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J Thorac Cardiovasc Surg 2004;128:949-950
© 2004 The American Association for Thoracic Surgery
Letter to the Editor |
Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
| The first 20% of the full text of this article appears below. |
To the Editor:
We read with interest the elegant article by De Wet and associates,1 who demonstrated that inhaled prostacyclin (PGI2) prevents pulmonary hypertension, right-heart dysfunction, and refractory hypoxemia after cardiothoracic surgery. We would like to add some observations regarding the mechanisms of action that might be of interest and of possible value in the further clinical implementation of inhalational PGI2.
First, pulmonary hypertension is associated with increased superoxide (O2·-) formation that is largely mediated by an upregulation of intravascular reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.2-5 O2·- reacts with endogenous nitric oxide (NO)
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