Health information needs of the pregnant adolescent.
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Biomedical subjects
Publications and source records attributed to S Belknap.
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Ascites labeled albumin and water kinetics were studied at steady state by intercompartmental clearances in cirrhotic patients whose ascites volumes ranged from 6.4 to 25.2 L. In 20 patients mean (+/- SD) ascitic fluid albumin clearance (equivalent to lymphatic absorption) was 3.5 +/- 1.9 L/day. In seven of them, lymphatic absorption was 3.4 +/- 0.8 L/day, total water absorption from ascitic fluid (outflow equals inflow at steady state) was 125.8 +/- 21.5 L/day. Vascular capillary water absorption (total minus lymphatic) was 122.4 +/- 21.4 L per 24 hours. Lymphatic absorption was less than 4% of total but accounted for all albumin absorbed (13.2 +/- 6.2 gm/day). Maximum lymphatic absorption was less than 10 L per 24 hours; peritoneovenous shunting augmented this function. Mean inflow water albumin concentration was 0.11 +/- 0.06 gm/L. If plasma albumin were diluted to concentration in ascites, calculated water inflow required would be 2.82 L/day. Actual inflow was 47 times that required. The major volume outflow path was through peritoneal venous capillaries; water and small-radius solute absorption through this route increased inflow water albumin concentration to ascites level. Concurrently, whole ascitic fluid was absorbed without sieving through lymphatics. Observed ascites albumin concentration in subjects with advanced cirrhosis was produced by water absorption from a large volume of dilute solution rather than dilution of a small inflow volume, in which albumin concentration originally was hyperoncotic to ascitic fluid. Large-volume transperitoneal water diversion from sources in high-pressure, extrahepatic splanchnic capillaries to absorption through parietal nonportal, low-pressure, peritoneal venous capillaries would significantly reduce portal plasma flow into liver and have deleterious systemic hemodynamic consequences.
The kallikrein-kininogen-kinin system (KKK) has been implicated in the renal sodium excretion response to changes in dietary sodium. However, both increases and decreases in the activity of this system have been observed when urinary sodium excretion is augmented by a variety of maneuvers. To further evaluate the potential physiologic role of this system, we measured three components of the KKK system in urine. Total kallikrein, intact kininogen, and kinin were measured twice in normal individuals during balance on both a high (250 mEq/day) or low (10 mEq/day) sodium intake. A consistent and significant reduction in the activity of all three components of the KKK system was noted during the high salt intake. Furthermore, during the high sodium intake, further acute reductions in components of this system were observed when an acute saline but not water load was administered. The consistent response of the various components of the KKK system to both acute and chronic sodium loading suggests that the system is physiologically linked to the regulation of sodium balance. However, the directional changes argue against a primary natriuretic effect of this system.
Previous estimates of PRL pharmacokinetics have been made using radioiodinated human PRL (hPRL) infusions or by measuring serum PRL disappearance following prolactinoma resection. The recent purification of hPRL in significant quantities made it possible to measure the clearance and volume of distribution directly. Studies were also carried out to determine absorption and clearance after im injection. In five normal men whose endogenous PRL secretion was suppressed by dopamine, a loading dose of hPRL (70-90 micrograms) followed by a constant infusion (1.39-2.9 ng/min) produced steady state serum PRL levels of 15.2-25.4 ng/mL by 30-60 min. The calculated mean volume of distribution was 7.3 +/- 2.9 (+/- SD) L. The calculated MCR was 71 +/- 19 mL/min X m2, and the calculated production rate was 802 +/- 377 micrograms/24 h X m2. The plasma disappearance half-life following discontinuation of the infusion was 37 +/- 10 min. The PRL infusate consisted primarily (75.6%) of a 22.5 K dalton species, probably PRL monomer, a component eluting at 45K daltons (16.1% of the total radioimmunoreactivity), probably dimer, and a small amount of a larger mol wt species. Serum obtained during dopamine infusion but before hPRL infusion contained 68.1% of the 22.5K, 7.2% of the 45K, and 24.7% of the larger mol wt moieties. During hPRL infusion in two men there was a relative decrease in the proportion of PRL monomer to 55% and 69% and a relative increase in the PRL dimer to 33% and 18%, respectively. hPRL was injected im in doses of 1, 2, 4, and 8 micrograms/kg without prior dopamine infusion. No significant changes in serum PRL levels occurred after the 1 and 2 micrograms/kg doses (n = 5). After the 4 micrograms/kg dose (n = 8), mean serum PRL levels rose from 10.0 +/- 1.8 (+/- SEM) ng/mL to peak levels of 13.1 +/- 1.8 ng/mL (P less than 0.01). After the 8 micrograms/kg dose (n = 7), PRL levels rose from 9.3 +/- 1.6 to 16.5 +/- 1.8 ng/mL (P less than 0.01). The PRL rise began between 60 and 80 min after injection; peak levels occurred at 160-180 min. In two men given 8 micrograms/kg who were sampled for an additional 3 h, PRL levels peaked at 200-220 min and began to fall by 220-240 min, but had not returned to baseline by 6 h. There were no side-effects of PRL administration, although the 8 micrograms/kg dose caused transient local discomfort.(ABSTRACT TRUNCATED AT 400 WORDS)
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The excretion kinetics of cocaine (C) and its two major metabolites, benzoylecgonine (BZ) and ecgonine methyl ester (EME), were determined by collecting all urine for 30 h from 5 cocaine users (subjects C, D, E, F, and G) given bolus doses followed by exponential cocaine infusions that delivered doses of 253 (subject C), 444 (subjects D, E, and F), and 700 mg (subject G). Plasma cocaine, urine cocaine, BZ, and EME were measured by gas chromatography, with a nitrogen detector. Elimination half-times for EME and BZ, estimated from semilog plots of excretion rates vs. time, averaged 3.1 and 4.5 h respectively, in agreement with our previous report. Urinary recovery in D, E, and F was 27-41% of the dose, with 14-17% as BZ, 12-21% as EME, and 2% as cocaine. Subject C excreted very little EME--5-6-fold less than the mean for the other subjects and amounting to only 3% of the dose. Cocaine disposition in subject G, who received the largest dose and attained plasma levels of 3000 ng/mL, showed some characteristics of a nonlinear process.