Effects of Formed Elements on Xenograft Rejection in an Ex Vivo Organ Perfusion Model

1991 ◽  
pp. 405-425
Author(s):  
B. A. Bryan ◽  
M. L. Henry ◽  
L. K. Han ◽  
D. D. Sedmak ◽  
R. M. Ferguson
Keyword(s):  
Ex Vivo ◽  
Organ Perfusion ◽  
Xenograft Rejection ◽  
Perfusion Model

Early Predictors of Late Renal Dysfunction in Subnormothermic Ex-Vivo Organ Perfusion Model

2016 ◽  
Vol 223 (4) ◽  
pp. S147
Author(s):  
Matthew F. Blum ◽  
Daniel Urcuyo ◽  
Qiang Liu ◽  
Basem Soliman ◽  
David A. Goldfarb ◽  
...  
Keyword(s):  
Renal Dysfunction ◽  
Ex Vivo ◽  
Organ Perfusion ◽  
Perfusion Model ◽  
Early Predictors

Prostanoid Release from Ex Vivo Perfused Canine Arteries and Veins: Effects of Prolonged Perfusion, Intermittent Perfusion, as well as Exposure to Exogenous Arachidonic Acid, Thrombin and Bradykinin

1989 ◽  
Vol 62 (03) ◽  
pp. 1034-1039 ◽  
Author(s):  
Jan S Brunkwall ◽  
James C Stanley ◽  
Timothy F Kresowik ◽  
Linda M Graham ◽  
William E Burkel ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Ex Vivo ◽  
Fold Increase ◽  
Ex Vivo Perfusion ◽  
Cyclooxygenase Activity ◽  
Perfusion Model ◽  
Prostanoid Production ◽  
Slow Decline ◽  
Arteries And Veins ◽  
Nonpulsatile Flow

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.

scholarly journals 474: Placenta transfer of sildenafil citrate in the ex-vivo human cotyledon perfusion model

2017 ◽  
Vol 216 (1) ◽  
pp. S280 ◽  
Author(s):  
FRANCESCA M. RUSSO ◽  
SIGRID CONINGS ◽  
PIETER ANNAERT ◽  
TIM VAN MIEGHEM ◽  
JAAN TOELEN ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Sildenafil Citrate ◽  
Perfusion Model

scholarly journals Generation of vascular chimerism within donor organs

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shahar Cohen ◽  
Shirly Partouche ◽  
Michael Gurevich ◽  
Vladimir Tennak ◽  
Vadym Mezhybovsky ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Patient Specific ◽  
Machine Perfusion ◽  
Organ Perfusion ◽  
Perfusion Process ◽  
Hind Limbs ◽  
Porcine Organs ◽  
Immunological Barrier

AbstractWhole organ perfusion decellularization has been proposed as a promising method to generate non-immunogenic organs from allogeneic and xenogeneic donors. However, the ability to recellularize organ scaffolds with multiple patient-specific cells in a spatially controlled manner remains challenging. Here, we propose that replacing donor endothelial cells alone, while keeping the rest of the organ viable and functional, is more technically feasible, and may offer a significant shortcut in the efforts to engineer transplantable organs. Vascular decellularization was achieved ex vivo, under controlled machine perfusion conditions, in various rat and porcine organs, including the kidneys, liver, lungs, heart, aorta, hind limbs, and pancreas. In addition, vascular decellularization of selected organs was performed in situ, within the donor body, achieving better control over the perfusion process. Human placenta-derived endothelial progenitor cells (EPCs) were used as immunologically-acceptable human cells to repopulate the luminal surface of de-endothelialized aorta (in vitro), kidneys, lungs and hind limbs (ex vivo). This study provides evidence that artificially generating vascular chimerism is feasible and could potentially pave the way for crossing the immunological barrier to xenotransplantation, as well as reducing the immunological burden of allogeneic grafts.

