muramidase and Brain-Ischemia

Insoluble ubiquitin conjugates (UC) in the mitochondrial fraction of the gerbil cortex were analyzed following transient forebrain ischemia. At 1 h of reperfusion after 2-10 min of ischemia, UC increased as the duration of ischemia was prolonged. Pre-treatment with pentobarbital, rather than post-treatment immediately after recirculation, reduced the increase of UC at 1 h of reperfusion following 5 min of ischemia. Pentobarbital had no effect on in vitro ubiquitination of heat-denatured lysozyme by the extract of gerbil cortex. These results suggest that increase in UC is dependent on ischemic damage and pentobarbital attenuates the increase of UC by relieving injury during ischemia.

Topics: Adenosine Triphosphate; Animals; Brain Ischemia; Gerbillinae; Immunoblotting; Male; Muramidase; Phenobarbital; Reperfusion; Time Factors; Ubiquitins

The material comprised 15 cases of ischemic brain stroke at the age of 45 to 101 years. Six brain of subjects deceased at the age of 45 to 57 years and 9 brains of those deceased at the age of 80 to 101 years were studied. Phagocytic cell immunoreactivity in both age groups during the first 5 days and on the 11th and 12th were compared. Phagocytic reactivity in cases of patients who died on the 6th, 15th and 35th days after stroke onset was also estimated. Colliquative necrosis with cavitation was observed in middle-aged cases from the 3rd infarction day. In the senile group the beginning of tissue breakdown was noted on the 5th day, but colliquative necrosis with cavitation was found on the 11th infarction day. Senile alterations in the biochemical components in various brain tissue elements are probably the cause of the different course and dynamics of the pathological process.

Topics: Aged; Aging; Autopsy; Brain; Brain Ischemia; Female; Humans; Immunohistochemistry; Male; Middle Aged; Muramidase; Necrosis; Phagocytes