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The Biological Lifetime of Nitric Oxide: Implications for the Perivascular Dynamics of NO and O2
Douglas D. Thomas, Xiaoping Liu, Stephen P. Kantrow and Jack R. Lancaster Jr.
Proceedings of the National Academy of Sciences of the United States of America
Vol. 98, No. 1 (Jan. 2, 2001), pp. 355-360
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3054679
Page Count: 6
You can always find the topics here!Topics: Hepatocytes, Blood vessels, Respiration, Half lives, Oxygen, Oxygen consumption, Body tissues, Oxides, Electrodes, Tissue oxygenation
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Endothelial nitric oxide (nitrogen monoxide) is synthesized at the intravascular/extravascular interface. We previously have reported the intravascular half-life of NO, as a result of consumption by erythrocytes, as approximately 2 ms. We report here studies designed to estimate the lifetime of NO in the parenchymal (extravascular) tissue and describe the implications of these results for the distribution of NO and oxygen concentration gradients away from the blood vessel. The rate of consumption of NO by parenchymal cells (hepatocytes) linearly depends on both NO and O2 concentration. We estimate that the extravascular half-life of NO will range from 0.09 to > 2 s, depending on O2 concentration and thus distance from the vessel. Computer modeling reveals that this phenomenon, coupled with reversible NO inhibition of cellular mitochondrial oxygen consumption, substantially extends the zone of adequate tissue cellular oxygenation away from the blood vessel, with an especially dramatic effect during conditions of increased tissue work (oxygen consumption). This represents a second action of NO, in addition to vasodilation, in enhancing tissue cellular respiration and provides a possible physiological function for the known reversible inhibition of mitochondrial respiration by low concentrations of NO.
Proceedings of the National Academy of Sciences of the United States of America © 2001 National Academy of Sciences