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Ann Thorac Surg 1996;62:1586-1587
© 1996 The Society of Thoracic Surgeons

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Invited Commentary

Invited Commentary

Department of Medicine, Columbia University College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032

The first 20% of the full text of this article appears below.

See also page 1580.

After every breath that we take, we exhale a measurable amount of NO [1], evidence for the tremendous capacity of the lungs to synthesize NO from the percursor L-arginine. Recent data even suggest that one of the prime functions of the lungs is to synthesize NO, to be unloaded by hemoglobin in distal tissues [2]. Within the lungs themselves, NO serves important vascular homeostatic functions, which become deranged after ischemia due to the nearly instantaneous quenching of NO by superoxide generated during reperfusion. The plummeting NO levels are associated with a decline in tissue cyclic guanosine monophosphate levels [3], which, in combination with a failure of the cyclic adenosine monophosphate second messenger pathway [4. . . [Full Text of this Article]

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Ann. Thorac. Surg. 1996 62: 1580-1586. [Abstract] [Full Text]