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The intestinal absorption of sodium taurocholate was studied in the near-term fetal and neonatal dog. Absorption rates were measured in vivo in isolated loops of fetal jejunum and ileum. Absorption was also measured in vitro in everted sacs and rings of fetal and neonatal jejunum and ileum. The maximal rates of taurocholate absorption observed after instillation of 1 micronmol taurocholate into closed segments of fetal jejunum and ileum with intact blood supply were not significantly different (P less than 0.2), and equalled 0.282+/-0.026 (mean+/-SEM) and 0.347+/-0.051 micronmol/h per 10-cm segment length jejunum and ileum, respectively. Similarly, the rates of absorption from open segments of jejunum and ileum perfused with 0.4 and 1.0 mM taurocholate were nearly identical (0.232+/-0.040 and 0.255+/-0.039, respectively at 0.4 mM, and 0.470+/-0.065 and 0.431+/-0.013, respectively at 1.0 mm) (P greater than 0.2). At perfusate concentrations of 4.0 mM, moreoever, jejunal absorption exceeded ileal absorption (1.490+/-0.140 and 0.922+/-0.200, respectively (P less than 0.05). As expected, concentration of taurocholate by the mucosa was readily demonstrated in adult ileal, but not in adult jejunal everted rings. In contrast, there were no significant differences in mucosal uptake of taurocholate by fetal jejunal and ileal rings. Fetal ileal mucosal concentrations were not significantly above those in the incubation medium after 1-h exposure of the mucosa to 0.003, 0.03, and 0.3 mM taurocholate. Uptake was proportional to incubation medium concentration over the full range of values. This was also true of tissues from 1-wk-old neonates. However, by 2 wk of age, ileal mucosal concentration of taurocholate was evident and adult levels were attained by 5 wk of age. It is concluded that taurocholate is absorbed by the fetal gut and that ileal absorption is no more efficient than jejunal absorption. Although active glucose transport was demonstrable in both jejunum and ileum, it was not possible to demonstrate an ileal mechanism for active transport of taurocholate in the fetus. Active ileal transport was not demonstrable in the newborn until at least 2 wk after birth.
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PMID:Fetal bile salt metabolism. The intestinal absorption of bile salt. 86 98

Nine newborn lambs between 24 and 48 hr of age were studied before and after infusion of furosemide (2 mg/kg) over 1-2 min. Plasma renin activity (PRA) increased within 8 min after furosemide from a baseline value of 12.6 +/- 3.5 ng/ml/hr (mean and SEM) to a level of 24.1 +/- 8.6 ng/ml/hr (P less than 0.05), and peaked 20 mins after the furosemide infusion at a level of 33.1 +/- 8.0 ng/ml/hr. Plasma aldosterone concentration increased from a baseline of 12.2 +/- 3.1 to 22.8 +/- 9.1 ng/dl 35 min after the furosemide infusion, P less than 0.05. There were no changes in plasma sodium or blood hemoatocrit and minimal changes in blood pressure and plasma protein concentrations during the first 35 min after the furosemide infusion. The results indicate that the renin-angiotensin-aldosterone system responds promptly to furosemide stimulation despite initially high PRA and aldosterone levels.
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PMID:The renin-angiotensin-aldosterone system in the newborn lamb: response to furosemide. 87 6

Fourteen pregnant women with oedema and inappropriate weight gain were treated with hydrochlorothiazide, 50 mg daily. Plasma renin activity (PRA) increased form 2.89 +/- 0.44 (mean +/- SEM) to 10.46 +/- 1.61 ng/ml/h after one week and remained high (10.07 +/- 1.36 ng/ml/h) after three weeks of drug therapy. Eight women were considered to be "responsers" because of a marked increase of PRA) (greater than 9.5 ng/ml/h) and six subjects ranked as "weak responders", with PRA increases of less than 6.0 ng/ml/h. These subgroups had different patterns of sodium excretion, weight loss and systolic blood pressure. The different reactivity of the renin-angiotensin system suggests that there may be at least two, basically different, types of pathophysiology in pregnancy associated edema.
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PMID:Plasma renin activity in pregnant women with oedema treated with hydrochlorothiazide. 88 59

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.
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PMID:Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure. 88 11

