LUNDVALL, J., S. MELLANDER, H. WESTLING and T. WHITE. Fluid transfer between blood and tissues during exercise. Acta physiol. scand. 1972. 85. 258-269.

No abstract

Lower body negative pressure (LBNP) is a stimulus frequently used to study reflex circulatory responses in humans. Studies have provided data on LBNP-induced blood pooling; however, the possibility that LBNP also might be associated with an important loss of plasma fluid has attracted little attention. Therefore this problem was analysed in male volunteers exposed to prolonged (10 min) high (70-75 mmHg) LBNP. Data on LBNP-induced blood pooling that were more reliable than in previous literature were also provided. LBNP caused early pooling of more than 870 ml of blood. Rapid filtration of plasma into the exposed tissues occurred throughout LBNP. The cumulative oedema in the legs and buttocks averaged as much as 460 ml, and additional quite large volumes of plasma apparently accumulated in other parts of the lower body. Concomitantly, there was compensatory absorption of extravascular fluid in the upper body. The net decrease in plasma volume (PV) was still large and averaged 491 +/- 29(SE) ml. Two aspects of the demonstrated process of transcapillary fluid fluxes and PV decline may be emphasized. Firstly, in conjunction with the primary large redistribution of intravascular volume, it certainly implies that LBNP is a potent stimulus as also indicated by a progressive increase in heart rate (HR) and a progressive decline in systolic pressure throughout experimental intervention. In fact, LBNP-induced circulatory stress clearly has bearings on the extreme hypovolaemic situation provided by the pressure-bottle haemorrhage technique used in animals. Secondly, it not only offers an interesting example of the dynamics of PV but appears to have more general validity with regard to states characterized by gravitational shifts of blood (hydrostatic load), like upright exercise and quiet standing.

Compensatory, net fluid transfer across the capillaries was studied in the arm of man with plethysmographic technique during experimental hypovolaemia induced by lower body negative pressure (LBNP). Thirty, 60, and 110 cmH2O LBNP evoked rapid transfer of fluid from tissue to blood at average rates of 0.053, 0.088 and 0.147 ml min-1 100 ml-1 soft tissue, i.e. graded responses typical for a true homeostatic regulation. Other experiments demonstrated a net fluid absorption not only from the arm but also from a wide range of skeletal muscle and skin regions in the body during experimental hypovolaemia, i.e. the more or less generalized response required if the absorption process is to contribute importantly to plasma volume regulation. In a third series of experiments it was shown that gradually applied LBNP was a much less efficient stimulus for fluid gain into the circulation than rapidly instituted LBNP, tentatively explaining the fairly slow plasma volume refill in main in previous literature after experimental, true and necessarily slow blood loss. Taken together, the findings described warrant the conclusion that the described process of fluid gain into the circulation may be a very important component in the overall homeostatic circulatory regulation in states of hypovolaemia. The data in fact suggest that the process might be capable of increasing plasma volume by as much as 600 ml within only 10 min, suggesting that such plasma volume control might be much more potent than previously believed.

The hypothesis was tested that the hemoconcentration observed during standing provides erroneous information about the induced plasma volume (PV) decline. Male volunteers (n = 10) stood quietly for 15 min after supine rest. On standing arterial hemoglobin (Hb) rose slowly to reach an increase of 5.9 +/- 0.3% (SE) after 15 min. Early after resuming the supine position, Hb increased further to 9.2 +/- 0.5% above control level and then declined gradually. Venous antecubital blood from the left arm supported horizontally at heart level in both the supine and standing positions (no hydrostatic load) showed very similar changes. However, Hb in venous blood collected during standing from the right arm held in the natural dependent position rose much more markedly than that in arterial blood and in venous blood from the horizontal arm (470 +/- 122, 105 +/- 24, and 55 +/- 7% greater increase at 5, 10, and 15 min, respectively). Taken together, these observations indicated that 1) analyses of arterial blood sampled from the standing subject grossly underestimated the prevailing "overall" hemoconcentration and PV decline, a phenomenon ascribed to incomplete mixing of blood between dependent and nondependent regions; 2) arterial blood sampled from the recumbent subject early (60 s) after completion of standing reflected the "true" overall intravascular hemoconcentration, with a calculated PV decline of no less than 511 +/- 27 ml, because the supine position facilitated proper mixing of blood between circulatory compartments; 3) data from common venous sampling from the dependent arm during standing primarily reflected a regional hemoconcentration (fluid loss) in the arm rather than PV decline; and 4) short-term quiet standing caused a more prominent and hemodynamically important decrease in PV than usually believed.