Based on the results of head-down simulation studies and the results of parabolic flights, the hypothesis was tested that central venous pressure (CVP) in humans increases during microgravity (weightlessness) compared with during the ground-based supine position. CVP was recorded with an intravascular pressure transducer in seven healthy humans during short (20-s) periods of microgravity created by parabolic-flight maneuvers and in one astronaut before, during, and up to 3 h after launch of the Spacelab D-2 mission (Space Transport System-55). When the subjects were supine during the parabolic maneuver, CVP decreased during microgravity from 6.5 +/- 1.3 to 5.0 +/- 1.4 mmHg (P < 0.05). during the Spacelab D-2 mission, CVP was 6.2 mmHg during the initial minutes of microgravity, which was very similar to the value of 6.5 mmHg in the supine position 3.5 h before launch of the space shuttle. During the subsequent 3 h of weightlessness, CVP during rest varied between 2.0 and 6.2 mmHg. We conclude that CVP during short (20-s) and longer (3-h) periods of microgravity is close to or below that of the supine position on the ground.
Changes in plasma volume (PV) throughout 12 h of thermoneutral (34.5 degrees C) water immersion (WI) were evaluated in eight subjects by an improved Evans blue (EB) technique and by measurements of hematocrit (Hct), hemoglobin (Hb), and plasma protein concentrations (Pprot). Appropriate time control studies (n = 6) showed no measurable change in PV. At 30 min of immersion, EB measurements demonstrated an increase in PV of 16 +/- 2% (457 +/- 70 ml). Calculations, however, based on concomitant changes in Hct, Hb, and Pprot showed an increase in PV of only 6.9 +/- 0.9 to 10.0 +/- 0.8% at 30 min of WI. PV values based on EB measurements subsequently declined throughout WI to (but not below) the preimmersion level. Concomitantly, changes in PV calculated from Pprot values remained increased, whereas estimations of changes in PV based on Hct and Hb values returned to prestudy levels after 4 h of immersion. It is concluded that PV initially increases by 16 +/- 2% during WI and does not decline below preimmersion and control levels during 12 h of immersion despite a loss of 0.9 +/- 0.2 liter of body fluid. Furthermore, changes in Hct, Hb, and Pprot do not provide accurate measures of the changes in PV during WI in humans.
Central venous pressure (CVP) was measured in 14 males during 23.3 +/- 0.6 s (mean +/- SE) of weightlessness (0.00 +/- 0.05 G) achieved in a Gulfstream-3 jet aircraft performing parabolic flight maneuvers and during either 60 or 120 s of +2 Gz (2.0 +/- 0.1 Gz). CVP was obtained using central venous catheters and strain-gauge pressure transducers. Heart rate (HR) was measured simultaneously in seven of the subjects. Measurements were compared with values obtained inflight at 1 G with the subjects in the supine (+1 Gx) and upright sitting (+1 Gz) positions, respectively. CVP was 2.6 +/- 1.5 mmHg during upright sitting and 5.0 +/- 0.7 mmHg in the supine position. During weightlessness, CVP increased significantly to 6.8 +/- 0.8 mmHg (P less than 0.005 compared with both upright sitting and supine inflight). During +2 Gz, CVP was 2.8 +/- 1.4 mmHg and only significantly lower than CVP during weightlessness (P less than 0.05). HR increased from 65 +/- 7 beats/min at supine and 70 +/- 5 beats/min during upright sitting to 79 +/- 7 beats/min (P less than 0.01 compared with supine) during weightlessness and to 80 +/- 6 beats/min (P less than 0.01 compared with upright sitting and P less than 0.001 compared with supine) during +2 Gz. We conclude that the immediate onset of weightlessness induces a significant increase in CVP, not only compared with the upright sitting position but also compared with the supine position at 1 G.
To investigate whether prolonged water immersion (WI) results in reduction of central blood volume and attenuation of renal fluid and electrolyte excretion, these variables were measured in connection with 12 h of immersion. On separate days, nine healthy males were investigated before, during, and after 12 h of WI to the neck or during appropriate control conditions. Central venous pressure, stroke volume, renal sodium (UNaV) and fluid excretion increased on initiation of WI and thereafter gradually declined but were still elevated compared with control values at the 12th h of WI. Atrial natriuretic peptide (ANP) concentration in plasma initially increased threefold during WI and thereafter declined to preimmersion levels, whereas plasma renin activity, plasma aldosterone, and norepinephrine remained constantly suppressed. It is concluded that, compared with the initial increases, central blood volume (central venous pressure and stroke volume) is reduced during prolonged WI and renal fluid and electrolyte excretion is attenuated. UNaV is still increased at the 12th h of WI, whereas renal water excretion returns to control values within 7 h. The WI-induced changes in ANP, plasma renin activity, plasma aldosterone, and norepinephrine may all contribute to the initial increase in UNaV. The results suggest, however, that the attenuation of UNaV during the later stages of WI is due to the decrease in ANP release.
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