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Biomedical subjects

F C Luft

Publications and source records attributed to F C Luft.

At least 505 records · Page 28Linked to original sources
PubMed1983

The morphology of the renal microvasculature in glycerol- and gentamicin-induced acute renal failure.

To elucidate abnormalities in the renal microvasculature that could account for the functional disturbances occurring in two well-established models of acute renal failure, we gave rats a single intramuscular injection of glycerol (50%, 10 ml/kg) or daily subcutaneous doses of gentamicin (100 mg/kg/day). Afferent arteriolar diameters were determined by measuring methacrylate vascular casts with SEM. The filtration barrier was examined by both SEM and TEM. The EF area was quantitated. By 3 hr, the glycerol treatment markedly decreased PADs and DADs (PAD 19.1 to 12.0 micrometers, DAD 13.8 to 7.4 micrometers, p less than 0.05). The changes were similar for both inner and outer cortical regions. By 3 days the vasoconstriction was alleviated; however, renal failure persisted. At that time, however, EF area was decreased to 43% of normal. After 10 days of gentamicin treatment, only minimal vasoconstriction occurred in the outer cortex; however, EF area was decreased to a similar degree as observed with the 3-day glycerol-treated animals. There are two phases to glycerol-induced acute renal failure. The first phase (described as readily reversible) is characterized by intense vasoconstriction. The second phase, which is not immediately reversible, is associated with a decreased EF area. Smaller outer cortical afferent arterioles and a decreased fenestral diameter and density of the glomerular endothelium are seen only after gentamicin-induced renal failure is well established (after 10 days of treatment).

Acute Kidney Injury↗
PubMed1983

The effect of dietary sodium and protein on urine volume and water intake.

To test the notion that water intake and urine volume are related to dietary sodium or protein intake in free-living persons, we studied normal men at three levels of sodium intake and two levels of protein intake. Twenty-four men received 10, 200, and 400 mEq/day sodium intake for 7 days while protein and caloric intake were maintained constant. Eight men received 80 or 180 gm/day protein intake for 7 days while caloric and sodium intake were maintained constant. Although sodium, solute, and urea nitrogen excretion changed appropriately according to the regimens, there was no demonstrable influence of sodium or protein intake on water intake and urine volume. We conclude that in normal free-living American man, water consumption is independent of either sodium or protein intake.

Adult↗
PubMed1982

Sodium sensitivity and resistance in normotensive humans.

To identify characteristics that may contribute to sodium susceptibility, we conducted, studies in normal subjects who are at risk for hypertension, namely, blacks, subjects older than 40 years of age and first-degree relatives of patients with essential hypertension. All three groups exhibited a decreased natriuretic capacity when compared with control subjects. Blacks and older subjects had consistently low renin values, while the plasma renin activity values of the relatives were greater than those in control subjects. Studies in twins showed that natriuretic capacity and several factors influencing sodium excretion are heritable. When blacks were subjected to extremely high sodium intake, a greater increase in blood pressure developed than in whites. These observations are consistent with an intrinsic renal abnormality in blacks and older subjects resulting in modest volume expansion. In the normotensive relatives of hypertensive patients, the renin system may be responsible for the decreased sodium excretory capacity. These alterations are possibly inherited.

Adult↗
PubMed1982

The blood pressure-raising effects of high dietary sodium intake: racial differences and the role of potassium.

Fourteen normotensive men (7 black, 7 white) were studied following equilibration during dietary sodium intake of 10, 300, 600, 800, 1200, and 1500 mEq sodium per day. Significant (p less than 0.05) increases in mean arterial blood pressure were seen after sodium intake of 800 mEq/d. Blood pressure increased at lower levels of sodium intake (800 mEq/d) and to a greater magnitude (21 mm Hg) in blacks than in whites (1200 mEq/d; 13 mm Hg). Sodium loading was associated with marked suppression of plasma renin activity, aldosterone and norepinephrine, and increases in cardiac index. At higher levels of sodium intake urinary potassium loss was seen. A subsequent experiment replacing urinary potassium losses as they occurred in six subjects demonstrated attenuation of the blood pressure increases seen in response to dietary sodium loading. These studies demonstrate a potential role for sodium and potassium in blood pressure regulation in normotensive man, and suggest that heterogeneity of response may be involved in the development of hypertension in individuals predisposed to avid sodium conservation.

Adolescent↗
PubMed1982

Pharmacokinetics of moxalactam in patients with normal and impaired renal function.

Moxalactam is the first representative of a new class of potent beta-lactam antibiotics. To establish dosage recommendations, the kinetics of moxalactam elimination were studied in 20 patients with various degrees of renal dysfunction. After a 1-g intravenous bolus injection, the elimination half-life increased from 2.2 +/- 0.1 hr in normal subjects to 22.3 +/- 1.7 hr in anuric patients. Similar correlations were shown between the rate of creatinine clearance and the rate of plasma clearance, the rate of renal clearance, and the overall elimination rate constant of moxalactam. No changes in the distribution volumes or metabolic clearance rates of moxalactam were detected. A nomogram for adjustment of moxalactam dosage in patients with any level of renal function was generated, and specific recommendations for moxalactam dosage are discussed.

