The indirect action of subcutaneous injections of glycerol on the renal tubules in the rat

Finckh, E.S.

doi:10.1002/path.1700780121

Cited by 24 publications

(13 citation statements)

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“…The mean pressure in 51 proximal tubules of ten dehydrated control rats was 15.0 + 0.2 cm HO, a pressure slightly less than that of nondehydrated control rats, significant at the 5% confidence limit (Figure 3). Fifteen (31)(32)(33)(34)(35)(36)(37)(38). The histologic lesions produced in this manner have been well described, and seem to be consistent from study to study.…”

Section: Resultssupporting

confidence: 58%

“…The histologic lesions produced in this manner have been well described, and seem to be consistent from study to study. In appearance, distribution, and reversibility they closely resemble the lesions seen in the kidney of man with acute renal failure due to transfusion accidents or crush injury (33).…”

Section: Resultsmentioning

confidence: 54%

“…Glycerol itself is not toxic to tubular epithelium (33,37), and hemoglobinuria per se has been shown not to cause acute renal failure in the rat (38,39). Carroll, KovAcs, and Tapp have postulated recently that glycerol predisposes to the development of acute tubular necrosis by producing a combination of hemoglobinuria and renal ischemia (38).…”

Section: Resultsmentioning

confidence: 99%

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Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Oken¹,

Arce²,

Wilson³

1966

J. Clin. Invest.

217

126

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The oliguria of acute renal failure has been attributed to tubular obstruction (1-12), "leakage" of the glomerular filtrate through rents in the tubular wall (13)(14)(15)(16)(17)(18)(19), and vascular mechanisms of various types (20)(21)(22)(23)(24)(25). In a previous paper, it was shown that the oliguria of mercury-induced acute renal failure in the rat reflects a primary decrease in glomerular filtration rate and cannot be attributed to tubular mechanisms (26). The applicability of these findings to most types of acute renal failure occurring in humans may be questioned, however, because of the very dissimilar etiologies and the known effect of large doses of mercury on the renal circulation (27). The present study concerns hours before glycerol injection. They lost an average of 8% of body weight in the period of dehydration, during which time their food intake was one-third less than that of nondehydrated animals. Blood samples were obtained by cardiac puncture from a number of glycerolinjected animals and dehydrated control rats that were exempted from micropuncture studies to determine the change in their blood urea nitrogen (BUN) occurring over a 48-hour period. BUN was measured on 0.2-ml samples by a modification of the urease method of Gentzkow (28). Urinary osmolalities were determined with an Advanced osmometer.Acute renal failure was induced by injecting 50%o glycerol in water into the muscle of both hind limbs at a total dose of 10 ml per kg of body weight. Within 2 hours after this injection, the urine was found to be burgundy red in color due to the presence of heme pigments.The animals were subjected to micropuncture experiments at times ranging from 30 minutes to 26 hours after glycerol injection. They were anesthetized with sodium pentobarbital given intraperitoneally at a dose of 40 to 50 mg per kg body weight. Their blood pressure was monitored as described earlier (26) either by a tail cuff microphone method or intra-arterial manometry. Although hypotension typically did not occur, animals whose mean arterial blood pressure was less than 85 mm Hg were excluded from micropuncture study. The left kidney was exposed through an abdominal incision and carefully dissected free of the perirenal fat. The renal hilus was disturbed as little as possible, and the renal capsule was left intact. The kidney was placed in a Lucite holder to minimize its displacement with respiration. Its surface was covered with warm mineral oil to prevent drying and to aid in visualization of the renal structures.Micropuncture methods were those described in an earlier paper (26). In short, proximal tubular hydrostatic pressure was measured by a modification of the manometric method of Wirz (29), using a water manometer to obtain maximal definition of the end point. The manometer was calibrated at zero pressure before each measurement. Glomerular filtration rate and fractional water absorption were determined at least 30 minutes after the injection of 40 ,uc of "C-labeled inulin 1 in 0.3 to 0.5 ml of 140 mM NaCl. Labele...

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Section: Resultssupporting

confidence: 58%

Section: Resultsmentioning

confidence: 54%

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Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Oken¹,

Arce²,

Wilson³

1966

J. Clin. Invest.

217

126

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“…Glycerol is not toxic per se (Finck, 1959;Mason, Alexander & Teschan, 1963). Finck (1959Finck ( , 1965 attributed renal insufficiency to a number of vascular mechanisms.…”

Section: Discussionmentioning

confidence: 98%

The Effect of Indomethacin and Prostaglandin (PGE2) on Renal Failure Due to Glycerol in Saline-Loaded Rats

et al. 1975

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1. Acute renal failure was induced in conscious rate by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE2) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.

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“…He found that intraperitoneally administered glycerol failed to produce hemoglobinuria, yet it evoked a renal lesion identical histologically to that after glycerol injection by the subcutaneous or intramuscular routes. This question remains unresolved, however, since Carroll, Kovacs, and Tapp (14), using a larger dose of glycerol than that given by Finckh (13), did note hemoglobinuria associated with the renal lesion that followed intraperitoneal injection of glycerol. In any event, the lesion after glycerol injection appears to resemble morphologically that produced by nephrotoxic substances (15), and Oken and his co-workers have noted identical functional changes in that lesion and the one produced by mercury in the rat (1, 2).…”

Section: Discussionmentioning

confidence: 99%

The Renal Lesion Associated with Hemoglobinemia: A Study of the Pathogenesis of the Excretory Defect in the Rat*

Jaenike¹

1967

J. Clin. Invest.

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Summary. The role of renal ischemia in the pathogenesis of the renal failure produced by hemoglobin injection in the rat is evaluated. The data indicate that in the initial hours of this lesion renal blood flow is consistently reduced and that during its subsequent evolution blood flow rises towards normal levels, in some animals, while inulin clearance remains severely depressed. Volume expansion during the initial stage of the lesion may effect a rise in renal blood flow to normal levels with little effect on inulin clearance rate, further demonstrating the relative lack of dependence of the excretory defect on concomitant renal ischemia. These observations indicate that renal ischemia is probably a necessary factor in the initial production of the lesion; that it persists during its initial phase, up to 24 hours in most rats; and that, although it may contribute to the observed excretory defect, it is not the predominant etiologic factor.Other functional data indicate that renal blood is perfusing nephrons in which the excretory capacity is impaired but which retain the ability to extract Diodrast from the peritubular capillaries. This functional pattern indicates an excretory defect secondary either to intratubular obstruction or to a primary reduction of glomerular filtration rate of undefined etiology. The morphological findings of numerous dense intratubular hemoglobin casts and, in the well-perfused kidney, dilatation of proximal tubules, are suggestive of an obstructive lesion. However, the data do not conclusively distinguish between these two pathogenetic mechanisms. Introduction Acute renal failure in man occurs in a variety of clinical settings, reflecting the diversity of basic etiologic factors implicated in this syndrome. The

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The indirect action of subcutaneous injections of glycerol on the renal tubules in the rat

Cited by 24 publications

References 1 publication

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

The Effect of Indomethacin and Prostaglandin (PGE2) on Renal Failure Due to Glycerol in Saline-Loaded Rats

The Renal Lesion Associated with Hemoglobinemia: A Study of the Pathogenesis of the Excretory Defect in the Rat*

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