Neurologic and Cardiovascular Effects of Hypotension in the Monkey

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Abstract

SUMMARY

Thirty monkeys were exposed to controlled systemic hypotension of different magnitudes and durations to determine factors leading to brain injury or cardiovascular failure. Fourteen monkeys developed brain injury. Of these, 6 survived indefinitely and 8 were sacrificed or died within 12-62 hours due to neurologic deterioration accompanied by respiratory failure. Sixteen animals did not develop brain injury, but 9 of these died within 24 hours from documented cardiovascular failure while the remaining 7 survived indefinitely. A highly reproducible threshold for the development of brain injury was found at a mean arterial blood pressure (MABP) of 25 mm Hg. Maintenance MABP was < 25 mm Hg in 13 of 14 lesioned monkeys and > 2S mm Hg in IS of 16 non-lesioned monkeys. Maintenance MABP averaged 20.1 ± 1.1 mm Hg in lesioned and 32.1 ± 1.7 mm Hg in non-lesioned animals (p < 0.001). Among the non-lesioned animals, death from delayed cardiovascular failure ensued when MABP was maintained between 27 and 35 mm Hg for 90 min or longer. Animals exposed to this range of hypotension for < 90 min or to MABP exceeding 35 mm Hg for as long as 3 h survived intact. EEG changes occurring during hypotension most accurately predicted neurologic outcome. The threshold MABP required to produce cerebral electric silence was 21-22 mm Hg. Monkeys developing marked brain injury had > 25 minutes of EEG flattening, while slightly injured animals had it for 5-15 minutes and those without injury for < 5 min. Changes in acid-base state, common carotid artery blood flow, and cerebral uptake of glucose and oxygen during hypotension also correlated with neurologic and cardiovascular outcome. Hypoxemia and hypercarbia were not contributory factors in the production of brain injury in this study.

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