Placental transfer of rosiglitazone in the ex vivo human perfusion model

2006 ◽  
Vol 195 (6) ◽  
pp. 1715-1719 ◽  
Author(s):  
Heather J. Holmes ◽  
Brian M. Casey ◽  
Roger E. Bawdon
Keyword(s):  
Placental Transfer ◽  
Ex Vivo ◽  
Perfusion Model

scholarly journals Placental Passage of Humulone and Protopine in an Ex Vivo Human Perfusion System

Planta Medica ◽  
2021 ◽  
Author(s):  
Deborah Spiess ◽  
Vanessa Fabienne Abegg ◽  
Antoine Chauveau ◽  
Andrea Treyer ◽  
Michael Reinehr ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Positive Control ◽  
Placental Perfusion ◽  
Perfusion Model ◽  
Beta Human Chorionic Gonadotropin ◽  
Pathologic Findings ◽  
Age Appropriate ◽  
Placental Passage

AbstractThe placental passage of humulone and protopine was investigated with a human ex vivo placental perfusion model. The model was first validated with diazepam and citalopram, 2 compounds known to cross the placental barrier, and antipyrine as a positive control. All compounds were quantified by partially validated U(H)PLC-MS/MS bioanalytical methods. Only a small portion of humulone initially present in the maternal circuit reached the fetal circuit. The humulone concentration in the maternal circuit rapidly decreased, likely due to metabolization in the placenta. Protopine was transferred from the maternal to the fetal circuit, with a steady-state reached after 90 min. None of the study compounds affected placental viability or functionality, as glucose consumption, lactate production, beta-human chorionic gonadotropin, and leptin release remained constant. Histopathological evaluation of all placental specimens showed unremarkable, age-appropriate parenchymal maturation with no pathologic findings.

Ex Vivo Organ Perfusion Studies in Xenograft Research

1991 ◽  
pp. 395-403
Author(s):  
K. E. Otte ◽  
D. Steinbruchel ◽  
E. Kemp
Keyword(s):  
Ex Vivo ◽  
Organ Perfusion ◽  
Perfusion Studies

Platelet-Vessel Wall Interactions in von Willebrand’s Disease

1979 ◽  
Author(s):  
M.I. Barnhart ◽  
R.M. Wilkins ◽  
J.M. Lusher
Keyword(s):  
Vessel Wall ◽  
Ex Vivo ◽  
Umbilical Vein ◽  
Vein Wall ◽  
Qualitative And Quantitative ◽  
Perfusion Model ◽  
Vascular Defect ◽  
Umbilical Cords ◽  
Wall Interactions ◽  
Scanning Electron

Adhesion of von willehrand (vW) platelets (P) from 12 patients was tested in an ex vivo human umbilical vein perfusion model. Experiments (42) employed twelve umbilical cords from Caesarian sections and P (fetal, adult and vW) either washed (with apyrase protection) or used as P rich plasma or whole blood. FVIII antigen (FVIII:ag), Ristocetin co-factor (RCF) and FVIII procoagulant were measured in blood and umbilical vein effluents. Either hypoxia or epinephrine pretreatment of vein released FVIII:ag and RCF into perfusates. Binding of a marker (latex linked anti-human FVIII:ag) demonstrated that FVIII:ag became exposed at endothelial surfaces. Scanning electron microscopy displayed vWP-vessel interactions. Although vWP adhered to injured vein wall, both qualitative and quantitative differences existed which related to the plasma RCF level. The vWP were less adhesive to exposed subendothelium than were control fetal or adult P. The vWP had less surface activity, spreading and fewer pseudopods. Vein pretreatment with FVIII antibody partly blocked P adhesion. Perfusion of cryoprecipitate with vWP improved their adhesion, activation and aggregation. These observations further establish the model's utility and validity for studies aimed at discovering the nature and extent of the vascular defect in various P disorders. The model seems especially well suited for testing impacts of P and/or endothelial cell reactive agents on platelet-vessel wall interactions.

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