This was a search for endogenous inhibitors of the cation pump enzyme in normal and ischemic gerbil brain. The first model of ischemia was bilateral common carotid clamping for 30 minutes followed by reperfusion periods of 0, 1, 2.5, and 4 hours. After bilateral clamping, K-paranitrophenylphosphatase (K-pNPPase) activity fell significantly after 0, 1, and 2.5 hours of reflow but only slightly by 4 hours. The second model was decapitation with timed delays of 0, 15, 60 and 240 minutes. There was no decline in K-pNPPase activity after total ischemia produced by decapitation. Thus, the model of partial ischemia was more deleterious to the cation pump enzyme than was the model of total ischemia. All brains contained endogenous K-pNPPase inhibitors. Boiled supernatant fractions inhibited K-pNPPase activity by about 50-60% while Amicon filtrates of brain homogenate inhibited about 12%. Factors in normal and ischemic brain may modify the activity of the cation pump enzyme, but no differences in inhibitory effects were found between normal and ischemic brain extracts.
|Original language||English (US)|
|Number of pages||8|
|State||Published - 1988|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)