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J Appl Physiol 91: 363-370, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 1, 363-370, July 2001

Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs

Toshiyuki Ogasa1, Hitoshi Nakano1, Hiroshi Ide1, Yasushi Yamamoto1, Nobuhiko Sasaki1, Shinobu Osanai1, Yuji Akiba1, Kenjiro Kikuchi1, and Jun Iwamoto2

1 Department of Medicine and 2 Division of Applied Physiology, School of Nursing, Asahikawa Medical College, Asahikawa 078-8510, Japan

The effects of changing perfusate flow on lung nitric oxide (NO) production and pulmonary arterial pressure (Ppa) were tested during normoxia and hypoxia and after NG-monomethyl-L-arginine (L-NMMA) treatment during normoxia in both blood- and buffer-perfused rabbit lungs. Exhaled NO (eNO) was unaltered by changing perfusate flow in blood-perfused lungs. In buffer-perfused lungs, bolus injections of ACh into the pulmonary artery evoked a transient increase in eNO from 67 ± 3 (SE) to 83 ± 7 parts/billion with decrease in Ppa, whereas perfusate NO metabolites (pNOx) remained unchanged. Stepwise increments in flow from 25 to 150 ml/min caused corresponding stepwise elevations in eNO production (46 ± 2 to 73 ± 3 nl/min) without changes in pNOx during normoxia. Despite a reduction in the baseline level of eNO, flow-dependent increases in eNO were still observed during hypoxia. L-NMMA caused declines in both eNO and pNOx with a rise in Ppa. Pulmonary vascular conductance progressively increased with increasing flow during normoxia and hypoxia. However, L-NMMA blocked the flow-dependent increase in conductance over the range of 50-150 ml/min of flow. In the more physiological conditions of blood perfusion, eNO does not reflect endothelial NO production. However, from the buffer perfusion study, we suggest that endothelial NO production secondary to increasing flow, may contribute to capillary recruitment and/or shear stress-induced vasodilation.

pulmonary endothelium; shear stress; recruitment


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