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Biomedical subjects

C W Gottschalk

Publications and source records attributed to C W Gottschalk.

At least 37 records · Page 2Linked to original sources
PubMed1978

Structural changes of experimental glomerulonephritis in rats as revealed by microdissection.

Microdissection revealed striking alterations in the nephrons of animal models AICN and anti-GBMN. The most severely damaged AICN kidney in the series presented marked heterogeneity in the size and deformity of the proximal tubules, corresponding to the diverse and variegated nephrons described by Oliver in chronic Bright's disease. The severely damaged anti-GBMN kidneys revealed widespread alterations in the proximal tubules, which, however, tended to be fairly uniform among the affected nephrons. This uniformity, perhaps, reflected the shorter duration of disease in the anti-GBMN animals. The most characteristic proximal tubular alteration in either the AICN or anti-GBMN animals was that combining atrophy of the pars convoluta and hypertrophy of the pars recta in same tubule. The largest and smallest nephrons encountered in the entire study were found in the most severly damaged kidney in the AICN. This finding reflected the simultaneous existence of regressive and progressive changes in this kidney, as certain nephrons underwent hypertrophy to compensate for the atrophy and disappearance of others. The remarkable functional glomerulotubular balance of single nephrons known to exist in both AICN and anti-GBMN was matched by the evidence presented here of structural glomerulotubular balance among the severely altered nephrons of a representative kidney from each group. Microdissection studies directed toward the characterization of the nephronic alterations in both membranous glomerulonephritis and proliferative glomerulonephritis of man should be of interest in relation to the findings in these experimental rat models of human disease.

Animals↗
PubMed1976

Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption.

The renal responses to sympathetic nerve stimulation were studied in saline-expanded rats. The left kidney was partially denervated by crushing the left greater splanchnic nerve. Then the distal portion of the nerve was stimulated with square wave pulses of 0.5 ms duration, voltage twice threshold, and 1 or 2 Hz frequency while monitoring the compound action potential. Fibers with conduction speeds of 13-17 m-s-1 and of 0.7-1 m-s-1 were identified. Only stimulation of the latter appeared to produce changes in renal Na and water excretion. Whole kidney and individual nephron studies were performed alternating control and nerve stimulation periods. Nerve stimulation produced approximately a 25% reduction of the left kidney urine volume and sodium excretion. Glomerular filtration rate and renal plasma flow remained unchanged. Right kidney Na and water excretion, glomerular filtration rate, and renal plasma flow remained constant. In the left kidney, during nerve stimulation, the tubular fluid to plasma inulin concentration ratio increased significantly in the late proximal tubule. We conclude that the antidiuresis and antinatriuresis seen during sympathetic nerve stimulation were caused by increased sodium and water reabsorption in the proximal tubule, probably mediated by the stimulation of slowly conducting unmyelinated fibers. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes.

Absorption↗
PubMed1975

Autoregulation of blood flow in the rat kidney.

We present evidence showing that renal blood flow (RBF) in the anesthetized nondiuretic rat can be measured reliably and accurately using a noncannulating flow transducer and an electromagnetic flowmeter. In vitro calibration yielded a linear relationship (r=0.998) between flowmeter output voltage and blood flow rates from 0.2 to 10.3 ml/min. Excellent agreement was observed between simultaneous determinations of RBF by the flowmeter and the PAH clearance technique. Glomerular filtration rate and RBF for a kidney with a flow transducer around its renal artery did not differ significantly from corresponding values for the undisturbed contralateral kidney. The relationship of mean RBF with steady-state variations in perfusion pressure was evaluated in 13 nondiuretic rats. RBF averaged 6 ml/min.g kidney wt at arterial pressures (AP) above 100 mmHg. A high degree of autoregulatory efficiency was observed when mean AP varied between 105 and 145 mmHg. Over this pressure range RBF changed only 3% as changes in intrarenal vascular resistance and AP were directly related (r=0.994). Below 95-105 mmHg RBF decreased in a curvilinear fashion with the concavity toward the pressure axis.

Aminohippuric Acids↗
PubMed1975

Uric acid excretion by the rat kidney.