Previous studies of heavy metal salt-induced acute renal failure demonstrated abnormalities of fluid and solute transport by nephron segments and alterations in glomerular filtration rate and renal hemodynamics. To determine the direct effects of uranyl nitrate (UN) or HgCl2 on ion transport, their effects were studied on the isolated urinary bladder of the turtle. Unidirectional 24Na+ and 36Cl- fluxes were measured across short-circuited bladders. The addition of 0.1 mM UN to the mucosal solution resulted in a 69.9 +/- 4% (SEM) decrease in short-circuit current (SCC) without change in transepithelial resistance. Net Na+ flux (7.95 +/- 0.81 mueq/h per 8 cm2) decreased by the same magnitude as the SCC, primarily due to a 5.75 +/- 0.76 mueq/h per 8 cm2 decrease in the mucosal- (M) to-serosal (S) Na+ flux. Net Cl- flux decreased also primarily due to a decrease in M-to-S Cl- flux. Addition of 0.4 mM UN to S did not measurably affect the SCC or ion fluxes. The addition of 10 muM HgCl2 in another group of bladders reduced SCC and M-to-S Na+ flux by 81 +/- 7% without change in Cl- fluxes or resistance. The removal of either UN or HgCl2 from M by washing did not reverse the decreased SCC, but after washing addition of either dithiothreitol, 2 mM, or amphotericin B, 20 mug/ml, to M completely reversed the effects of UN or HgCl2 on SCC. These studies suggest that heavy metal salts inhibit Na+ transport by the turtle bladder without altering passive ion fluxes.
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PMID:Heavy metal-induced alterations in ion transport by turtle urinary bladder. 93 49

We used micropuncture techniques to examine the intrarenal response to an acute elevation of the renal perfusion pressure. In one series of studies (epinephrine, group I) the renal perfusion pressure was acutely increased by intravenous epinephrine infusion; in another series, by bilateral carotid occlusion and vagotomy. A third series of studies (epinephrine, group II) was performed identically to the epinephrine, group I, studies except that the renal perfusion pressure was held constant during the epinephrine infusion by suprarenal aortic constriction. After epinephrine infusion (group I) and following bilateral carotid occlusion and vagotomy the renal perfusion pressure increased, from 119 +/- 1.0 (SEM) to 166 +/- 1.85 mm Hg and from 122 +/- 5.9 to 168 +/- 3.1 mm Hg, respectively. Fractional sodium excretion rose from 2.31 +/- 0.34% to 5.09 +/- 0.58% (P less than 0.001) after epinephrine and from 1.80 +/- 0.71 to 6.40 +/- 1.0% (P less than 0.01) following carotid occlusion and vagotomy. In neither study, however, did we find that the increase in renal perfusion pressure changed the glomerular filtration rate (GFR) (both kidneys) or fractional sodium delivery from the superficial cortical late distal tubule. Furthermore, we found that epinephrine infusion at a constant renal perfusion pressure (epinephrine, group II) did not affect fractional sodium excretion, although a small, but significant, decrease in the GFR and sodium delivery from the superficial late distal tubule occurred. These data suggest that the natriuresis which follows an acute elevation of the renal perfusion pressure cannot be attributed to enhanced sodium delivery from superficial nephrons but must result from (1) inhibition of sodium reabsorption in inner cortical nephrons or (2) an effect on sodium transport in the collecting system.
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PMID:The effect of an acute increase in renal perfusion pressure on sodium transport in the rat kidney. 97 57

The hemodynamic response to vasodilator therapy with sodium nitroprusside has been assessed in 33 patients with severe coronary artery disease (CAD) during coronary artery operation. The patients were divided into three groups; Group 1 included seven patients with CAD and normal left ventricular filling pressure (LVFP less than 12 mm Hg); Group 2 included 18 patients with CAD and chronic left ventricular (LV) dysfunction (LVFP greater than 12 mm Hg) and Group 3 included eight patients with CAD and acute LV dysfunction (LVFP greater than 12 mm Hg) associated with an intraoperative hypertensive episode. Nitroprusside was administered intraoperatively at an initial infusion rate of 10-15 mcg/min and the rate was gradually increased thereafter until the criteria for effective therapy were satisfied. The effective dose ranged from 10-120 mcg/min with an average of 52 +/- 4 (SEM) mcg/min. In all three groups, pulmonary and systemic arterial pressure, right and left ventricular filling pressure, and pulmonary and systemic vascular resistance decreased significantly with nitroprusside infusion. Heart rate increased significantly in Group 1 and remained unchanged in Group 2 and 3. Heart rate X systolic arterial pressure decreased significantly in Group 1 and 3 and did not change in Group 2. Stroke index increased significantly in both groups of patients with elevated control LVFP (Group 2 and 3) and remained unchanged in patients with normal left ventricular function (Group 1). Left ventricular stroke work index decreased in Group 1, increased in Group 2, and remained unchanged in Group 3. Right ventricular stroke work index decreased significantly in all groups. These findings suggest that judicious intraoperative administration of sodium nitroprusside improves left ventricular function in patients with acute or chronic elevation of LVFP and LV dysfunction associated with severe CAD. Furthermore, nitroprusside is an effective drug for control of intraoperative hypertensive episodes in such patients.
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PMID:Hemodynamic effects of nitroprusside infusion during coronary artery operation in man. 99 24

