Abstract
Study hypothesis: We attempted to determine whether the reduced egress of mRNA from brain nuclei following in vivo ischemia and reperfusion is caused by direct damage to the nuclear pore-associated NTPase that impairs the system for nuclear export of polyadenylated, or poly (A)+, mRNA. Design: Prospective animal study. Interventions: NTPase activity and poly(A)+ mRNA transport were studied in nuclear envelope vesicles (NEVs) prepared from canine parietal cortex isolated after 20 minutes of ischemia or 20 minutes of ischemia and 2 or 6 hours of reperfusion. Results: Brain NEV NTPase Michaelis-Menten constant (K m) and maximum uptake velocity (V max) and the ATP-stimulated poly(A)+ mRNA egress rates were not significantly affected by ischemia and reperfusion. In vitro exposure of the NEVs to the OH× radical-generating system completely abolished NTPase activity. Conclusion: We conclude that brain ischemia and reperfusion do not induce direct inhibition of nucleocytoplasmic transport of poly(A)+ mRNA. This suggests that the nuclear membrane is not exposed to significant concentrations of OH× radical during reperfusion. [Tiffany BR, White BC, Krause GS: Nuclear-envelope nucleoside triphosphatase kinetics and mRNA transport following brain ischemia and reperfusion. Ann Emerg Med June 1995;25:809-817.]. © 1995 Mosby, Inc. All rights reserved.