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Excerpt
My objective is to describe the effects of inhaling low levels of nitric oxide (NO) on the haemodynamic and gas exchange function of both the normal and diseased lung. Attention will be paid to the safety and hazards of inhaled-NO therapy. During the past decade, remarkable progress has been made in understanding the NO-guanylate cyclase signal transduction system. Inhaled NO has been the subject of considerable clinical investigation in pulmonary artery hypertension, neonatal respiratory failure and adult respiratory distress syndrome (ARDS) patients. Pulmonary hypertension with severe hypoxemia may complicate the care of patients with diseases such as acute and chronic pulmonary hypertension, ARDS, newborn respiratory failure, chronic respiratory failure and congenital heart disease, as well as after cardiopulmonary bypass. I will review the present status of the acute and chronic uses of inhaled nitric oxide.
I will describe both the present and novel future uses of inhaled NO. Numerous vasodilator therapies aimed at reducing pulmonary hypertension have been tested. Systemic vasodilation and hypotension may occur with all the currently available intravenous vasodilators tested in dosages sufficient to reduce the pulmonary artery pressure. In addition, intravenous infusions of systemic vasodilators, such as nitroprusside or prostacyclin (PGI2), markedly increase the venous admixture. Thus, the widespread appeal of inhaled NO as a pulmonary selective vasodilator has led to its therapeutic use in many respiratory diseases. I will describe the rationale for exploring novel uses of inhaled NO, especially efforts to extend its therapeutic duration with PDE5 inhibition, as well as examining red cell, white cell and platelet effects of inhaled NO for beneficial effects during ischaemia-reperfusion injury, thrombolysis and to prevent restenosis. After a decade of research on inhaled NO, there remains a great deal more to learn about the value of this important therapeutic advance.
