. These results suggest that NO, plus other lipopolysaccharide-induced products, are necessary to impair responsiveness to inhaled NO in a murine sepsis model.

In Reply: Inhaled Nitric Oxide Trials: "Vive la différence!"

PEDIATRICS ◽  
1996 ◽  
Vol 97 (3) ◽  
pp. 438-439
Author(s):  
STEVEN H. ABMAN ◽  
JOHN P. KINSELLA
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Clinical Care ◽  
Inhaled Nitric Oxide ◽  
Multicenter Studies ◽  
Therapeutic Role ◽  
Inappropriate Use ◽  
Recent Commentary ◽  
Potential Therapeutic Role

Dr Davidson misinterprets our recent commentary on the pathophysiology of persistent pulmonary hypertension of the newborn (PPHN) and potential therapeutic role of inhaled nitric oxide (I-NO) as suggesting the lack of a need for multiple studies that investigate different questions regarding its efficacy. In contrast, we clearly state that "multicenter studies play vital roles in improving clinical care, and the absence of such studies may lead to the inappropriate use of ineffective or harmful therapies."

THE ROLE OF INHALED NITRIC OXIDE IN END-STAGE LIVER DISEASE

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 420A
Author(s):  
M A E Ramsay ◽  
K Lynch ◽  
H A T Hein ◽  
K Ramsay ◽  
R I Simpson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Disease ◽  
Inhaled Nitric Oxide ◽  
End Stage Liver Disease ◽  
End Stage

Abstract 12177: Inhaled Nitric Oxide During Cardiopulmonary Resuscitation Improves Functional Outcome and Increases 7-Day-Survival After Prolonged Cardiac Arrest in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Anne Brücken ◽  
Christian Bleilevens ◽  
Matthias Derwall ◽  
Michael Fries
Keyword(s):  
Nitric Oxide ◽  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Functional Outcome ◽  
Statistical Significance ◽  
Spontaneous Circulation ◽  
Left Ventricular ◽  
Inhaled Nitric Oxide ◽  
Sprague Dawley ◽  
Pulmonary Vasodilator

Introduction: Precordial compressions during cardiac arrest (CA) increase pulmonary vascular resistance (PVR), potentially impeding survival by limiting left ventricular preload. Although used as selective pulmonary vasodilator there is accumulating evidence that inhaled nitric oxide (iNO) also attenuates I/R injury. Hypothesis: Applying iNO during cardiopulmonary resuscitation (CPR) increases resuscitation rates and improves functional outcome after cardiac arrest in rats. Methods: Thirty male Sprague-Dawley rats were subjected to 10 mins of CA and 3 mins of CPR. Animals were randomized to receive either 20 ppm or 40 ppm iNO during CPR until 30 mins after ROSC (return of spontaneous circulation) or no iNO treatment. For all animals a neurological deficit score (NDS) was calculated daily for seven days following the experiment. Results: Inhalation of 20 ppm iNO increased ROSC rates in comparison to animals treated with 40 ppm or without iNO treatment, however this failed to reach statistical significance (control: 7/10; 20ppm iNO: 10/10; 40ppm iNO 6/10). 20 ppm iNO significantly decreased time to ROSC, resulting in a significant reduction of post-arrest lactate levels. Also, significantly higher mean arterial pressures in comparison to control animals were observed. Furthermore, 20 ppm iNO resulted in a significantly higher seven-day-survival in comparison to controls (control: 4/10; 20 ppm iNO: 10/10). All iNO treated animals showed better neurological outcomes, being significant in animals treated with 20 ppm iNO on postoperative day 2- 7. Conclusions: Our study demonstrates that 20 ppm but not 40 ppm iNO during CPR significantly decreases time to ROSC. Furthermore, significantly better seven-day-survival and neurological outcome was noted for 20 ppm iNO in comparison to controls.

scholarly journals The role of inhaled nitric oxide in brain inflammation

2007 ◽  
Vol 54 (S1) ◽  
pp. 44303-44303
Author(s):  
Gilbert Blaise ◽  
QI. Yanqin ◽  
Rame Taha ◽  
Walid Elybayed
Keyword(s):  
Nitric Oxide ◽  
Inhaled Nitric Oxide ◽  
Brain Inflammation
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