Ischemia and tubule obstruction during acute renal failure in dogs: mannitol in protection.

T. J. Burke, R. E. Cronin, K. L. Duchin, L. N. Peterson, R. W. Schrier

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Abstract

The pathogenetic factors involved in norepinephrine- (NE) induced reversible acute renal failure (ARF) were examined in untreated (U) and mannitol-treated (M) animals. At 3 and 24 h after NE infusion renal blood flow (RBF) was significantly higher in M compared to U animals (174 vs. 138 and 191 vs. 148 ml/min, respectively, both P less than 0.05). At 3 h, glomerular filtration rate (GFR) was higher in M animals (8 vs. 4 ml/min, P less than 0.01), while at 24 h protection was even greater (18 vs. 3 ml/min, P less than 0.01). In U animals proximal tubule pressure (Pt) was lower at 1 h than before NE (13 vs. 23 mmHg, P less than 0.01); from 1 to 3 h Pt increased to elevated levels in parallel with restoration of RBF (r = 0.62, P less than 0.01). At 3 h in U animals stop-flow pressure (SFP), as an index of glomerular capillary pressure, was below normal (35 vs. 44 mmHg, P less than 0.05) yet Pt was increased (35 vs. 23 mmHg, P less than 0.05). Thus little transglomerular pressure gradient was present for ultrafiltration. Further evidence of tubular obstruction was obtained by microperfusion at 6 nl/min, which increased Pt from 30 to 45 mmHg (P less than 0.001), a finding not present in unobstructed tubules. Delayed excretion (approximately 20 min) of microinjected [3H]inulin also was compatible with renal ischemia and tubule obstruction. Microinjection studies provided no evidence for backleak of tubular fluid. At 1 h, Pt was higher in M vs. U animals (31 vs. 13 mmHg, P less than 0.05). In M animals at 3 h SFP was normal (50 vs. 44 mmHg) and Pt was below SFP (32 vs. 50 mmHg, P less than 0.01), thus preserving a substantial transglomerular pressure gradient for ultrafiltration. In summary, reduced GFR in U animals is characterized by a combination of reduced glomerular capillary pressure and tubule obstruction. In contrast, animals receiving mannitol were protected against ARF through maintenance of glomerular capillary pressure and prevention of tubular obstruction, perhaps by increasing Pt within the first hour of the NE insult.

Original languageEnglish (US)
JournalThe American journal of physiology
Volume238
Issue number4
StatePublished - Apr 1980

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Mannitol
Acute Kidney Injury
Ischemia
Dogs
Pressure
Norepinephrine
Renal Circulation
Ultrafiltration
Glomerular Filtration Rate
Inulin
Microinjections

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Burke, T. J., Cronin, R. E., Duchin, K. L., Peterson, L. N., & Schrier, R. W. (1980). Ischemia and tubule obstruction during acute renal failure in dogs: mannitol in protection. The American journal of physiology, 238(4).

Ischemia and tubule obstruction during acute renal failure in dogs : mannitol in protection. / Burke, T. J.; Cronin, R. E.; Duchin, K. L.; Peterson, L. N.; Schrier, R. W.

In: The American journal of physiology, Vol. 238, No. 4, 04.1980.