The renal excretion of uric acid was studied in nondiuretic (ND) male Wistar rats and in the same animals subsequently made diuretic (D) by the infusion of hypertonic saline. Clearances of endogenous urate and of inulin, determined chemically, were compared with the simultaneous clearance of 14C infused as [6(-14)C]urate or [2(-14)C]urate. In rats infused with [6(-14)C]urate the isotope/inulin clearance ratios were 0.29 +/- 0.09 (ND) and 0.31 +/- 0.11 (D) ml/min; the simultaneous urate (chemical)/inulin ratios were 0.21 +/- 0.07 (ND) and 0.24 +/- 0.08 (D) ml/min. In rats infused with [2(-14)C]urate the isotope/inulin clearance ratios were 1.02 +/- 0.5 (ND) and 1.13 +/- 0.9 ml/min (D); the simultaneous urate (chemical)/inulin clearance ratios were much lower-0.19 +/- 0.09 (ND) and 0.32 +/- 0.19 (D) ml/min. Thin-layer chromatography of urine after [6(-14)C]urate inl uric acid. In contrast, a similar analysis of urinary radioactivity after [2(-14)C]urate infusion revealed that more than 70% of the 14C was excreted as allantoin and not as uric acid.

Allantoin↗
PubMed1975

Pathogenesis of acute renal failure following temporary renal ischemia in the rat.

In this study, we characterized the sequence of several intrarenal events and evaluated their relative importance in the pathogenesis of unilateral oliguric acute renal failure induced experimentally in rats by complete occlusion of a renal artery for 1 hour. Kidneys were studied prior to occlusion and 1-3 hours and 22-26 hours after release of the temporary occlusion. Renal blood flow measured by an electromagnetic flow transducer was reduced to 40-50% of control during both postocclusion periods. Flow of tubular fluid was markedly reduced, and the damaged kidneys were oliguric. Proximal and distal convolutions were filled with fluid and dilated 1-3 hours after occlusion; their pressures were greatly heterogeneous and were elevated, on the average, to 31 and 16 mm Hg, respectively. Glomerular capillary pressure at this time was normal or slightly increased. Histological sections showed extensive tubular obstruction. We conclude that initially the oliguria is primarily due to intraluminal obstruction in the absence of predominant increases in preglomerular vascular resistance. Observations at 22-26 hours after occlusion indicated acute tubular necrosis. Moreover, the combined involvement of preglomerular vasoconstriction, presisting tubular obstruction, and passive backflow of tubular fluid appeared to be important in the maintenance of the oliguria. Glomerular capillary, proximal intratubular, and peritubular capillary hydrostatic pressures were reduced below control values. After acute volume expansion, the reduced pressures and renal blood flow were reversed, yet the experimental kidneys remained oliguric. Thus, it is clear that tubular obstruction is a significant factor responsible for both the genesis and the maintenance of oliguria in this experimental model of ischemia-induced acute renal failure.

Acute Kidney Injury↗
PubMed1975

Effects of acute unilateral renal denervation in the rat.

Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and the mechanisms involved in these responses. Denervation was produced in anesthetized nondiuretic rats by application of phenol to the left renal artery. Studies were also performed in sham-denervated nondiuretic rats. Whole kidney and individual nephron studies were performed before and after denervation or sham denervation. Denervation increased urine volume from the left kidney to about twice its control value (P less than 0.001) and increased urinary sodium excretion from 332 neq min minus -1 to 1,887 neq min minus -1 (P less than 0.001). Glomerular filtration rate (GFR) and renal plasma flow (RPF) remained unchanged in both kidneys after the procedure. The innervated right kidney showed no changes in urine volume or in sodium excretion. After denervation, late proximal ratio of tubular fluid inulin concentration to that of plasma [(F/P)In] decreased from 2.23 to 1.50 (P less than 0.001) while single nephron GFR remained unchanged. Absolute reabsorption decreased from 16.5 to 9.9 n. min minus -1 (P less than 0.001). (F/P)In ratios were also decreased in early distal (from 6.21 to 3.18, P less 0.001) and late distal convolutions (from 16.41 to 8.33, P less than 0.001) during the experimental period. (F/P)Na ratios remained unchanged in the early distal convolutions, but increased from 0.18 to 0.38 (P less than 0.01) in late distal convolutions after denervation. Absolute Na reabsorption after denervation increased in the loop of Henle, distal convolution, and collecting ducts. Any changes in intrarenal hydrostatic pressures after denervation were always small. There were no changes in GFR, RPF, urine volume, urinary sodium excretion, or late proximal (F/P)In after sham denervation. We conclude that the diuresis and natriuresis seen after acute renal denervation were caused by a marked depression of sodium and water reabsorption in the proximal tubule with partial compensation in more distal nephron segments. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes. The results demonstrate an effect of the renal nerves on proximal tubular function.

Aminohippuric Acids↗
PubMed1975

Hyperoncotic albumin infusion in experimental glomerulonephritis in rats: A micropuncture study.

