INTRODUCTION: This study measured total and regional cerebral blood flow (BF) in baboons during +Gz-induced loss of consciousness (G-LOC) and during recovery from G-LOC. METHODS: Flowprobes (Transonic Inc., T201, Ithaca, NY) were placed on the common carotid and internal carotid arteries of five male baboons for continuous measurement of total cephalic and cerebral BF, respectively. Radiolabeled microspheres were used to measure regional central nervous system BF at discrete timepoints. G-LOC was determined from visual observations of the animals and from EEG recordings. RESULTS: Cerebral blood flow was maintained and animals remained conscious during 60 s exposure to +4 Gz. In contrast, G-LOC was observed during the first 16-25 s (mean = 20.3 +/- 3.7 s) of exposure to +8 Gz in all five animals. Internal and common carotid artery BF decreased rapidly to zero during the first few seconds of +8 Gz. BF always appeared to cease prior to the occurrence of G-LOC. During early recovery from G-LOC there was no hyperemic response recorded with flowprobes, whereas a hyperemic response was recorded following 60 s exposures to +4 Gz in which the animals did not experience G-LOC. Microsphere measurements of the regional distribution of BF are consistent with the hypothesis of a +Gz-induced differential perfusion deficit throughout the brain and central nervous system during G-LOC. CONCLUSIONS: We conclude that G-LOC is preceded by cessation of cerebral BF. The fact that the hyperemic response following +Gz exposure is less when G-LOC occurs than when G-LOC does not occur suggests CNS energy conservation during G-LOC.
INTRODUCTION: This study measured total and regional cerebral blood flow (BF) in baboons during +Gz-induced loss of consciousness (G-LOC) and during recovery from G-LOC. METHODS: Flowprobes (Transonic Inc., T201, Ithaca, NY) were placed on the common carotid and internal carotid arteries of five male baboons for continuous measurement of total cephalic and cerebral BF, respectively. Radiolabeled microspheres were used to measure regional central nervous system BF at discrete timepoints. G-LOC was determined from visual observations of the animals and from EEG recordings. RESULTS: Cerebral blood flow was maintained and animals remained conscious during 60 s exposure to +4 Gz. In contrast, G-LOC was observed during the first 16-25 s (mean = 20.3 +/- 3.7 s) of exposure to +8 Gz in all five animals. Internal and common carotid artery BF decreased rapidly to zero during the first few seconds of +8 Gz. BF always appeared to cease prior to the occurrence of G-LOC. During early recovery from G-LOC there was no hyperemic response recorded with flowprobes, whereas a hyperemic response was recorded following 60 s exposures to +4 Gz in which the animals did not experience G-LOC. Microsphere measurements of the regional distribution of BF are consistent with the hypothesis of a +Gz-induced differential perfusion deficit throughout the brain and central nervous system during G-LOC. CONCLUSIONS: We conclude that G-LOC is preceded by cessation of cerebral BF. The fact that the hyperemic response following +Gz exposure is less when G-LOC occurs than when G-LOC does not occur suggests CNS energy conservation during G-LOC.