No abstract

The authors report dose-response relationships for atropine in their rat model of human delirium. In this model, anticholinergic mechanisms are an important cause and may be a neurochemical final common pathway for diverse etiologies of delirium. Four intravenous (i.v.) bolus doses of atropine (27.5, 13.5, 6.875, and 3.44 mg/kg) were studied along with the originally reported dose of 55 mg/kg and saline control. Subsequent iv infusions were also proportionately reduced. EEG frequency and amplitude, maze performance, and subjective behavioral descriptions were taken over 320-minute study periods. Repeated-measures analysis of variance compared data between groups, and effect sizes were calculated. Dosages to be used in future studies are discussed.

This study compared the effects of 3 hours of cardiac arrest performed at 2 different levels of profound hypothermia in totally exsanguinated, blood substituted dogs. Dogs (N = 10) were anesthetized and esophageal temperature was lowered to 24 degrees at which time exsanguination began. Once exsanguination was complete and the heart had arrested, continuous whole body perfusion of an oxygenated blood substitute solution was performed for 3 hours. Core temperature during this period remained below 10 degrees C and reached nadirs of 1.3 degrees C in Group 1 (N = 5) versus 7.3 degrees C in Group II (N = 5). Once the dog was allowed to rewarm to 10 degrees C replacement of the perfusate with blood was begun. All dogs survived the procedure but 2 dogs from each group died by 4 days following the experiment. The remaining 6 dogs were observed for between 10 and 85 days. The group perfused with blood substitute at the warmer nadir had a faster recovery of motor behavior and showed smaller changes from normal in several biochemical and hematological parameters. These findings indicate that profound hypothermia and total blood substitution can be successfully achieved at either temperature nadir, but the warmer level appears to be associated with a faster recovery.