-Due to the short half-life (45 min) of propentofylline,may be advantageous to test continuous administration of the substance in future clinical studies. In one previous of nerve and glial function by adenosine-role in the development of
ischemic damage. controlled study in 30 patients with acute stroke. Patients Kreutzberg GW. Modulation of intracellular formation of reactive
received a continuous i.v. infusion over 7 days and oxygen intermediates in peritoneal macrophages and microglia /
repeated measurements of glucose metabolism with brain macrophages by propentofylline. J Cereb Blood Flow Metab
[18F]deoxyglucose positron emission tomography (PET)
[14] DeLeo J, Toth L, Schubert P, Rudolphi K, Kreutzberg GW. showed an increased glucose metabolism in the prop- Ischemia-induced neuronal cell death, calcium accumulation, and
entofylline treatment group 14 days after onset of therapy glial response in the hippocampus of the mongolian gerbil and
as compared with placebo [29]. protection by propentofylline In conclusion, we have shown in a permanent MCA Metab 1987;7:745–51.
occlusion model that propentofylline has a neuroprotective brain damage using propentofylline in gerbils. Stroke potential against ischemic brain damage; however, this 1988;19:1535–9.
neuroprotective effect was only significant after continuous treatment over 48 h. Shorter-term administration with (HWA 285) against focal cerebral infarction in rats. Neurosci Lett
delayed postmortem analysis was not effective due to the 1994;178:235–8.
short half-life of propentofylline. These data suggest that of ischemic brain damage by the preischemic administration prior to its evaluation in clinical trials, propentofylline of propentofylline (HWA 285) in arat focal ischemia. Brain Res
should be tested in long term animal experiments using