This observation is consistent with the proposal that, because the rate of NO diffusion exceeds any rate of NO oxidation, cellular SNO formation involves NO that has first diffused out of, then back into a given cell (54).
However, with the inclusion of the diffusion process, the response significantly deviates from the no diffusion state.
Experiments were carefully designed for accurate measurements of the apparent NO diffusion coefficient D and the partition coefficient α in the aortic wall.
The NO diffusion coefficient in the aortic wall is nearly fourfold smaller than the reported diffusion coefficient in solution at 37°C, indicating that NO diffusion in the vascular wall is no longer free, but markedly dependent on the environment in the tissue where these NO molecules are.
The variation in NO diffusion rates through different polymer systems is explained by considering the characteristics of the polymers and, when applicable, the influence of plasticizer content.
In this study, a modified Clark-type NO electrode attached with a customized aorta holder was used to directly measure the flux of NO diffusion across the aortic wall at 37°C.
These results imply that the NO diffusion rate in the vascular wall may be upregulated and downregulated by certain physiological and/or pathophysiological processes affecting the composition of tissues.
The degree of polarization was much more modest when compared to the no diffusion case, but the dynamic range was still broad.
Solid clusters, for example, show virtually no diffusion, but the particles of a liquid cluster can and do diffuse.
Diffusivity of interstitial solute in austenite is treated as concentration dependent and no diffusion is allowed in cementite and ferrite.
There is no diffusion limitation of the exchange of carbon dioxide because this gas is more soluble than oxygen in the alveolar capillary membrane, which facilitates carbon dioxide exchange.
