scholarly journals Intrarenal Distribution of Blood Flow in Dogs during Hemorrhagic Hypotension

1966 ◽  
Vol 19 (1) ◽  
pp. 167-179 ◽  
Author(s):  
SERGE CARRIERE ◽  
GEOFFREY D. THORBURN ◽  
CHARLES C. C. O'MORCHOE ◽  
A. CLIFFORD BARGER
1995 ◽  
Vol 268 (5) ◽  
pp. F839-F846 ◽  
Author(s):  
F. Vetterlein ◽  
F. Hoffmann ◽  
J. Pedina ◽  
M. Neckel ◽  
G. Schmidt

The question was studied of whether myoglobin (Mb), when released into the general circulation during hemorrhagic hypotension (HH), causes disturbances of renal blood flow. In anesthetized rats 250 mg/kg Mb was intravenously infused within 1 h; HH at 50 mmHg with subsequent retransfusion was induced for 30 min. By allowing two dyes to circulate for 1 and 3 min, respectively, and detecting their localization histologically after rapid freezing of the organ, intrarenal distribution of capillary blood flow was studied. In contrast to the results obtained with Mb or HH alone, when Mb was infused during HH, the development of large areas within cortex and medulla lacking any capillary perfusion was observed. In > 70% of the tissue, a distance > 60 microns to the next dye-labeled capillary was found (in controls 0%). At this time total renal flow had decreased from 5.3 to 0.20 ml/min (HH without Mb: 5.1 to 1.1 ml/min). It is concluded that the observed changes in renal blood flow contribute to the known direct nephrotoxic potential of Mb.


1991 ◽  
Vol 75 (3) ◽  
pp. A822-A822
Author(s):  
R D Vincent ◽  
D H Chestnut ◽  
S L Sipes ◽  
C S Thompson ◽  
S A Bleuer ◽  
...  

1973 ◽  
Vol 225 (2) ◽  
pp. 319-323 ◽  
Author(s):  
Y Abe ◽  
T Okahara ◽  
T Kishimoto ◽  
K Yamamoto ◽  
J Ueda

1966 ◽  
Vol 4 (3) ◽  
pp. 351
Author(s):  
B. Truniger ◽  
S. M. Rosen ◽  
H. Kriek ◽  
J. P. Merrill ◽  
J. E. Murray

Author(s):  
Yoshinori Kikuta ◽  
Otowa Moritsune ◽  
Hiroaki Kawabata ◽  
Shinkichi Tezuka ◽  
Kazuo Okada ◽  
...  

1964 ◽  
Vol 206 (2) ◽  
pp. 383-390 ◽  
Author(s):  
Julius J. Cohen ◽  
Evelyn W. Randall

Does alkalosis per se or does the associated lactacidemia determine the rate of PAH or Diodrast transport? How is net renal uptake of lactate related to Tmpah? Tmpah, renal extraction of I131-Diodrast (Ediod) and net renal lactate uptake were studied in anesthetized (pentobarbital) dogs. In clearance experiments, Tmpah is elevated (facilitated) by isohydric increases in blood [lactate]; alkalosis has no further effect on the facilitated (by lactate) Tmpah. In contrast to the effects of alkalosis on Tmpah, no rise in Ediod occurs during alkalosis. However, when Ediod is depressed by [PAH] sufficiently high to achieve Tmpah, a rise in blood lactate does enhance Ediod. Thus, lactate enhances Ediod when the transport mechanism common to it and PAH is saturated. Net renal uptake of endogenous lactate is decreased during alkalosis; no net renal production of lactate has been observed. Therefore, the increases in Tmpah and Ediod are not related to a rise in net renal uptake of lactate but are probably more related to the blood [lactate]. It is postulated that Tmpah and Ediod may be more dependent on the metabolic mixture presented to the kidney, and thus on extrarenal metabolism, than on intrarenal distribution of blood flow or rate of renal blood flow.


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