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British Journal of Anaesthesia, 2001, Vol. 87, No. 2 179-183
© 2001 The Board of Management and Trustees of the British Journal of Anaesthesia

Editorial

Editorial I

Nitric oxide as mediator, marker and modulator of microvascular damage in ARDS

N. Marczin and D. Royston

In this issue, Stuart-Smith and Jeremy join an interesting series of international debates regarding mechanisms of microvessel damage in acute respiratory distress syndrome (ARDS), in particular the role of endothelium derived relaxing factors (EDRF) in the pathophysiology and treatment of this disease.1 Their review seems to promote the idea of endothelium-derived hyperpolarizing factor playing a primary role in ARDS whereas nitric oxide (NO), a prominent endothelium derived relaxing factor and regulator of intercellular communication, is attributed only as a minor component. The major claim of the authors, as reflected in the title, is that NO may not be the answer to microvessel damage in ARDS. This claim should certainly be investigated in the context of specific questions and in the context of our success or failure in understanding this life-threatening condition.

Do we understand the biology of ARDS?

The main characteristics of ARDS is non-cardiogenic pulmonary oedema and a mild degree of hypertension that results from acute . . . [Full Text of this Article]

NO as regulator of pulmonary function and mediator of lung injury

NO as a marker of lung injury

NO as modulator of lung injury

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N. Marczin, T. Kovesis, D. Royston, B. H. Cuthbertson, S. A. Stott, and N. R. Webster
Exhaled nitric oxide as a marker of lung injury in coronary artery bypass surgery
Br. J. Anaesth., January 1, 2003; 90(1): 101 - 105.
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