The swelling of mitochondria from nitrogen gas; a possible cause of reperfusion damage.

Electron photomicrograph evidence is presented which suggests that the in vivo swelling of mitochondria may result from the uptake of nitrogen gas bubbles which coalesce to fill the intramitochondrial space during tissue anoxia. These observations have led to the hypothesis that nitrogen-filled mitochondria are unable to take up oxygen resulting in cell death. A test of this hypothesis also represents a probable treatment for stroke, namely the total body washout of nitrogen. This can be achieved by the inhalation of an oxygen-helium mixture with exhaled gases shunted to ambient atmosphere. This washout should facilitate nitrogen egress from the interior of affected mitochondria, allow oxygen uptake and a resumption of oxidative metabolism. This hypothesis generally fits well with the literature on luxury perfusion following stroke. In cases of luxury perfusion the venous blood exiting the lesion is red indicating a decreased transfer of oxygen to the extracellular and cytosolic fluids. However, whereas luxury perfusion assumes blood flow adequate for delivery of oxygen to the tissues, this hypothesis interjects a blockade at the level of oxygen uptake into mitochondria, and unless this blockade is reversed it will lead to cell death and brain tissue necrosis in the affected regions.