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Biomedical subjects

S B Bates

Publications and source records attributed to S B Bates.

10 recordsLinked to original sources
PubMed1987

Effects of dietary protein on uranyl-nitrate-induced acute renal failure.

The effects of dietary protein both before and after uranyl-nitrate-induced acute renal failure were investigated. Male Sprague-Dawley rats were maintained on high-protein (60%), normal-protein (20%), low-protein (5%) and no-protein diets for 8 days prior to intravenous administration of uranyl nitrate (10 mg/kg). Immediately following uranyl nitrate injection, some rats on normal-protein diets were switched to no-protein, low-protein or high-protein diets, while some of the rats on high-protein diets were switched to low-protein diets. Serum and urine creatinine levels and urine volumes were monitored for 2 weeks following uranyl nitrate treatment. Rats conditioned to no-protein and low-protein diets exhibited significantly lower mortalities than rats maintained on normal-protein diets. Rats maintained on high protein diets exhibited better renal function than rats maintained on lower dietary protein regimes, but these rats had mortality rates similar to rats maintained on normal-protein diets. Shifting the rats on normal-protein diets to low- or no-protein diets immediately after uranyl nitrate administration did not improve their renal function or survival rates. However, shifting the rats on normal-protein diets to high-protein diets immediately following uranyl nitrate injection resulted in significantly higher mortalities (93%) than in rats maintained on either normal or high dietary protein throughout the experimental period. Finally, shifting rats on high dietary protein to low-protein diets immediately following uranyl nitrate administration resulted in both improved renal function and survival compared with rats shifted from normal to restricted dietary protein (5%) immediately following uranyl nitrate injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1986

Dietary protein prior to renal ischemia dramatically affects postischemic kidney function.

Male Sprague-Dawley rats were maintained on high protein (60%), normal protein (20%), low protein (5%), or no protein (0%) diets for two or four weeks prior to 45 minutes of renal ischemia induced by renal pedicle clamping. Most (93%) of the rats on the high protein diet died within three days following renal ischemia. In addition, 69% of the rats on normal protein diets also died, most before the fourth day following ischemic insult. In contrast, 88% of the rats on the low protein diet lived, although some exhibited elevated serum creatinine levels for up to one to two weeks following ischemia. Finally, all of the rats on no protein diets lived, and most (75%) exhibited normal serum creatinine levels by the fourth day following ischemia. Shifting the diets of high protein and normal protein adapted rats to no protein diets immediately following ischemia did not improve postischemic survival. Also, changing the diets of no protein adapted rats to high protein diets immediately following ischemia did not significantly affect postischemic recovery. When rats were maintained on no protein diets for shorter periods of time prior to ischemia, it was found that approximately a week on this diet is necessary to provide maximum protection from postischemic acute renal failure. These findings demonstrate a dramatic effect of dietary protein prior to ischemic induced acute renal failure, and suggests that preoperative dietary protein intake should be an important consideration in those situations which are predisposed to postoperative acute renal failure.

Acute Kidney Injury↗
PubMed1985

Dose-dependent movement of cationic molecules across the glomerular wall.

Different concentrations of the polycation polyethyleneimine (PEI) were administered by single intravenous injections or by constant vascular perfusion to the kidneys of Sprague-Dawley rats. At a fixed time interval after administration of PEI, the kidneys were fixed and the distribution of PEI in the glomerular wall was evaluated by electron microscopy. At the lower concentrations (e.g., 0.005%), PEI bound only to the glomerular endothelial glycocalyx and preferentially to microvillous projections on this endothelium. At higher concentrations (e.g., 0.05%), PEI also bound to discrete anionic sites in the lamina rara interna (LRI) but was rarely seen in the lamina rara externa (LRE). As the concentration of PEI was further increased (e.g., 0.5%), PEI moved deeper into the glomerular basement membrane (GBM) and bound extensively to discrete anionic sites in the lamina rara externa. Although anionic sites in the LRI and LRE appeared nearly saturated following infusion of 0.5% PEI, this cationic molecule was rarely seen to cross filtration slits and pass into the urinary space. At still higher concentrations (e.g., 2%), however, PEI moved freely across the filtration slits, bound extensively to the glomerular epithelial glycocalyx, and induced a narrowing of the filtration slits. When PEI was mechanically perfused through the kidney vasculature for 3 minutes, PEI binding to the epithelial glycocalyx caused very extensive adherence of adjacent podocyte processes and the narrowing and loss of filtration slits. Also in these latter samples, discrete anionic sites in the LRE were no longer apparent and a dense band of PEI was seen under the foot processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Evaluation of a flushing solution designed to protect kidneys from in situ ischemia.

