Tumor Pathophysiology: the Perfusion Model

Author(s):  
P. M. Gullino
Keyword(s):  
1989 ◽  
Vol 62 (03) ◽  
pp. 1034-1039 ◽  
Author(s):  
Jan S Brunkwall ◽  
James C Stanley ◽  
Timothy F Kresowik ◽  
Linda M Graham ◽  
William E Burkel ◽  
...  

SummaryRegulation of prostanoid release from ex vivo perfused vessel segments is not fully understood. A series of perfusion experiments were performed with canine arteries and veins to define certain regulatory phenomena. Arteries were perfused with pulsatile flow of 90 ml/min at a pressure of 100 mmHg, and veins with nonpulsatile flow of 90 ml/min at a pressure of 7 mmHg. Segments were perfused with Hanks' balanced salt solution for five 15-min periods with the perfusate exchanged after each study period. With onset of perfusion, there was an initial burst of prostacyclin release to 127 ± 40 pg/mm2, declining to 32 ± 10 pg/mm2 after 60 minutes (p <0.005). If perfusion continued for 5.5 hours, there was a stable release period between 1 and 3 hours, followed by a very slow decline. At that time addition of arachidonic acid (AA) increased prostacyclin release six-fold (p <0.01). Vessels perfused for 1 hour and then rested for another hour, responded to reperfusion at the second onset of flow with a two-fold increase in prostacyclin release (p <0.01). Vessels perfused with thrombin, bradykinin or A A (either added to each perfusate or only to the last perfusate) exhibited greater prostacyclin release than did control segments. Release of thromboxane steadily declined with time in all parts of the study, and only increased with the addition of A A to the perfusate. These data indicate that vessel segments subjected to ex vivo perfusion do not maximally utilize enzyme systems responsible for prostanoid production, and after 1 hour perfusion have not depleted their phospholipids, and maintain functioning levels of phospholipase and cyclooxygenase activity. This perfusion model allows for the study of prostacyclin and thromboxane release from arteries and veins and their response to various drugs and other stimuli.


2017 ◽  
Vol 216 (1) ◽  
pp. S280 ◽  
Author(s):  
FRANCESCA M. RUSSO ◽  
SIGRID CONINGS ◽  
PIETER ANNAERT ◽  
TIM VAN MIEGHEM ◽  
JAAN TOELEN ◽  
...  

2006 ◽  
Vol 3 (6) ◽  
pp. 686-694 ◽  
Author(s):  
Jae-Seung Kim ◽  
Stefanie Mitchell ◽  
Paul Kijek ◽  
Yasuhiro Tsume ◽  
John Hilfinger ◽  
...  

2006 ◽  
Vol 195 (6) ◽  
pp. 1715-1719 ◽  
Author(s):  
Heather J. Holmes ◽  
Brian M. Casey ◽  
Roger E. Bawdon

1989 ◽  
Vol 257 (2) ◽  
pp. G210-G220 ◽  
Author(s):  
X. Deroubaix ◽  
T. Coche ◽  
E. Depiereux ◽  
E. Feytmans

Compartmental analysis was used to study the hepatobiliary transport of taurocholate (TC) in the rat in vivo. The available data are the following: [14C]TC kinetics in blood and bile, weighting factors associated with these data and computed from a theoretical variability model, and TC excretion rate in bile. The lumped model that best fits the data contains five compartments: three compartments for TC distribution in blood and two compartments for the liver. It includes a compartmental representation of the laminar flow of bile in the collecting catheter. This model overestimates TC concentration in blood. A perfusion model that includes a compartment representing explicitly the sinusoidal TC concentration gradient was developed. TC concentration in blood estimated by this model is in good agreement with direct measurements, showing that the perfused model has a better descriptive capacity than the lumped model. The amounts of TC estimated in the two hepatic compartments are similar to values previously published.


2013 ◽  
Vol 54 (3) ◽  
pp. 1698 ◽  
Author(s):  
Vikas Gulati ◽  
Shan Fan ◽  
Cassandra L. Hays ◽  
Thomas W. Samuelson ◽  
Iqbal Ike K. Ahmed ◽  
...  

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