The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: Examination of a model

Abstract

The hypothesis that iv dextrose infusion prior to - and head position during - cerebral ischemia would influence the severity and pattern of neurologic injury was tested in primates. Fifteen pigtail monkeys weighing 3.3 ± 0.2 kg (mean ± SE) were subjected to 17 min complete cerebral ischemia followed by 24 h intensive care treatment and neurologic assessment for an additional 72 h. Monkeys were given 50 ml iv infusions of either dextrose 5% in 0.45% saline solution (n = 8) or lactated Ringer's solution (n = 7) during the preparatory period. This volume corresponds to approximately 1 l/70 kg individual. These same monkeys were placed in either the lateral (n = 3), prone (n = 5), or supine (n = 7) position during the ischemic period. Two monkeys failed to meet preestablished protocol criteria and were excluded from data analysis. Blood glucose immediately preischemia in the dextrose-treated group (181 ± 19 mg·dl-1) was not significantly greater than in the group given lactated Ringer's solution (140 ± 6 mg·dl-1; P = 0.07). Dextrose infusion resulted in significantly greater cerebral injury at 96 h postischemia when comparing both neurologic (P < 0.05) and histopathology (P < 0.05) scores. Specifically, dextrose administration resulted in the greatest injury to the insular cortex, thalamus, Purkinje cells, and substantia nigra. Although blood glucose was <250 mg·dl-1 in all monkeys at the time of complete cerebral ischemia, there was a high correlation between blood glucose rank and neurologic function rank (r(s) = 0.76; P < 0.005). The authors were unable to note any effect of head position on the distribution of histopathologic lesions. Prior to removing the brain for histopathologic studies, four monkeys were given repeat infusions of 50 ml dextrose 5% in 0.45% saline solution over 11 ± 1 min. These infusions produced increases in blood glucose from 56.7 ± 7.6 to 244 ± 24.9 mg·dl-1 (P < 0.01) and increases in brain glucose from 1.64 ± 0.22 to 5.11 ± 0.48 μmol·g-1 (P < 0.01).