• Andrew P Blaber, Helmut Hinghofer-Szalkay, and Nandu Goswami.
• School of Kinesiology, Simon Fraser University, Burnaby, B.C., Canada.
• Aviat Space Envir Md. 2013 Jan 1;84(1):59-64.

BackgroundThe goal of this study was to investigate the contribution of splanchnic volume redistribution and lower limb vasoconstriction in the maintenance of blood pressure during progressive central hypovolemia induced by graded lower body negative pressure (LBNP). It was hypothesized that splanchnic blood volume loss during LBNP would buffer decreases in thoracic blood volume.MethodsThere were 15 healthy subjects (8 men, 7 women) who participated in the study. We used LBNP of -10, -20, -30, and -40 mmHg with segmental impedance analysis to determine central and splanchnic volume changes, and near infrared spectroscopy (NIRS) to assess calf venous volume changes and vasoconstrictor tone.ResultsIn relation to baseline, LBNP to -40 mmHg resulted in a 57% increase in deoxygenated blood in the calf, indicating venous pooling in the lower limbs. These events led to a decrease in venous return and a 28% decline in cardiac output. Total upper body impedance increased by 6.6% with a 2.4% change in thoracic and a 13.1% increase in splanchnic impedance with progressive LBNP. Splanchnic blood volume contributed to more than 50% of the volume redistribution to the thoracic compartment during hypovolemia. Both men and women increased their heart rate, but only men vasoconstricted (4.4%) with increasing LBNP. The net result of these events was the maintenance of mean arterial blood pressure with no presyncopal symptoms in these subjects.DiscussionOur results suggest that splanchnic blood volume redistribution--rather than leg vasoconstriction--plays an important role in blood pressure regulation during central hypovolemia.

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