Rw. Hyde et al., DETERMINATION OF PRODUCTION OF NITRIC-OXIDE BY LOWER AIRWAYS OF HUMANS-THEORY, Journal of applied physiology, 82(4), 1997, pp. 1290-1296
Exercise and inflammatory lung disorders such as asthma and acute lung
injury increase exhaled nitric oxide (NO). This finding is interprete
d as a rise in production of NO by the lungs (VNO) but fails to take i
nto account the diffusing capacity for NO (DNO) that carries NO into t
he pulmonary capillary blood. We have derived equations to measure VNO
from the following rates, which determine NO tension in the lungs (PL
) at any moment from I)production (VNO); 2) diffusion, where DNO(PL) =
rate of removal by lung capillary blood; and 3) ventilation, where VA
(PL)/(PB - 47) = the rate of NO removal by alveolar ventilation (VA) a
nd PB is barometric pressure. During open-circuit breathing when PL is
not in equilibrium, d/dt PL[V-L/(PB - 47)] (where V-L is volume of NO
in the lower airways) = VNO - DNO(PL) - VA(PL)/(PB - 47). When PL rea
ches a steady state so that d/dt = 0 and VA is eliminated by rebreathi
ng or breath holding, then PL = VNO/DNO. PL can be interpreted as NO p
roduction per unit of DNO. This equation predicts that diseases that d
iminish DNO but do not alter VNO will increase expired NO levels. Thes
e equations permit precise measurements of VNO that can be applied to
determining factors controlling NO production by the lungs.