Intratubul�rer Druck, glomerul�rer Capillardruck und Glomerulumfiltrat w�hrend Mannit-Diurese

A B S T R A C T Glomerular filtration (GF) during progressive reduction of renal perfusion pressure by aortic clamping was studied in hydropenic rats and in rats infused with isotonic saline, hypertonic saline, or mannitol. As judged by visual observation of Lissamine green movements in superficial nephrons, GF was absent in hydropenic or saline-loaded rats at 40 mm Hg aortic pressure, but continued in some nephrons of all rats infused with mannitol and of some rats infused with hypertonic saline. Urine flow persisted only in rats infused with mannitol. By use of the qualitative Hanssen technique, it was found that all glomeruli in superficial and deep portions of the cortex were perfused at 40 mm Hg in all groups of rats. By the same method, GF continued in 1% of nephrons in hydropenic rats, 12% of nephrons in isotonic saline-loaded rats, and 78% of nephrons in rats infused with mannitol. By means of a quantitative Hanssen technique, GF was 5.8 nl/min per nephron in mannitol-infused rats and not measurable (<0.5 nl) in hydropenic rats. Superficial and deep nephrons were similar in both qualitative and quantitative studies. Although urine flow did not persist in rats infused with hypertonic saline, GF was detected in four of seven studies by the Hanssen method (mean, 9.1 nl/min per nephron). In additional experiments, mannitol infused after perfusion pressure had already been-lowered to 40 mm Hg in hydropenic rats reestablished urine flow and GF (mean, 9.8 nl/min). Furosemide, isotonic and hypertonic saline did not restart urine flow; however, GF (Lissamine green) was restarted by hypertonic saline. We conclude that mannitol can maintain or reestablish by an extratubular mechanism GF which otherwise would not occur during renal hypoperfusion. Hypertonic saline has a similar effect on GF in some cases, but urine

Section: Introductionsupporting

confidence: 72%

Restoration and maintenance of glomerular filtration by mannitol during hypoperfusion of the kidney

Morris¹,

Alexander²,

Bruns³

et al. 1972

“…The assumption common to each of these latter studies is that these methods for elevation of PT permit encroachment on the value for PGC without significantly disturbing it. Since reported estimates of PGC using these stop-flow techniques in the rat have been higher than 80 cm H20 (11)(12)(13)(14), often in excess of 100 cm H20, and therefore much higher than values measured directly in the present study, this assumption may be invalid. In all liklihood, autoregulatory adjustments are initiated in response to progressive elevations in PT (17) and yield values of approximately 250 X 10-1 ml/sec per cm H20/cm2.…”

Section: Methodscontrasting

confidence: 52%

“…Hydraulic output from the servo-system was channeled via a strain gauge to a recorder. Accuracy, frequency response, and stability features of this servo-system will be described in detail elsewhere (Brenner et (11)(12)(13)(14). The assumption common to each of these latter studies is that these methods for elevation of PT permit encroachment on the value for PGC without significantly disturbing it.…”

Section: Methodsmentioning

confidence: 99%

The Dynamics of Glomerular Ultrafiltration in the Rat

Brenner¹,

Troy²,

Daugharty³

1971

280

105

A B ST R A CT Using a unique strain of \VNistar rats endowed with glomeruli situated directly on the renal cortical surface, we measured glomerular capillary pressures using servo-nulling micropipette transducer techniques. Pressures in 12 glomerular capillaries from 7 rats averaged 60 cm H20, or approximately 50% of mean systemic arterial values. Wave form characteristics for these glomerular capillaries were found to be remarkably similar to those of the central aorta. From similarly direct estimates of hydrostatic pressures in proximal tubules, and colloid osmotic pressures in systemic and efferent arteriolar plasmas, the net driving force for ultrafiltration was calculated. The average value of 14 cm H20 is lower by some two-thirds than the majority of estimates reported previously based on indirect techniques. Single nephron GFR (glomerular filtration rate) was also measured in these rats, thereby permitting calculation of the glomerular capillary ultrafiltration coefficient.

“…Unfortunately, estimates of this value vary widely. In the rat direct and indirect measurements have yielded conflicting results (46)(47)(48).…”

mentioning

confidence: 99%

Renal Distribution Volumes of Indocyanine Green, [51Cr]EDTA, and 24Na in Man during Acute Renal Failure after Shock. IMPLICATIONS FOR THE PATHOGENESIS OF ANURIA

Reubi¹,

Vorburger²,

Tuckman³

1973

A Bs T R A C T The mechanism responsible for the anuria in acute renal failure after shock is still controversial.Suppressed glomerular filtration and/or tubular backdiffusion of the filtrate are major possible causes. In the present investigation, seven patients with acute anuria, three of these seven again in the polyuric phase, six patients with moderate renal impairment, four patients with chronic renal failure, and eight subjects with normal renal function were studied by a multiple indicatordilution method in which the total renal blood flow and renal distribution volumes of indocyanine green, ['Cr]-EDTA, and 'Na were determined. In normal subjects the average values for one kidney were 582 ml/min, 42 ml, 92 ml, and 139 ml, respectively. The measurements in the patients with moderate renal impairment were similar to those in the normal subjects, but were decreased in chronic renal failure. In acute anuria, the average values were 269 ml/min, 40 ml, 101 ml, and 114 ml and the kidney volume, estimated radiographically, was increased by 40%. When expressed as milliliters per milliliters kidney, the average distribution volume of 'Na was decreased from 0.64 to 0.38. This decrease is consistent with the hypothesis that suppressed filtration is largely responsible for the anuria and that back-diffusion is, at most, a contributory factor. The apparent contradiction between the relatively well-preserved total blood flow and the suppressed filtration may be due to a combination of afferent vasoconstriction and efferent vasodilatation. This view is supported by the observation that low filtration fractions were found in clearance measurements performed during the polyuric phase.