Brain lactic acidosis and ischemic cell damage: quantitative ultrastructural changes in capillaries of rat cerebral cortex.
Excessive tissue lactic acidosis has earlier been shown to aggravate structural damage of both neurons and glial cells in the rat cerebral cortex. To study the reactions of cortical capillaries, light- and electronmicroscopic morphometry was used. Rats were subjected to severe incomplete ischemia (cerebral blood flow below 5% of normal) for 30 min by clamping their carotid arteries and by lowering the blood pressure. Lactate production during ischemia was modified by preischemic administration of either saline (low lactic acidosis group) or glucose (high lactic acidosis group). In the animals with low lactic acidosis, only minimal vascular changes were seen after both 5 min and 90 min recirculation. In the high lactic acidosis group, the endothelial cells were swollen after 5 min of recirculation, and the changes grew markedly worse during 90 min of recirculation. Nuclear chromatin coarsened and mitochondria swelled up. Morphometry showed that the lumen narrowed as a result of endothelial swelling. In spite of variable degree of perivascular astrocytic edema, the outer capillary diameter was little changed in the experimental groups. It seems likely that endothelial swelling hampers postischemic circulation in incomplete ischemia accompanied by high lactic acidosis.
D000138:Acidosis / Q000473:pathology*; D000818:Animals; D002196:Capillaries / Q000648:ultrastructure*; D002540:Cerebral Cortex / Q000098:blood supply / Q000648:ultrastructure*; D002843:Chromatin / Q000648:ultrastructure; D004727:Endothelium / Q000648:ultrastructure; D002546:Ischemic Attack, Transient / Q000473:pathology*; D007773:Lactates; D008297:Male; D008854:Microscopy, Electron; D008928:Mitochondria / Q000648:ultrastructure; D051381:Rats; D013997:Time Factors
D002843:Chromatin; D007773:Lactates