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Juhani Partanen, MD; Markku S. Nieminen, MD
Helsinki, Finland

Arch Intern Med. 1996;156(5):588.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Morris is partly right. We do not have definite direct evidence that our patient's death was caused by the effects of inhaled nitric oxide therapy.¹ Therefore, we wrote: "It is suggested that this [decrease of blood pressure probably due to nitric oxide] provoked an irreversible cardiogenic shock. Thus, inhaled nitric oxide may be dangerous...."

The severely disturbed hemodynamics of our patient remained stable before nitric oxide was administered during the first 15 hours after insertion of the pulmonary and radial artery catheters. Then, after institution of the inhaled nitric oxide therapy, her circulation deteriorated progressively with clear peripheral vasodilatation until she died 11 hours later. In the study of Wessel et al² cited by Morris and us, inhaled nitric oxide increased the plasma levels of vasodilatatory systemic cyclic guanosine monophosphate. In that investigation, nitric oxide also decreased mean blood pressure significantly by 7% (from 65.8 to 60.9 mm . . . [Full Text PDF of this Article]

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