Inhaled nitric oxide in combination with volume resuscitation refines a porcine model of endotoxic shock

2001 ◽  
Vol 170 (3) ◽  
pp. 172-175 ◽  
Author(s):  
N. A. Herity ◽  
J. D. Allen ◽  
B. Silke ◽  
A. A. J. Adgey
Author(s):  
Patrick J. Offner ◽  
Hiroshi Ogura ◽  
Bryan S. Jordan ◽  
Basil A. Pruitt ◽  
William G. Cioffi

1998 ◽  
Vol 115 (3) ◽  
pp. 700-708 ◽  
Author(s):  
Michael Argenziano ◽  
David A. Dean ◽  
Nader Moazami ◽  
Daniel J. Goldstein ◽  
Eric A. Rose ◽  
...  

1997 ◽  
Vol 114 (3) ◽  
pp. 461-466 ◽  
Author(s):  
Daniel J. Goldstein ◽  
David A. Dean ◽  
Arthur Smerling ◽  
Mehmet C. Oz ◽  
Daniel Burkhoff ◽  
...  

2004 ◽  
Vol 56 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Lara S Shekerdemian ◽  
Daniel J Penny ◽  
Pia K Ryhammer ◽  
Jayne A Reader ◽  
Hanne B Ravn

2020 ◽  
pp. 204887262091871 ◽  
Author(s):  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jacob Gammelgaard Schultz ◽  
Mads Dam Lyhne ◽  
Asger Andersen ◽  
...  

Background Inhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE. Methods Anesthetized pigs ( n = 18) were randomized into three subgroups. An acute PE iNO-group ( n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals ( n = 6) received PE, but no active treatment. A third group of sham animals ( n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements. Results The administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p < 0.0001), pulmonary vascular resistance (vehicle vs sham; 847.5 vs 82.0 dynes, p < 0.0001) and right ventricular arterial elastance (vehicle vs sham; 1.2 vs 0.2 mmHg/ml, p < 0.0001). Significant mPAP reduction by iNO was preserved at 12 hours after the onset of acute PE (vehicle vs iNO; 0.5 vs –3.5 mmHg, p < 0.0001). However, this response was attenuated over time ( p = 0.0313). iNO did not affect the systemic circulation. Conclusions iNO is a safe and effective pulmonary vasodilator both in the immediate and prolonged phase of acute PE in an in-vivo porcine model of intermediate-risk PE.


1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 323A-323A
Author(s):  
William E Truog ◽  
Jihan Youssef ◽  
Donald W Thibeault ◽  
Ikechukwu I Ekekezie

Nitric Oxide ◽  
2021 ◽  
Author(s):  
Barbara Adamik ◽  
Claes Frostell ◽  
Urszula Paslawska ◽  
Barbara Dragan ◽  
Stanislaw Zielinski ◽  
...  

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