Abstract:In this study, we evaluated the protective effects of inhaled nitric oxide in a pulmonary air embolism setting. Nitric oxide attenuated the hemodynamic changes induced by pulmonary air embolism without improving pulmonary oxygenation.
“…The inhalation of 3 ppm NO attenuated pulmonary hypertension and the decrease in CI and MAP after an acute massive pulmonary air embolism without improving pulmonary oxygenation [14]. Other studies have also shown positive hemodynamic effects of NO inhalation after acute pulmonary embolism with microspheres [11±13].…”
Section: Discussionmentioning
confidence: 97%
“…The concentration of 3 ppm was chosen because this amount of NO improves hemodynamics after massive air embolism [14]. NO 40 ppm was administered because this concentration produces maximum pulmonary vasodilation [24,25].…”
Section: Methodsmentioning
confidence: 99%
“…Favorable hemodynamic effects were demonstrated after acute pulmonary microsphere embolism [11±13]. Similarly, previous inhalation of a low dose of NO (3 ppm) attenuates the hemodynamic changes associated with a massive pulmonary air embolism, without improving pulmonary oxygenation [14].…”
Nitrate/nitrite concentrations were unaltered after VAI in dogs. NO therapy attenuated TxA(2) release and improved hemodynamics, but not blood oxygenation, in dogs with a VAI. There were no differences between the responses to 3 ppm and 40 ppm NO.
“…The inhalation of 3 ppm NO attenuated pulmonary hypertension and the decrease in CI and MAP after an acute massive pulmonary air embolism without improving pulmonary oxygenation [14]. Other studies have also shown positive hemodynamic effects of NO inhalation after acute pulmonary embolism with microspheres [11±13].…”
Section: Discussionmentioning
confidence: 97%
“…The concentration of 3 ppm was chosen because this amount of NO improves hemodynamics after massive air embolism [14]. NO 40 ppm was administered because this concentration produces maximum pulmonary vasodilation [24,25].…”
Section: Methodsmentioning
confidence: 99%
“…Favorable hemodynamic effects were demonstrated after acute pulmonary microsphere embolism [11±13]. Similarly, previous inhalation of a low dose of NO (3 ppm) attenuates the hemodynamic changes associated with a massive pulmonary air embolism, without improving pulmonary oxygenation [14].…”
Nitrate/nitrite concentrations were unaltered after VAI in dogs. NO therapy attenuated TxA(2) release and improved hemodynamics, but not blood oxygenation, in dogs with a VAI. There were no differences between the responses to 3 ppm and 40 ppm NO.
“…It has been shown that activation of the nitric oxide (NO)-cyclic guanosine monophosphate pathway attenuates acute pulmonary embolism-induced hemodynamic derangements (15)(16)(17)(18)(19)(20)(21), maybe through mechanisms including negative modulation of lung MMP-2 and MMP-9 activities after APE (7). Another way to activate the NO-cyclic guanosine monophosphate pathway is by using statins (22)(23)(24).…”
These results suggest that pretreatment with atorvastatin attenuates APE-induced pulmonary hypertension and increases 24-hr survival rate by mechanisms that result in attenuated increases in lung activated MMP-9 after APE.
“…In the presence of pulmonary vasoconstriction, the higher pulmonary vascular resistance then the greater the inhaled NO vasodilator effect. Recently it has been demonstrated that inhaled NO could attenuate the pulmonary vasoconstriction caused by active mediators in an experimental model of massive air pulmonary embolism (PE) [2]. …”
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