The circadian rhythm of plasma renin activity during continuous recumbency was determined fifty-one times in thirty subjects who either slept at night or remained awake for 24 h. Both groups had maximum values between 2400 and 0800 h, despite absence of the expected early morning fall in blood pressure, pulse, and glomerular filtration rate in the awake subjects. Infusion of normal saline between 2300 and 0300 h initially suppressed renin, but did not prevent its subsequent rise regardless of the amount of sodium appearing in the urine. Of thirteen patients tested two to five times, twelve had recurrence of the zenith within a single 4 h period on retesting, despite differences in sodium intake, basal blood pressure, and mean plasma renin activity. Peaks of lesser magnitude were also frequently noted, most commonly at 1000 h and 1800-2000 h. Minimum PRA values were not restricted to a particular time of day and did not generally recur at the same time upon retesting. The mean ratio of maximum to minimum PRA in each study was 246% +/- 18.3% (+/- 1 SEM). The circadian rhythm of renin appears to be independent of known renal mechanisms responsible for regulating renin release. It is possible that this rhythm is controlled by the central nervous system.
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PMID:The circadian rhythm of renin. 100 16

Metoclopramide is known to enhance gastric emptying and stimulate duodenal and small-intestinal peristaltic activity. The effect of the drug on peroral jejunal biopsy was examined in a controlled, double-blind, randomized trial. Forty-nine patients (24 females and 25 males) who required jejunal biopsy for diagnostic purposes were admitted to the study. All the biopsies were performed by the same operator using the Quinton multipurpose suction biopsy tube and applying the same technique. Twenty-four patients ranging in age from 18 to 67 years (mean 44.5) received placebo intravenously (sodium metabisulfite), and 25 patients from 16 to 73 years old (mean 39.9) received 10 mg of metoclopramide intravenously prior to the jejunal intubation. Objective parameters of the study were (1) time in minutes required for the intubation at the biopsy site, ie, the area at the ligament of Treitz, and (2) fluoroscopy time. Intubation time in the placebo group was 22.3 +/- 1.9 min (mean +/- SEM) vs 11.3 +/- 1.4 min in the metoclopramide group (P less than 0.001). Fluoroscopy exposure time was 2.47 +/- 0.25 in the placebo group vs 1.40 +/- 0.12 min in the metoclopramide group (P less than 0.001). Subjective clinical evaluation of the operator's assessment of the procedure was based on a 0-4 scale (much easier = 0, easier = 1, average = 2, harder = 3, and much harder = 4). Metoclopramide administration resulted in a significantly easier performance of the procedure (P less than 0.001) but did not influence patient tolerance. Three patients who received metoclopramide and one receiving placebo developed mild to moderate drowsiness of short duration. The results of this controlled trial indicate that metoclopramide significantly shortens the time required for jejunal biopsy and reduces fluoroscopy exposure. Its regulatory action on gastrointestinal motility contributes to the easier performance of a valuable diagnostic procedure.
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PMID:The role of metoclopramide in peroral jejunal biopsy: a controlled randomized trial. 101 96

Experiments to investigate pressure-induced antagonism of the effects of general anaesthetics in isolated peripheral nerve from the frog are described. The doses of four gaseous general anaesthetic agents required to reduce electrically evoked action potentials by 50% (mean +/- SEM) were nitrous oxide 490 +/- 40.4 kPa, ethylene 665 +/- 212 kPa, dichlorodifluoromethane 108 +/- 17.2 kPa and cyclopropane 70 +/- 5 kPa. The combination of high pressure and the anaesthetic agent partially or completely restored the action potential amplitudes for the gaseous and some of the volatile agents (chloroform, diethyl ether, helothane). However, reversal of the effects of other volatile agents (ethanol, butanol), sodium pentobarbitone and two local anaesthetic agents (procaine, dibucaine) did not occur. The pressures used to effect a reversal were less than anticipated. This apparent inconsistency with the critical volume hypothesis for anaesthesia is discussed.
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PMID:Pressure antagonism of anaesthetic-induced conduction failure in frog peripheral nerve. 101 41


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