Regional assessment of pathophysiological changes in acute cerebral ischemia: multiparametric histochemical study
Kim, S.H.
Nihon Geka Hokan. Archiv für Japanische Chirurgie 54(6): 417-440
1985
ISSN/ISBN: 0003-9152 PMID: 3834861 Document Number: 242696
Regional changes of histochemical multiparameters including brain mitochondrial redox State (NADH), ATP content, tissue pH (pH), tissue potassium (K+) and brain dopamine nerve terminals (DA) in the caudate nucleus were assessed in a various degree of experimental acute cerebral ischemia. Ischemia was produced by permanent or transient occlusion of the left common carotid artery for various duration in normally fed mongolian gerbils. The degree of ischemia was evaluated by the severity of neurological symptoms, and animals were classified into three groups; symptomatic, borderline and asymptomatic. The changes of each parameters on the ligated side were well corresponded to the degree of ischemia. However, regional differences were observed among these parameters. In 5 minutes and 60 minutes of occlusion, there were three different types of ischemic changes; (1) acidosis with marked increase of NADH and depletion of ATP, (2) acidosis with mild increase of NADH and no depletion of ATP, (3) acidosis without changes of NADH and ATP. Acidosis extended wider than areas of NADH and ATP changes. These differences might be caused by facilitated anaerobic glycolysis in acute stage of ischemia. In 180 minutes occlusion of symptomatic gerbils on the other hand, the acidotic area was almost consistent with the areas of NADH and ATP changes with marked depletion of tissue K+. The results might indicate that mild ischemic changes of energy metabolism were exacerbated by brain edema in symptomatic group in spite of recovery in borderline group. In transient ischemia, symptoms and changes of parameters recovered with residual acidosis in 60 minutes reperfusion after 60 minutes of ischemic insult. On the other hand the black area on NADH fluorescence was noted with depletion of ATP and tissue K+ and persistent acidosis in the hippocampus, thalamus and caudate nucleus in 60 minutes of reperfusion after 180 minutes of ischemic insult. These tissue damage and disturbance of energy metabolism might be related to the postischemic hyperoxidation. DA fluorescence in the caudate nucleus on the ligated side decreased heterogeneously in acute stage of ischemia. Preservation of DA fluorescence was noted around the small vessels with thick walls, probably arterioles. The heterogeneity was more apparent in borderline group of 60 minutes occlusion and in 5 minutes occlusion of the symptomatic group. This heterogeneity of DA might be due to the difference of perfusion pressure at the microcirculation in the acute stage of incomplete cerebral ischemia. The present study indicates the importance of multiparametric regional study to elucidate the pathophysiology of acute cerebral ischemia.