Engineering functional microvessels in synthetic polyurethane random-pore scaffolds by harnessing perfusion flow

Biomaterials ◽  
2020 ◽  
Vol 256 ◽  
pp. 120183
Author(s):  
Meghan EE. Wright ◽  
Jonathan K. Yu ◽  
Devika Jain ◽  
Azusa Maeda ◽  
Shu-Chi A. Yeh ◽  
...  
Keyword(s):  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Satoshi Miyamoto ◽  
Zu Soh ◽  
Shigeyuki Okahara ◽  
Akira Furui ◽  
Taiichi Takasaki ◽  
...  

AbstractThe need for the estimation of the number of microbubbles (MBs) in cardiopulmonary bypass surgery has been recognized among surgeons to avoid postoperative neurological complications. MBs that exceed the diameter of human capillaries may cause endothelial disruption as well as microvascular obstructions that block posterior capillary blood flow. In this paper, we analyzed the relationship between the number of microbubbles generated and four circulation factors, i.e., intraoperative suction flow rate, venous reservoir level, continuous blood viscosity and perfusion flow rate in cardiopulmonary bypass, and proposed a neural-networked model to estimate the number of microbubbles with the factors. Model parameters were determined in a machine-learning manner using experimental data with bovine blood as the perfusate. The estimation accuracy of the model, assessed by tenfold cross-validation, demonstrated that the number of MBs can be estimated with a determinant coefficient R2 = 0.9328 (p < 0.001). A significant increase in the residual error was found when each of four factors was excluded from the contributory variables. The study demonstrated the importance of four circulation factors in the prediction of the number of MBs and its capacity to eliminate potential postsurgical complication risks.


Author(s):  
Mark George ◽  
Jaime Tierney ◽  
Adam Luchies ◽  
Shannon Faley ◽  
Kathryn Ozgun ◽  
...  
Keyword(s):  

1978 ◽  
Vol 234 (5) ◽  
pp. R201-R208 ◽  
Author(s):  
C. M. Wood ◽  
B. R. McMahon ◽  
D. G. McDonald

A whole trout preparation (Salmo gairdneri) externally ventilated with water and internally perfused with artificial medium via a cardiac pump is discribed for the study of O2 exchange and vascular resistance. As cardiac output (Q) was raised, ventral and dorsal aortic pressures increased while branchial (Rg) and systemic (Rs) vascular resistances fell, reflecting considerable passive distensibility. Arterial oxygenation was negative at low Qs due to significant internal O2 demand by the gill tissue, but increased to zero or positive values at intermediate Qs, and eventually declined at high Qs because of transit time limitation. O2 uptake from the ventilatory flow rose with increasing Q. Epinephrine (10(-5) M) decreased Rg, increased Rs, and enhanced arterial oxygenation. Artificial elevation of dorsal aortic pressure decreased Rg but did not affect arterial oxygenation. A 10-fold elevation of ventilatory flow increased arterial oxygenation but did not alter Rg or Rs. Endogenous metabolism of branchial tissue accounted for 11.7% of resting O2 uptake in vivo, and comprised an internal component taking O2 from perfusion flow and an external component drawing O2 from ventilatory flow.


1991 ◽  
Vol 261 (5) ◽  
pp. F779-F786 ◽  
Author(s):  
J. Radermacher ◽  
B. Klanke ◽  
S. Kastner ◽  
G. Haake ◽  
H. J. Schurek ◽  
...  

The effect of L-Arg depletion on glomerular hemodynamics and tubular function of isolated rat kidneys perfused with a medium containing 21 amino acids has been studied. A cyclooxygenase inhibitor was added throughout for blockade of prostaglandin synthesis. Arg depletion caused significant (approximately 30%) reductions in renal perfusion flow rate (PFR, 13.9 +/- 1.2 vs. 19.8 +/- 0.6 ml.min-1.g (kidney wt-1), glomerular filtration rate (GFR, 598 +/- 79 vs. 924 +/- 42 microliters.min-1.g kidney wt-1), and urine flow rate (139 +/- 38 vs. 192 +/- 13 microliters.min-1.g kidney wt-1) compared with control kidneys, which were perfused with a physiological concentration of Arg (200 microM). Filtration fraction (FF) increased with Arg depletion (5.1 +/- 0.4 vs. 4.4 +/- 0.4%). Arg-depleted kidneys had a lower absolute sodium (TNa, 75.7 +/- 8.8 vs. 107.9 +/- 6.0 mumol.min-1.g kidney wt-1) and glucose reabsorption (T glucose, 3.7 +/- 0.6 vs. 5.6 +/- 0.5 mumol.min-1.g kidney wt-1), corresponding to a lower sodium and glucose filtration. Potassium handling and reabsorption of free water were not changed. Oxygen consumption (QO2) was lower in Arg-depleted kidneys (4.6 +/- 0.3 vs. 5.5 +/- 0.5 mumol.min-1.g kidney wt-1). The effects of Arg depletion were completely reversed by the addition of Arg (1 mM) at 120 min and partly reversed by the addition of citrulline (1 mM). Ornithine depletion or addition had no effect on PFR, GFR, FF, TNa, T glucose, and QO2. N omega-methyl-L-arginine, a specific inhibitor of nitric oxide endothelium-derived relaxing factor, produced the same effect as Arg depletion.(ABSTRACT TRUNCATED AT 250 WORDS)