An in situ flushing solution was evaluated with regard to the following: (1) its ability to protect the kidney during 60, 90, and 120 minutes of normothermic ischemia; (2) the effects of using an intracellular versus extracellular electrolyte composition in the flushing solution; and (3) the ability of the flushing solution to complement in situ hypothermia as a protective measure during long-term ischemia. Rat kidneys were briefly flushed in situ with an isotonic phosphate buffered solution (pH 7.2) containing 50 milliosmole of sucrose. The left renal pedicle was then immediately clamped to render the kidney ischemic and to hold the flushing solution in the kidney. Following removal of the pedicle clamp, a contralateral nephrectomy of the right kidney was performed and daily serum creatinine levels determined to evaluate postischemic renal function. The results indicate the following: (1) the flushing procedure is very effective in preventing postischemic acute renal failure following 60 minutes of normothermic ischemia, but is considerably less effective for ischemic times of 90 minutes or more; (2) an intracellular electrolyte composition in the flushing solution does not improve the protective effects of this solution; and (3) the flushing procedure can significantly improve on the protection otherwise provided by in situ hypothermia.

Acute Kidney Injury↗
PubMed1985

Improving Euro-Collins flushing solution's ability to protect kidneys from normothermic ischemia.

In this investigation, we describe a modification of Euro-Collins flushing solution which enables this solution to be effective in preventing normothermic postischemic acute renal failure. The left kidneys of Sprague-Dawley rats were briefly flushed in situ by vascular perfusion with Euro-Collins solution and the renal pedicle clamped to render the kidney ischemic and hold the flushing solution in the kidney. Following 1 h of in situ normothermic ischemia, the pedicle clamp was removed and a contralateral nephrectomy of the right kidney performed. In two other groups of rats the same experimental protocol was followed using Euro-Collins solution in which the dextrose in this solution was replaced with a similar osmolal contribution of either sucrose (64 g/l) or mannitol (35 g/l). Rats with kidneys flushed with the standard Euro-Collins solution containing dextrose (n = 24) exhibited significantly higher postischemic daily serum creatinine levels, a greater degree of tubular necrosis, and a higher mortality (75, versus 31%) than unflushed ischemic controls (n = 22). Rats with kidneys flushed with Euro-Collins, containing either sucrose (n = 25) or mannitol (n = 22) in place of dextrose, all survived, exhibited only focal tubular damage as observed by electron microscopy, and most returned to normal serum creatinine levels within 72 h following ischemia. These findings, together with other reports that mannitol- and sucrose-based flushing solutions provide excellent protection during prolonged cold ischemia, strongly argue for the substitution of sucrose, mannitol or other similar protective impermeant agents for dextrose in flushing solutions such as Euro-Collins.

Acute Kidney Injury↗
PubMed1984

Filamentous actin bundles in the kidney.

The distribution of filamentous actin bundles in the rat kidney was studied using a fluorescent phallotoxin label and transmission electron microscopy. The microvillous brush border lining proximal tubules, smooth muscle in renal vessels, and renal corpuscles were the structures most intensely labeled with rhodamine phalloidin. Closer evaluation of renal corpuscles revealed intense labeling of filamentous actin within podocyte foot processes enveloping the glomerular capillary loops. Rhodamine phalloidin also labeled basal bands of filamentous actin in the parietal epithelium and basal bands of actin in proximal and distal tubules. Finally, a band of filamentous actin was evident along the innermost aspect of the kidney capsule, within cells which often joined to form sinus-like compartments.

Actins↗
PubMed1982

Computer-assisted measurement of the thickness of biological structures.

A digitizer-microcomputer method has been developed for the determination of the average thickness or width of biological structures of a relatively long, thin nature. Test models were used to confirm the accuracy and reproducibility of the method. Although the method does not eliminate all subjectivity (e.g., estimation of pericyte areas in capillaries) or human error (i.e., stability of the tracing) it does not involve the tedium and subjectivity of repeated individual measurements and estimations of ruler-type measurements. It furthermore allows for more rapid measurements than other methods currently in use. The method provides a precise, quick, reproducible, relatively non-subjective method for routine analyses. The system used is relatively inexpensive and readily available.

Basement Membrane↗
PubMedDate not supplied

Dietary protein as a risk factor in gentamicin nephrotoxicity.

The effects of dietary protein on renal function and structure, both prior to and after initiation of daily gentamicin treatment, were investigated. Male Sprague-Dawley rats were pair-fed on low-protein (LP, 5%), normal-protein (NP, 20%), or high-protein (HP, 60%) diets for 10 days prior to gentamicin treatment. Gentamicin was administered as daily subcutaneous injections (150 mg/kg) for 6 days. Immediately after beginning daily gentamicin injections some of the rats on NP diets were switched to LP or HP diets, and some of the rats on HP diets were switched to LP diets. Renal function was monitored by evaluating serum creatinine levels and 24-h urine volumes; renal histology was evaluated by light and electron microscopy; and gentamicin uptake was determined using radioimmunoassay. Our findings indicate that conditioning to higher dietary protein prior to gentamicin administration results in less uptake of gentamicin by the kidneys. If rats on HP diets are placed on LP coincident with gentamicin administration, there is a significant improvement in survival. Switching rats from NP to LP protein coincident with gentamicin administration does not improve renal function, histology, or survival. However, switching rats from NP to HP coincident with gentamicin administration significantly increases mortality. Maintaining rats on LP both prior to and after gentamicin administration results in a significant improvement in survival but does not improve renal function. These results indicate that dietary protein both prior to and following the administration of gentamicin can significantly affect the nephrotoxicity of gentamicin.

Acute Kidney Injury↗