BACKGROUND: Circulatory changes occur during exposure to Lower Body Negative Pressure (LBNP). These changes may have some similarities to exposure to moderately and slowly increased G-loads in a relaxed subject without anti-G suit. HYPOTHESIS: Changes will also occur in cerebral blood circulation during a rapid release of LBNP. METHODS: Transcranial Doppler ultrasound (TCD) was used to measure middle cerebral artery blood flow velocity (CBFV) in 14 human subjects following rapid release of a ramped lower body negative pressure (LBNP) (0.33 mm Hg.s) to presyncope (mean peak negative pressure of -124 mm Hg). RESULTS: The mean CBFV decreased to an average of 60% (p < 0.05) of the baseline value at peak LBNP. Mean CBFV was still decreased to 65% and 84% of the baseline value (p < 0.05) at the third heart beat and 30 s, respectively, after pressure release. The systolic CBFV decreased similarly to 57% (p < 0.05) of baseline during peak LBNP, and was still 63% (p < 0.05) at the third heart beat after pressure release. Heart rate increased by a mean of 51% (p < 0.001) and systolic heart level blood pressure decreased by 28% (p < 0.001) during peak negative pressure. Both heart rate and blood pressure returned to baseline levels within 30 s after pressure release. CONCLUSIONS: Following a presyncopal LBNP, the CBFV is not fully restored up to 30 s after the release of the negative pressure. This delayed returning of cerebral circulation following orthostatic stress may have some similarities to what occurs after the release of a gradual onset G-load in a relaxed subject without anti-G suit.
BACKGROUND: Circulatory changes occur during exposure to Lower Body Negative Pressure (LBNP). These changes may have some similarities to exposure to moderately and slowly increased G-loads in a relaxed subject without anti-G suit. HYPOTHESIS: Changes will also occur in cerebral blood circulation during a rapid release of LBNP. METHODS: Transcranial Doppler ultrasound (TCD) was used to measure middle cerebral artery blood flow velocity (CBFV) in 14 human subjects following rapid release of a ramped lower body negative pressure (LBNP) (0.33 mm Hg.s) to presyncope (mean peak negative pressure of -124 mm Hg). RESULTS: The mean CBFV decreased to an average of 60% (p < 0.05) of the baseline value at peak LBNP. Mean CBFV was still decreased to 65% and 84% of the baseline value (p < 0.05) at the third heart beat and 30 s, respectively, after pressure release. The systolic CBFV decreased similarly to 57% (p < 0.05) of baseline during peak LBNP, and was still 63% (p < 0.05) at the third heart beat after pressure release. Heart rate increased by a mean of 51% (p < 0.001) and systolic heart level blood pressure decreased by 28% (p < 0.001) during peak negative pressure. Both heart rate and blood pressure returned to baseline levels within 30 s after pressure release. CONCLUSIONS: Following a presyncopal LBNP, the CBFV is not fully restored up to 30 s after the release of the negative pressure. This delayed returning of cerebral circulation following orthostatic stress may have some similarities to what occurs after the release of a gradual onset G-load in a relaxed subject without anti-G suit.