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.

Our previous studies strongly indicate that the capillary filtration coefficient (CFC) in skeletal muscle and skin of man is much larger than previously believed, or about 0.050 ml min-1 100 ml-1 mmHg-1. The hypothesis that this large capillary fluid permeability is a factor of primary importance for plasma volume control was approached. Experimental hypovolaemia induced by lower body negative pressure (LBNP of 70-95 cmH2O) was associated with a rapid net fluid gain from the studied upper arm into the circulation of 0.17 ml min-1 100 ml-1 tissue. The transcapillary driving force for this fluid transfer, probably caused by adrenergic adjustment of vascular resistance, with a decline of capillary pressure, was relatively small, or 1.7 mmHg on average. CFC was instead very high during LBNP, increasing from a control value of 0.054 +/- 0.004 (SE) to no less than 0.097 +/- 0.007 ml min-1 100 ml-1 mmHg-1, probably reflecting an increased number of effectively perfused capillaries. It is suggested that the large capillary fluid permeability in skeletal muscle and skin of man, with large tissue mass and fluid reservoir, may be of great functional importance for plasma volume control after blood loss and also in other (patho)physiological situations. As demonstrated, it can thus permit rapid transfer of large fluid volumes into the circulation and, perhaps of special importance, with only small transcapillary driving force (capillary pressure decline).(ABSTRACT TRUNCATED AT 250 WORDS)

We analyzed in the forearm of "comfortably warm" male volunteers 1) reflex sympathetic vascular resistance changes evoked by short-term graded [1.5-min exposure to 15, 40, 55, and 70 mmHg and high and barely tolerated (77-95 mmHg)] lower body negative pressure (LBNP) and 2) resistance changes evoked by abolition of control sympathetic vasoconstrictor tone (anesthetic axillary nerve block). Graded LBNP caused graded neurogenic vasoconstriction with pronounced average flow decline at high LBNP from 3.7 to 0.8 ml.min-1 x 100 ml-1 (77 +/- 2% decrease), corresponding to a drastic resistance increase from 25.4 to 127 mmHg.ml-1 x min x 100 ml (352 +/- 27% rise above control). Axillary nerve block caused marked increases in forearm blood flow from 4.3 +/- 0.4 to 15.7 +/- 1.4 ml.min-1 x 100 ml-1 [> 3-fold flow increase equivalent to an average resistance decline from 19.7 to 6.3 mmHg.ml-1 x min x 100 ml (72 +/- 5%)], reflecting a surprisingly high resting constrictor fiber vascular tone. The overall results indicate that the sympathetic skeletal muscle and skin resistance vessel control in men allows very large (almost 20-fold) alterations in blood flow and vascular resistance from complete inhibition of neurogenic vascular tone to maximal reflex nerve activation. This range of sympathetic control was clearly greater than that revealed in comparative experiments on the cat lower leg.

The concept that, in man, the sympathetic control of the resting limb vascular resistance is truly limited and thus strikingly different from animal species, was challenged in the present study. Analyses were performed in healthy male volunteers of reflex forearm vascular resistance changes evoked by lower body negative pressure (LBNP) ranging from low (15 mmHg) to high and barely tolerated (85 mmHg) levels. Graded LBNP was associated with graded increases in resistance. At high 85 mmHg LBNP the responses were pronounced with a rise in forearm resistance to no less than 120 mmHg ml-1 min 100 + ml soft tissue, on average, corresponding to a 377% increase above control. This drastic response seemed entirely neurogenic in origin and calculations, based on the likely assumption that a similar response occurred in all skeletal muscle and skin/(subcutaneous fat), showed that it permitted a marked increment in total systemic vascular resistance because of the fact that these tissues constitute so large a proportion of the body mass. The conclusion was reached that the studied tissues may serve as main targets for powerful homeostatic reflexes. It is also suggested, in contrast to current views, that the high-pressure arterial rather than the low-pressure cardio-pulmonary baroreceptors may be the main mediators of haemodynamically important vasoconstrictor responses.

Resting forearm vascular resistance changes elicited in male volunteers by graded reflex sympathetic activation evoked by graded lower body negative pressure (LBNP) were studied at room temperatures of 24-25 and 20-21 degrees C. The latter condition caused strong suppression of skin flow and permitted preferential analysis of muscle responses and, by comparison with responses at 24-25 degrees C, secondary estimation of circulatory reactions in the skin. Short-lasting LBNP-bouts (1.5 min) allowed analyses of reflex vascular reactions to high and barely tolerated LBNP (85 mmHg) and thereby to high levels of circulatory stress and sympathetic nerve discharge, yet without risks for the subjects under study. Both muscle and skin reacted intensely and in a graded manner to graded sympathetic activation with very pronounced resistance change (74-77% flow decline; 350-400% resistance rise above control level) at high LBNP. Therefore, the sympathetic vasomotor fibres can exert a very potent control of vascular resistance both in skeletal muscle and in skin under thermoneutral conditions, and both tissues apparently can serve as major targets for powerful sympathetic homeostatic baroreflexes. Evidence indicated that this control is exerted from both low-pressure cardiopulmonary and high-pressure arterial baroreceptor areas. These conclusions deviate from previous literature, in which baroreflex sympathetic vasoconstriction in the human limb has been proposed to be more or less selectively mediated from cardiopulmonary receptors and, further, muscle to respond fully already at mild circulatory stress without further constriction if the stimulus is increased.