Treatment of Transient Graft Dysfunction Following Lung Transplantation

Treatment of Transient Graft Dysfunction following Lung Transplantation  

Nitric oxide reduced pulmonary artery pressure to 29.4 3.1 mm Hg P 0.05), a mean percentage change of 24%, and pulmonary vascular resistance to 6.4 1.3 U m, a mean percentage change of 31%. The arterial oxygen tension tended to increase from 98 21 to 147 21 (P = 

FIGURE 9 The effects of 80-ppm nitric oxide (NO) inhalation in six patients with transient graft dysfunction after lung transplantation. Pulmonary artery pressure (PAp), pulmonary vascular resistance index (PVRI), and intrapulmonary shunt fraction (Qs/Qt) decreased significantly, while arterial oxygen pressure (PaOi increased. [Adapted and reproduced with permission from Adatia et al. (77).] 

The effectiveness of nitric oxide as a pulmonary vasodilator, together with the diminished response to acetylcholine in a variety of patients in whom endothelial injury is postulated, begs the question as to whether a deficiency of endogenously released nitric oxide is responsible for the elevation in pulmonary vascular tone. Nitric oxide is thought to be released continuously under basal conditions, and inhibition of basal release may lead to an increase in systemic vascular resistance. The perfusion of isolated human lungs with methylene blue, an inhibitor of nitric oxide-mediated vessel relaxation, leads to an increase in pulmnary vascular resistance. Thus, endothelial damage with a reduction in endogenous nitric oxide could account for pulmonary vasoconstriction. 

Alternatively, the increased pulmonary vascular resistance may be due to an increase in a circulating vasoconstrictor such as endothelin or thromboxane, both of which have been reported to be elevated in children with congenital heart disease following cardiopulmonary bypass. It is noteworthy that the excretion of thromboxane has been found to be elevated during a pulmonary hypertensive crisis ° and that in animal studies inhaled nitric oxide is effective in reversing the pulmonary vasoconstriction induced by thromboxane mimetics.  

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