The effect of infusion of hyperonciotic (25 g% salt-poor bovine plasma albumin) (0.06 g% of body weight) has been studied using clearance and micropuncture techniques in animals with two forms of immunologically induced experimental glomerulonephritis and in age-matched control rats. In control rats the significant natriuresis and diuresis after hyperoncotic albumin were associated with decreased fractional and absolute proximal reabsorption, decreased calculated efferent oncotic pressure, and a transitory rise in efferent arteriolar hydrostatic pressure. These findings, however, do not necessarily indicate a predominant role for peritubular "physical factors" in the control of proximal reabsorption. In glomerulonephritic rats a smaller diuresis and an insignificant natriuresis were found after hyperoncotic albumin, especially in anti-GBM nephritis, when no change in SNGFR or proximal absolute reabsorption occurred. In AICN there was a rise in SNGFR and a fall in absolute reabsorptive rate, especially in those nephrons with high filtration rates. There was no evidence that any alteration in efferent arteriolar hydrostatic pressure of calculated efferent oncotic pressure had occurred.

Animals↗
PubMed1974

Pathophysiology of experimental glomerulonephritis in rats.

Micropuncture, clearance, immunofluorescence and light microscopy techniques were used to study kidney structure and single nephron function in rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis developing over 5 to 20 mo, in the more acute and proliferative glomerular basement membrane (GBM) nephritis and in controls. Both models are known to have clinical counterparts in human disease. Kidney functional abnormalities correlated with the degree of architectural derangement. In both AICN and anti-GBM nephritis filtration fraction fell in direct proportion to the fall in glomerular filtration rate (GFR), renal plasma flow being unchanged. Fractional electrolyte excretion increased as the GFR fell. Despite marked heterogeneity of single nephron filtration rate (SNGFR) (AICN, 5-93 nl/min; anti-GBM, 0-50 nl/min) and of proximal tubular hydrostatic pressure (4-48 mm Hg), each nephron showed almost complete glomerulotubular balance, absolute reabsorption to the late proximal convolution varying directly with filtration rate. In addition SNGFR could be related both to proximal intratubular hydrostatic pressure and to calculated glomerular capillary pressure (Pg), being lowest in those nephrons with the highest intratubular pressure. Nephrons with very high filtration rates did not apparently reach filtration equilibrium. Mean SNGFR was significantly lower in the anti-GBM group, while calculated Pg was the same in both. This probably reflects the acute and diffuse involvement of the anti-GBM lesion with different filtration characteristics from the more chronic AICN disease. Tubular damage was more marked in AICN, and extraction of p-aminohippurate was reduced in this group.

Blood Proteins↗
PubMed1974

Nephron stop-flow pressure response to obstruction for 24 hours in the rat kidney.

Complete ureteral ligation of 24-h duration significantly reduced stop-flow and estimated glomerular capillary pressures in nephrons accessible to micropuncture in obstructed kidneys. In kidneys without ureteral obstruction, a similar response occurred in single tubules blocked for 24 h without affecting nearby unblocked tubules. Thus, the response to tubular obstruction occurs on an individual nephron basis and results from constriction of individual afferent arterioles. The mechanism leading to the response is unknown, but a feedback mechanism operating through the juxtaglomerular apparatus of individual nephrons is an attractive possibility.

Animals↗
PubMed1972

Renal tubular permeability during increased intrarenal pressure.

Renal tubular permeability was studied by microinjection techniques during increased intrarenal pressure in anesthetized diuretic rats. Intrarenal pressure, as evidenced by intratubular pressure (ITP), was increased by elevation of ureteral pressure, partial renal venous constriction, or massive saline diuresis. Various combinations of radioactive inulin, creatinine, mannitol, sucrose, and iothalamate in isotonic saline were microinjected into superficial proximal and distal convolutions, and recovery of the isotopes was measured in the urine. Inulin was completely recovered in the urine from the injected kidney at both normal and elevated ITP. Creatinine, mannitol, sucrose, and iothalamate were also completely recovered at normal ITP, but recoveries were significantly lower, averaging 73, 85, 89, and 85%, respectively, after early proximal injection when proximal ITP was increased to 30+/-2 mm Hg by elevation of ureteral pressure. Since transit time is prolonged under these conditions, mannitol recovery was also studied during aortic constriction, which prolongs transit time but lowers ITP. Recovery was complete. A significant loss of mannitol was observed during massive saline diuresis, which shortens transit time but increases ITP. During renal venous constriction producing a proximal ITP of 30+/-2 mm Hg, mannitol recovery was significantly less than 100% even after microinjection into distal convolutions, but the loss was greater injection at more proximal puncture sites. Mannitol recovery was complete during elevation of ureteral pressure in the contralateral kidney. These studies demonstrate a change in the permeability characteristics of all major segments of the renal tubule during elevation of intrarenal pressure. This change is rapidly reversible and does not appear to be due to a humoral factor which gains access to the general circulation.

Animals↗