PRESYNCOPE CAUSED BY CENTRAL HYPOVOLEMIA IS NOT PRECEDED BY EVOKED-POTENTIAL ALTERATIONS

被引:5
作者
LIGHTFOOT, JT
THAKOR, N
BISWIJIT, S
HANLEY, DF
机构
[1] JOHNS HOPKINS MED INST,DIV PHYSIOL,BALTIMORE,MD 21205
[2] JOHNS HOPKINS MED INST,DIV BIOMED ENGN,BALTIMORE,MD 21205
[3] JOHNS HOPKINS MED INST,DIV ANESTHESIOL NEUROSURG & NEUROL,BALTIMORE,MD 21205
来源
CLINICAL PHYSIOLOGY | 1992年 / 12卷 / 03期
关键词
CEREBRAL BLOOD FLOW; CEREBRAL OXYGEN CONSUMPTION; LBNP; PRESYNCOPE; SOMATOSENSORY EVOKED POTENTIALS;
D O I
10.1111/j.1475-097X.1992.tb00832.x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The mechanism(s) responsible for the onset of presyncope during a central hypovolaemic challenge have gone undefined for many years. It has been speculated that a decrease in cerebral blood flow initiates presyncopal responses, which in turn lead to greater decreases in cerebral oxygen delivery and unconsciousness. Somatosensory evoked potentials (SEP) were monitored as a measure of cerebral functioning in ten subjects during presyncopal symptom limiting lower body negative pressure (a central hypovolaemic challenge). SEP latency and amplitudes have been correlated with cerebral oxygen uptake, so SEP activity can serve as an indirect indicator of cerebral homeostasis. SEPs were generated by electrically stimulating the median nerve and recoding the resulting potentials over the contralateral cerebral cortex. While heart rate and mean blood pressure both fell at presyncope, there were no changes noted in either SEP latency or amplitude at any point before (latency = 22-9 +/- 9 ms; amplitude = 2.86 +/- 0.24-mu-V), during (22.6 +/- 0-9 ms; 2.68 +/- 0.2-mu-V), or after (22.7 +/- 0-9 ms; 2-37 +/- 0-23-mu-V) the occurrence of presyncope. We conclude that the onset of presyncope is not associated with a decrease in cerebral function.
引用
收藏
页码:267 / 275
页数:9
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