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Physiologie und Pathologische Physiologie / Physiology and by Bernard Fey, Felix Heni, Albert Kuntz, D. F. McDonald, Louis

By Bernard Fey, Felix Heni, Albert Kuntz, D. F. McDonald, Louis Quénu, Laurence G. Wesson Jr., Clifford Wilson (auth.)

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Additional resources for Physiologie und Pathologische Physiologie / Physiology and Pathological Physiology / Physiologie Normale et Pathologique

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GIBSON et al. DUNN et al. DUNN et al. Renal hematocrit values, measured as percent of large vessel hematocrit, which have been reported by various authors. Hematocrits of some other tissues are listed for comparison. In the "single passage" methods, known amounts of isotopically labelled red cells and albumin are injected into a renal artery. Hematocrit is then calculated either from transit times or from relative dilutions of the isotopes during passage through the kidney. In the "steady state" methods, hematocrit is calculated from relative intrarenal red cell and plasma spaces after continuous perfusion for some time by blood containing labelled red cells and plasma in constant concentration.

In acute experiments on anesthetized animals, section of the renal or splanchnic nerves quite regularly is followed by an increase in urine flow and sodium excretion. The hemodynamic functions of filtration rate and renal blood flow also increase indicating that active vasoconstrictor fibers have been interrupted by section. Although some investigators feel that the increase in sodium excretion is greater than can be explained as a simple consequence of the hemodynamic changes, data adequate to establish a specific effect of the nerves on tubular functions have not been published (WESSON 1957).

Hg, is exceeded. Thereafter, all three pressures, together with the peritubuIar capillary pressure, increase equally (WINTON 1933; GOTTSCHALK 1950, 1952; GOTTSCHALK and MYLLE 1956; SWANN, MONTGOMERY and LOWRY). Renal interstitial pressure also increases to 30 mm. Hg or more during diuresis from causes related to decreased reabsorption of water (WINTON 1933; MILES and DE WARDENER 1954; GOTTSCHALK and MYLLE 1956, 1957). Since the diuretic agent (chilling; cyanide administration; urea, mannitol, saline, or sulfate loading) does not usually increase blood flow or filtration rate and, by diminishing tubular reabsorption, actually lessens the fluid volume entering the interstitium, the pressure rise is probably caused by swelling of the tubules whose lumina can be observed to dilate (BRODIE and MACKENZIE; GOTTSCHALK and MYLLE 1957).

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