[Hemodynamics in hemorrhagic infarction--an experimental study].
Using our previously reported "thalamic infarction model in the dogs", it was found that hemorrhagic infarction can be produced at a high frequency following recirculation after 6-12 hours of vascular occlusion. In the present study, in order to elucidate the pathophysiology of hemorrhagic infarction, we have undertaken a study of the relations among the histological findings, degree of ischemia, circulatory dynamics, CO2 response and EEG findings after vascular occlusion of 6 hours. In all animals where rCBF was found to fall to less than 50% due to vascular occlusion, hemorrhagic infarction was found. The hemodynamics of those animals presenting hemorrhagic infarction was such that reflow resulted in a transient increase in rCBF followed by decrease within a short period. After a few hours, rCBF values had fallen to pre-occlusion levels. During the 6 hours occlusion, electrical activity became almost flat, and recovery following reflow was not seen. The CO2 response was found to be disturbed immediately following vascular occlusion and also did not recover following reflow. In contrast, among the animals in which hemorrhagic foci were not found, reflow resulted in recovery of rCBF to pre-occlusion levels within a short period. Electrical activity of the brain and CO2 response were found to be maintained throughout the period of occlusion and thereafter in these animals.
D000818:Animals; D002245:Carbon Dioxide; D002543:Cerebral Hemorrhage / Q000503:physiopathology*; D002544:Cerebral Infarction / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D004285:Dogs; D004569:Electroencephalography; D006439:Hemodynamics; D012039:Regional Blood Flow; D013788:Thalamus / Q000098:blood supply* / Q000503:physiopathology
D002245:Carbon Dioxide