Adult↗
PubMed1982

Effects of moxalactam and cefotaxime on rabbit renal tissue.

To determine and compare the effects of moxalactam and cefotaxime on kidneys, we gave these drugs in doses of 750 and 1,500 mg/kg to rabbits for 7 days. Cephaloridine was included as a positive control. Neither moxalactam nor cefotaxime at either dose caused lysosomal enzymuria, changes visible by light microscopy or increased plasma creatine. Both drugs caused minor alterations in glomerular ultrastructure at the higher dose. Cephaloridine, on the other hand, caused widespread renal functional and morphological damage. We conclude that in rabbits, both moxalactam and cefotaxime are remarkably nonnephrotoxic.

Acetylglucosaminidase↗
PubMed1982

The role of the sympathetic nervous system in the modulation of sodium excretion.

To investigate the existence of opposing renal noradrenergic and dopaminergic modulation of renal sodium excretion, urinary excretion rates of NE, DA and DOPAC were measured in different states of sodium balance. A natriuretic index, DOPAC/NE, was found to correlate closely with the state of sodium balance in normal men subjected to very low (10 mEq/d) or very high (800 mEq/d) sodium intake. Additional studies utilizing rapid sodium and volume expansion and contraction confirmed the utility of this natriuretic index. Hypertensive men demonstrated significantly lower values for this index than did normotensive subjects under similar study conditions. These studies provide new evidence of abnormalities in the adrenergic-dopaminergic system in human hypertension and support a link between these systems and renal sodium handling.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

The renin-angiotensin system in aminoglycoside-induced acute renal failure.

To examine the role of the renin-angiotensin system in aminoglycoside-induced acute renal failure, we gave rats gentamicin (80 mg/kg/day), gentamicin + captopril (an angiotensin-converting enzyme inhibitor), captopril alone or saline sham injections, for 10 days. Blood pressure, sodium excretion, urine osmolality and creatinine clearance were measured four times during treatment. Plasma renin activity, angiotensin I-converting enzyme and renal histology were determined at sacrifice. Although angiotensin I-converting enzyme activity was markedly suppressed by captopril treatment, the addition of captopril failed to consistently influence blood pressure or urine osmolality. In addition, it did not promote natriuresis in the face of gentamicin toxicity. Creatinine clearance decreased progressively in groups receiving gentamicin and was lowest (P less than .05) in the groups receiving gentamicin + captopril. Captopril did not prevent the development of tubular epithelial nor glomerular endothelial changes associated with gentamicin toxicity. In a separate experiment rats received captopril for 3 days prior, before receiving the gentamicin + captopril regimen for 10 days. Captopril pretreatment did not influence the results. This study does not support a pivotal role for the renin-angiotensin system in the production of the decreased glomerular filtration rate observed in nephrotoxic acute renal failure induced by gentamicin in rats.

Acute Kidney Injury↗
PubMed1981

The effect of sodium on aldosterone metabolic clearance.

The effect of sodium intake on the aldosterone metabolic clearance rate (MCR) was examined in 5 normal subjects. Measurements were made under conditions where dietary sodium ranged from 10 to 1500 meq/day. There were no consistent changes in MCR over these extremes of sodium intake, and the plasma level of aldosterone correlated only with the aldosterone urinary excretion rate. In an additional group of 6 normal subjects, a single dose of 100 meq sodium administered orally had no effect on the aldosterone MCR. The findings indicate that aldosterone metabolism is unaffected by sodium intake.

Adult↗
PubMed1981

Sodium intake alters the effects of norepinephrine on the renin system and the kidney.

To examine the interactions between sodium intake and the sympathetic nervous system and their influences on the blood pressure control system we studied eight normotensive men after high (800 mEq/d) and low (10 mEq/d) sodium intake. We measured blood pressure, arterial, venous and urinary norepinephrine (NE), glomerular filtration rate (GFR), renal blood flow (RBF), plasma renin activity (PRA) and aldosterone (PA), and the fractional excretion of sodium (FENa) and potassium (FEK) before and during incremental infusion of norepinephrine. High salt intake influenced the sensitivity to NE as well as subsequent pressor responses. The NE-induced decrease in RBF and GFR was not different on high and low sodium intakes. A significant decrease in FENa (p less than 0.05) with NE infusion could only be seen during high sodium intake. A significant increase in PRA (p less than 0.01) and PA (p less than 0.05) was induced by NE only during the low sodium period. These observations reveal previously unrecognized qualitative and quantitative interactions between sodium homeostasis and norepinephrine which are capable of influencing blood pressure in man.

Adult↗