Cardiac Output, Renal Blood Flow and Hepatic Blood Flow in Rats with Glycerol-Induced Acute Renal Failure

Nephron ◽  
1989 ◽  
Vol 53 (4) ◽  
pp. 353-357 ◽  
Author(s):  
T. Kishimoto ◽  
W. Sakamoto ◽  
T. Nakatani ◽  
T. Ito ◽  
K. Iwai ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Hepatic Blood Flow

scholarly journals Dissociation of glomerular filtration and renal blood flow in HgCl2-induced acute renal failure

1982 ◽  
Vol 22 (2) ◽  
pp. 162-170 ◽  
Author(s):  
Raymond C. Vanholder ◽  
Marleen M. Praet ◽  
Piet A. Pattyn ◽  
Isidoor R. Leusen ◽  
Norbert H. Lameire
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration ◽  
Renal Blood Flow

Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F490-F496 ◽  
Author(s):  
J. A. Winston ◽  
R. Safirstein
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Single Nephron ◽  
Renal Vascular

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 +/- 0.06 vs. 1.17 +/- 0.06 ml X min-1 X g kidney wt-1 and 5.30 +/- 0.62 vs. 8.25 +/- 0.43 ml X min-1 X g kidney wt-1, respectively; P less than 0.001), as were superficial nephron GFR and stop-flow pressure (20.2 +/- 2.1 vs. 34.5 +/- 2.0 nl X min-1 X g kidney wt-1 and 29.0 +/- 1.9 vs. 39.8 +/- 1.3 mmHg, respectively; P less than 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 +/- 0.07 ml X min-1 X g kidney wt-1, single nephron filtration rate increased to 29.9 +/- 3.5 nl X min-1 X g kidney wt-1 (P less than 0.005), and renal plasma flow increased to 5.62 +/- 0.60 ml X min-1 X g kidney wt-1 (P less than 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.

Noninvasive monitoring of renal blood flow characteristics during acute renal failure in man

1990 ◽  
Vol 16 (3) ◽  
pp. 153-158 ◽  
Author(s):  
P. E. Stevens ◽  
S. J. Gwyther ◽  
M. E. Hanson ◽  
J. E. Boultbee ◽  
W. J. Kox ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Flow Characteristics ◽  
Noninvasive Monitoring

Effect of renal ischemia on cortical microsomal calcium accumulation

1985 ◽  
Vol 249 (5) ◽  
pp. C476-C483 ◽  
Author(s):  
A. Schieppati ◽  
P. D. Wilson ◽  
T. J. Burke ◽  
R. W. Schrier
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Normal Level ◽  
Mitochondrial Respiration ◽  
Renal Cortex ◽  
Bilateral Renal Artery ◽  
Ischemic Acute Renal Failure

Mitochondrial respiration, Ca2+ content, and Ca2+ kinetics have been found to be profoundly altered in ischemic acute renal failure (ARF). The effect of clamping the bilateral renal artery for 50 and 90 min on microsomal Ca2+ uptake was therefore examined in the rat. The 50-min clamping produced a reversible model of nonoliguric ARF, and the 90-min clamping produced a model of nonreversible oliguric ARF. In the 50-min nonoliguric model, ATP-dependent Ca2+ uptake by microsomes from renal cortex (nmol X mg protein-1 X 30 min-1) was significantly impaired immediately before release of the clamp and before return of renal blood flow (reflow) (191 +/- 11 vs. 83 +/- 11, P less than 0.005). However, in this nonoliguric model of ischemic ARF, microsomal uptake returned completely to normal after 1 h of reflow (sham 189 +/- 11 vs. 167 +/- 14 at 1 h, NS) and persisted at this normal level at 24 h (sham 166 +/- 14 vs. 150 +/- 13 at 24 h, NS). In the oliguric model of ARF the microsomal Ca2+ uptake also was impaired immediately after the clamp release (sham 191 +/- 11 vs. 93 +/- 11, P less than 0.001) as well as after 1 h of reflow (sham 189 +/- 11 vs. 129 +/- 12, P less than 0.005) but not at 24 h (sham 166 +/- 14 vs. 173 +/- 13, NS). The results indicate that impaired microsomal Ca2+ uptake occurs early in both oliguric and nonoliguric ARF and persists after 1 h of reflow in the oliguric model.(ABSTRACT TRUNCATED AT 250 WORDS)

The Haemodynamic Effects of Metabolic Acidosis in the Rat

1976 ◽  
Vol 50 (3) ◽  
pp. 177-184 ◽  
Author(s):  
J. Yudkin ◽  
R. D. Cohen ◽  
Barbara Slack
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Renal Blood Flow ◽  
Hepatic Blood Flow ◽  
Conscious Rats ◽  
Blood Ph ◽  
Significant Difference

1. The effect of metabolic acidosis of 4–6 h duration on cardiac output, blood pressure, heart rate, and hepatic and renal blood flow has been studied in the rat. 2. In anaesthetized rats, blood pressure and heart rate fell linearly with blood pH in both sham-operated and nephrectomized rats. There was no significant difference between the two groups in the effect of acidosis on either variable. 3. Cardiac output showed a significant fall with increasing acidosis in the conscious rat. 4. Estimated hepatic blood flow in conscious rats showed a significant positive correlation with blood pH in both sham-operated and nephrectomized animals. There was no significant difference in estimated hepatic blood flow between the two groups of animals at any blood pH. 5. In conscious rats, increasing acidosis caused a progressive decrease in estimated renal blood flow. 6. It is concluded that the increase in the previously described apparent renal contribution to lactate removal in the acidotic rat cannot be explained by any circulatory effect mediated by the kidney. The possible relevance of the findings to lactate homeostasis is discussed.

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