AVP response to LBNP is attenuated in a hyperbaric environment.

Introduction: Accumulated evidence indicates attenuated vasopressin (AVP) release associated with hyperbaria in humans. The present study was designed to test the hypothesis that plasma AVP response to central hypovolemiawas attenuated in a hyperbaric environment. Methods: Response of AVP to central hypovolemic stress, in the form of lower-body negative pressure (LBNP), was measured in 10 men at 1 and 3 atmosphere absolute (ATA) air. The stress consisted of 4 min each of control and LBNP at -20 and -40 mmHg. Plasma AVP, plasma norepinephrine (NE), plasma osmolality, and hematocrit (Hct) were measured. Thoracic impedance (Zo), and leg volume were also determined. Results: The baseline AVP (0.9 ′ 0.3 pg . ml - 1 ) at 1 ATA increased significantly in response to -40 mmHg LBNP (1.8 ′ 0.6 pg . ml - 1 ), but the increase was attenuated at 3 ATA (1.2 ′ 0.8 pg . ml - 1 ). The baseline NE at 3 ATA was lower by 22.4 pg . ml - 1 than that of 1 ATA (226.5 pg . ml - 1 ). NE increased with increasing LBNP at both environmental pressures, but the increase was independent of the pressure. Changes in Zo, reflecting thoracic blood volume, were identical in both environments. Mean arterial pressure, plasma osmolality, and Hct remained constant throughout the experimental period. Leg volume increased stress dependently during LBNP (∼34 ml at -20 mmHg; ∼74 ml at -40 mmHg) and the increment was similar in the two environments. Conclusion: The present study revealed that hyperbaria attenuated the response of AVP and NE to hypovolemic stress. The attenuated AVP response to LBNP was associated with neither plasma osmolality nor intrathoracic blood shift.