Research output: Contribution to journalArticle

Burke, TJ, Cronin, RE, Duchin, KL, Peterson, LN & Schrier, RW 1980, 'Ischemia and tubule obstruction during acute renal failure in dogs: mannitol in protection.', The American journal of physiology, vol. 238, no. 4.
Burke, T. J. ; Cronin, R. E. ; Duchin, K. L. ; Peterson, L. N. ; Schrier, R. W. / Ischemia and tubule obstruction during acute renal failure in dogs : mannitol in protection. In: The American journal of physiology. 1980 ; Vol. 238, No. 4.
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abstract = "The pathogenetic factors involved in norepinephrine- (NE) induced reversible acute renal failure (ARF) were examined in untreated (U) and mannitol-treated (M) animals. At 3 and 24 h after NE infusion renal blood flow (RBF) was significantly higher in M compared to U animals (174 vs. 138 and 191 vs. 148 ml/min, respectively, both P less than 0.05). At 3 h, glomerular filtration rate (GFR) was higher in M animals (8 vs. 4 ml/min, P less than 0.01), while at 24 h protection was even greater (18 vs. 3 ml/min, P less than 0.01). In U animals proximal tubule pressure (Pt) was lower at 1 h than before NE (13 vs. 23 mmHg, P less than 0.01); from 1 to 3 h Pt increased to elevated levels in parallel with restoration of RBF (r = 0.62, P less than 0.01). At 3 h in U animals stop-flow pressure (SFP), as an index of glomerular capillary pressure, was below normal (35 vs. 44 mmHg, P less than 0.05) yet Pt was increased (35 vs. 23 mmHg, P less than 0.05). Thus little transglomerular pressure gradient was present for ultrafiltration. Further evidence of tubular obstruction was obtained by microperfusion at 6 nl/min, which increased Pt from 30 to 45 mmHg (P less than 0.001), a finding not present in unobstructed tubules. Delayed excretion (approximately 20 min) of microinjected [3H]inulin also was compatible with renal ischemia and tubule obstruction. Microinjection studies provided no evidence for backleak of tubular fluid. At 1 h, Pt was higher in M vs. U animals (31 vs. 13 mmHg, P less than 0.05). In M animals at 3 h SFP was normal (50 vs. 44 mmHg) and Pt was below SFP (32 vs. 50 mmHg, P less than 0.01), thus preserving a substantial transglomerular pressure gradient for ultrafiltration. In summary, reduced GFR in U animals is characterized by a combination of reduced glomerular capillary pressure and tubule obstruction. In contrast, animals receiving mannitol were protected against ARF through maintenance of glomerular capillary pressure and prevention of tubular obstruction, perhaps by increasing Pt within the first hour of the NE insult.",
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AU - Cronin, R. E.

AU - Duchin, K. L.

AU - Peterson, L. N.

AU - Schrier, R. W.

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N2 - The pathogenetic factors involved in norepinephrine- (NE) induced reversible acute renal failure (ARF) were examined in untreated (U) and mannitol-treated (M) animals. At 3 and 24 h after NE infusion renal blood flow (RBF) was significantly higher in M compared to U animals (174 vs. 138 and 191 vs. 148 ml/min, respectively, both P less than 0.05). At 3 h, glomerular filtration rate (GFR) was higher in M animals (8 vs. 4 ml/min, P less than 0.01), while at 24 h protection was even greater (18 vs. 3 ml/min, P less than 0.01). In U animals proximal tubule pressure (Pt) was lower at 1 h than before NE (13 vs. 23 mmHg, P less than 0.01); from 1 to 3 h Pt increased to elevated levels in parallel with restoration of RBF (r = 0.62, P less than 0.01). At 3 h in U animals stop-flow pressure (SFP), as an index of glomerular capillary pressure, was below normal (35 vs. 44 mmHg, P less than 0.05) yet Pt was increased (35 vs. 23 mmHg, P less than 0.05). Thus little transglomerular pressure gradient was present for ultrafiltration. Further evidence of tubular obstruction was obtained by microperfusion at 6 nl/min, which increased Pt from 30 to 45 mmHg (P less than 0.001), a finding not present in unobstructed tubules. Delayed excretion (approximately 20 min) of microinjected [3H]inulin also was compatible with renal ischemia and tubule obstruction. Microinjection studies provided no evidence for backleak of tubular fluid. At 1 h, Pt was higher in M vs. U animals (31 vs. 13 mmHg, P less than 0.05). In M animals at 3 h SFP was normal (50 vs. 44 mmHg) and Pt was below SFP (32 vs. 50 mmHg, P less than 0.01), thus preserving a substantial transglomerular pressure gradient for ultrafiltration. In summary, reduced GFR in U animals is characterized by a combination of reduced glomerular capillary pressure and tubule obstruction. In contrast, animals receiving mannitol were protected against ARF through maintenance of glomerular capillary pressure and prevention of tubular obstruction, perhaps by increasing Pt within the first hour of the NE insult.

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