Blood flow of experimental liver metastases in rat as evaluated by the locally injected 133-Xenon washout

1985 ◽  
Vol 185 (3) ◽  
pp. 207-215 ◽  
Author(s):  
C. Merkel ◽  
P. P. Cagol ◽  
P. P. Da Pian ◽  
M. Bolognesi ◽  
D. Sacerdoti ◽  
...  
Pharmaceutics ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 703
Author(s):  
Arturas Ziemys ◽  
Vladimir Simic ◽  
Miljan Milosevic ◽  
Milos Kojic ◽  
Yan Ting Liu ◽  
...  

Metastatic cancer disease is the major cause of death in cancer patients. Because those small secondary tumors are clinically hardly detectable in their early stages, little is known about drug biodistribution and permeation into those metastatic tumors potentially contributing to insufficient clinical success against metastatic disease. Our recent studies indicated that breast cancer liver metastases may have compromised perfusion of intratumoral capillaries hindering the delivery of therapeutics for yet unknown reasons. To understand the microcirculation of small liver metastases, we have utilized computational simulations to study perfusion and oxygen concentration fields in and around the metastases smaller than 700 µm in size at the locations of portal vessels, central vein, and liver lobule acinus. Despite tumor vascularization, the results show that blood flow in those tumors can be substantially reduced indicating the presence of inadequate blood pressure gradients across tumors. A low blood pressure may contribute to the collapsed intratumoral capillary lumen limiting tumor perfusion that phenomenologically corroborates with our previously published in vivo studies. Tumors that are smaller than the liver lobule size and originating at different lobule locations may possess a different microcirculation environment and tumor perfusion. The acinus and portal vessel locations in the lobule were found to be the most beneficial to tumor growth based on tumor access to blood flow and intratumoral oxygen. These findings suggest that microcirculation states of small metastatic tumors can potentially contribute to physiological barriers preventing efficient delivery of therapeutic substances into small tumors.


1983 ◽  
Vol 396 (2) ◽  
pp. 182-183 ◽  
Author(s):  
Ulrik Abildgaard ◽  
O. Amtorp ◽  
S. Hans� ◽  
P. Rosenkilde ◽  
P. Sejrsen

2002 ◽  
Vol 103 (2) ◽  
pp. 165-174 ◽  
Author(s):  
V. Muralidharan ◽  
C. Malcontenti-Wilson ◽  
Chris Christophi

1970 ◽  
Vol 4 (5) ◽  
pp. 446-446
Author(s):  
Pedro A Jose ◽  
Alexander G Logan ◽  
Gilbert M Eisner ◽  
Lawrence M Slotkoff ◽  
Charles E Hollerman ◽  
...  

2002 ◽  
Vol 106 (1) ◽  
pp. 173-178 ◽  
Author(s):  
Hideaki Karube ◽  
Hideki Masuda ◽  
Yukimoto Ishii ◽  
Tadatoshi Takayama

1978 ◽  
Vol 55 (s4) ◽  
pp. 85s-87s ◽  
Author(s):  
P. W. De Leeuw ◽  
H. E. Falke ◽  
R. Punt ◽  
W. H. Birkenhäger

1. In 20 subjects with uncomplicated essential hypertension, 10 of whom were on propranolol treatment, several blood samples were drawn simultaneously from the renal artery and vein after angiographic studies. In these samples we determined concentrations of noradrenaline, active renin, aldosterone and cortisol. 2. Renal blood flow was measured in all patients by Hippuran-clearance and xenon-washout. 3. Despite marked variations in the arteriovenous difference of noradrenaline, it was apparent in both groups that the kidney is able to release noradrenaline. 4. In the propranolol-treated group noradrenaline secretion by the kidney was enhanced when compared with untreated hypertensive patients.


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