SIMULTANEOUS DETERMINATION OF PLASMA VOLUME AND TRANSCAPILLARY ESCAPE RATE WITH 131 I-LABELLED ALBUMIN AND T-1824 IN THE NEWBORN

1973 ◽  
Vol 62 (3) ◽  
pp. 248-252 ◽  
Author(s):  
H.-H. PARVING ◽  
J. G. KLEBE ◽  
C. J. INGOMAR
1989 ◽  
Vol 77 (2) ◽  
pp. 149-155 ◽  
Author(s):  
J. Hilsted ◽  
N. J. Christensen ◽  
S. Larsen

1. The effect of intravenous catecholamine infusions and of intravenous insulin on plasma volume and intravascular mass of albumin was investigated in healthy males. 2. Physiological doses of adrenaline (0.5 μg/min and 3 μg/min) increased peripheral venous packed cell volume significantly; intravenous noradrenaline at 0.5 μg/min had no effect on packed cell volume, whereas packed cell volume increased significantly at 3 μg of noradrenaline/min. No significant change in packed cell volume was found during saline infusion. 3. During adrenaline infusion at 6 μg/min, packed cell volume increased, plasma volume decreased and intravascular mass of albumin decreased significantly. During noradrenaline infusion at 6 μg/min, packed cell volume increased and plasma volume decreased, but intravascular mass of albumin did not change. 4. Application of a hyperinsulinaemic, euglycaemic glucose clamp led to an increase in transcapillary escape rate of albumin and a decrease in intravascular mass of albumin. Packed cell volume remained constant, while plasma volume, measured by radiolabeled albumin, decreased. 5. We conclude that the previously reported changes in packed cell volume, plasma volume, intravascular mass of albumin and transcapillary escape rate of albumin during hypoglycaemia may be explained by the combined actions of adrenaline and insulin.


1982 ◽  
Vol 63 (s8) ◽  
pp. 415s-418s ◽  
Author(s):  
J. A. O'hare ◽  
J. B. Ferriss ◽  
B. M. Twomey ◽  
H. Gonggrijp ◽  
D. J. O'sullivan

1. We studied 12 normotensive non-ketotic diabetic patients during poor metabolic control, with sustained hyperglycaemia, and again, after an interval of 3 weeks, when metabolic control was improved. On each occasion we measured blood pressure, total exchangeable sodium, plasma volume, transcapillary escape rate of albumin, and plasma concentrations of angiotensin II and aldosterone. 2. With improved diabetic control there was a small but significant fall in arterial pressure. Total exchangeable sodium was normal when control was poor but rose significantly to above normal with improved control. 3. Plasma volume also rose significantly with improved control, and the transcapillary escape rate of albumin fell and the intravascular mass of albumin rose. 4. Plasma angiotensin II and aldosterone concentrations were significantly above normal during poor metabolic control, but fell to normal with improved control. 5. These findings indicate a resetting of the relationship between blood pressure and exchangeable sodium when diabetic control improves. The association between exchangeable sodium and concentrations of angiotensin II and aldosterone also appears altered in diabetic patients. These changes associated with varying metabolic control must be considered when studying cardiovascular disease in diabetic patients.


2005 ◽  
Vol 98 (6) ◽  
pp. 1991-1997 ◽  
Author(s):  
Nina S. Stachenfeld ◽  
Hugh S. Taylor

Adequate plasma volume (PV) and extracellular fluid (ECF) volume are essential for blood pressure and fluid regulation. We tested the hypotheses that combined progesterone (P4)-estrogen (E2) administration would increase ECF volume with proportional increases in PV, but that P4would have little independent effect on either PV or ECF volume. We further hypothesized that this P4-E2-induced fluid expansion would be a function of renin-angiotensin-aldosterone system stimulation. We suppressed P4and E2with a gonadotropin-releasing hormone (GnRH) antagonist in eight women (25 ± 2 yr) for 16 days; P4(200 mg/day) was added for days 5–16 (P4) and 17β-estradiol (2 × 0.1 mg/day patches) for days 13–16 (P4-E2). On days 2 (GnRH antagonist), 9 (P4), and 16 (P4-E2), we estimated ECF and PV. To determine the rate of protein and thus water movement across the ECF, we also measured transcapillary escape rate of albumin. In P4, [Formula: see text] increased from 2.5 ± 1.3 to 12.0 ± 2.8 ng/ml ( P < 0.05) with no change in [Formula: see text] (21.5 ± 9.4 to 8.6 ± 2.0 pg/ml). In P4-E2, plasma concentration of P4remained elevated (11.3 ± 2.7 ng/ml) and plasma concentration of E2increased to 254.1 ± 52.7 pg/ml ( P < 0.05). PV increased during P4(46.6 ± 2.5 ml/kg) and P4-E2(48.4 ± 3.9 ml/kg) compared with GnRH antagonist (43.3 ± 3.2 ml/kg; P < 0.05), as did ECF (206 ± 19, 244 ± 25, and 239 ± 27 ml/kg for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05). Transcapillary escape rate of albumin was lowest during P4-E2(5.8 ± 1.3, 3.5 ± 1.7, and 2.2 ± 0.4%/h for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05). Serum aldosterone increased during P4and P4-E2compared with GnRH antagonist (79 ± 17, 127 ± 13, and 171 ± 25 pg/ml for GnRH antagonist, P4, and P4-E2, respectively; P < 0.05), but plasma renin activity and plasma concentration of ANG II were only increased by P4-E2. This study is the first to isolate P4effects on ECF; however, the mechanisms for the ECF and PV expansion have not been clearly defined.


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