Cerebral hemodynamics and brain functional activity during lower body negative pressure.

INTRODUCTION: Exposure to high +Gz acceleration forces on a centrifuge or in an aircraft can severely decrease cerebral blood perfusion and cause rapid G-induced loss of consciousness. However, milder acceleration may gradually reduce cerebral blood flow and affect cognitive function in subtler ways. This study used lower body negative pressure (LBNP) to mimic +Gz circulatory effects in order to study cerebral hemodynamics and brain function. METHODS: Subjects were 15 healthy men, 19-21 yr of age. They were exposed to LBNP at two levels for 5 min each separated by a 10-min recovery period. The conditions were low (LO), -4.00 kPa (-30 mmHg) and high (HI), -6.67 kPa (-50 mmHg).Variables measured before, during, and after LBNP included cerebral blood flow velocity (CBFV) in the middle cerebral artery, blood oxygen saturation (SaO2), heart rate (HR), blood pressure, P300 of event-related EEG potentials, reaction time, and tracking error. RESULTS: LO significantly reduced CBFV at 4 and 5 min, increased HR, and decreased the amplitude of P300, but none of the other variables changed from baseline. In contrast, HI produced significant changes in most variables: CBFV decreased at 2 min and then fell further at 4 and 5 min, HR increased, and SaO2 decreased. Significant neurocognitive changes included increased latency and reduced amplitude of P300, slower reaction time, and greater tracking error. CONCLUSION: The higher level of LBNP used here reduced cerebral perfusion sufficiently to impair neurocognitive function. This model may be useful for further studies of these and other variables under closely controlled conditions.

[Changes of human cerebral blood flow velocity and blood oxygen saturation under lower body negative pressure in upright seated position].

Objective. To investigate the effect of lower body negative pressure (LBNP) in upright seated position on cerebral blood flow velocity, heart rate (HR), and blood oxygen saturation (SaO2) in human. Method. Fifteen young men were selected as subjects. Blood flow velocity in middle cerebral artery (VMCA), HR and SaO2 were measured at 0.5, 1, 2, 3, 4, and 5 min during LBNP and 1, 3, 5 min after -4.00 kPa and -6.67 kPa LBNP in upright seated position respectively. Result. Under -4.00 kPa LBNP, VMCA slowed down at 4, 5 min during LBNP (P<0.05), and HR speeded up at 3, 4, 5 min during LBNP (P<0.05). There were no significant changes of SaO2. Under -6.67 kPa LBNP, VMCA became slow at 2, 3 min (P<0.05), and at 4 and 5 min (P<0.01) during LBNP. At 1 min after release of LBNP, VMCA did not recover, after which it recovered to control level. HR significantly increased (P<0.01) and SaO2 decreased at 5 min (P<0.05) during LBNP. Conclusion. LBNP can cause blood pooling in lower body so that VMCA and brain blood volume decrease. Then it causes loss of consciousness. The results of this experiment may provide experimental data for diagnosis of flight syncope and orthostatic intolerance.