1999 ◽  
Vol 84 (4) ◽  
pp. 651-663 ◽  
Author(s):  
BOHUMÍR STEFL ◽  
JIRÍ A. MEJSNAR ◽  
ALENA JANOVSKÁ

1980 ◽  
Vol 239 (5) ◽  
pp. F427-F432 ◽  
Author(s):  
J. P. Briggs ◽  
J. Schnermann ◽  
F. S. Wright

Experiments were performed in Sprague-Dawley rats in order to distinguish between sodium chloride and total solute concentration as possible luminal signals capable of eliciting tubuloglomerular feedback responses. Early proximal flow rate (VEP), an index of nephron filtration rate, was measured without perfusion of the loop of Henle and during retrograde perfusion with solutions containing 20, 35, 60 to 100 mM NaCl and varying amounts of either urea or mannitol to achieve total solute concentrations of 130, 280, or 400 mosM. Perfusion flow rate was kept constant at 20 nl/min. Perfusion with a solution containing 20 mM NaCl and made hypo-, iso-, or hypertonic with urea or mannitol caused little or no change in VEP. Perfusion with a 35 mM NaCl solution made hypo-, iso-, or hypertonic with mannitol resulted in a fall of VEP of 6-7 nl/min. When NaCl concentration was 60 mM, VEP fell by 10-14 nl/min with solutions made hypo-, iso-, or hypertonic with urea or mannitol. With 100 mM NaCl solutions made hypo-, iso-, or hypertonic with mannitol, VEP fell approximately 12 nl/min. These results indicate that feedback responses are determined by the NaCl concentration of the perfusate and that this NaCl dependency is not modified by varying perfusate osmolarity between 130 and 400 mosM with urea or mannitol as osmotic agents.


2009 ◽  
Vol 17 (2) ◽  
pp. 180-185 ◽  
Author(s):  
Martin W. W. Janssen ◽  
Karl T. Druckrey-Fiskaaen ◽  
Leyla Omidi ◽  
Grzegorz Sliwinski ◽  
Christine Thiele ◽  
...  

1999 ◽  
Vol 84 (4) ◽  
pp. 651-663 ◽  
Author(s):  
Bohumír Štefl ◽  
Jiří A. Mejsnar ◽  
Alena Janovská

2009 ◽  
Vol 297 (5) ◽  
pp. F1256-F1264 ◽  
Author(s):  
Mona Oppermann ◽  
Yan Qin ◽  
En Yin Lai ◽  
Christoph Eisner ◽  
Lingli Li ◽  
...  

Adenosine 1 receptors (A1AR) in the kidney are expressed in the vasculature and the tubular system. Pharmacological inhibition or global genetic deletion of A1AR causes marked reductions or abolishment of tubuloglomerular feedback (TGF) responses. To assess the function of vascular A1AR in TGF, we generated transgenic mouse lines in which A1AR expression in smooth muscle was augmented by placing A1AR under the control of a 5.38-kb fragment of the rat smooth muscle α-actin promoter and first intron ( 12 ). Two founder lines with highest expression in the kidney [353 ± 42 and 575 ± 43% compared with the wild type (WT)] were used in the experiments. Enhanced expression of A1AR at the expected site in these lines was confirmed by augmented constrictor responses of isolated afferent arterioles to administration of the A1AR agonist N6-cyclohexyladenosine. Maximum TGF responses (0–30 nl/min flow step) were increased from 8.4 ± 0.9 mmHg in WT ( n = 21) to 14.2 ± 0.7 mmHg in A1AR-transgene (tg) 4 ( n = 22; P < 0.0001), and to 12.6 ± 1.2 mmHg in A1AR-tg7 ( n = 12; P < 0.02). Stepwise changes in perfusion flow caused greater numerical TGF responses in A1AR-tg than WT in all flow ranges with differences reaching levels of significance in the intermediate flow ranges of 7.5–10 and 10–15 nl/min. Proximal-distal single-nephron glomerular filtration rate (SNGFR) differences (free-flow micropuncture) were also increased in A1AR-tg, averaging 6.25 ± 1.5 nl/min compared with 2.6 ± 0.51 nl/min in WT ( P = 0.034). Basal plasma renin concentrations as well as the suppression of renin secretion after volume expansion were similar in A1AR-tg and WT mice, suggesting lack of transgene expression in juxtaglomerular cells. These data indicate that A1AR expression in vascular smooth muscle cells is a critical component for TGF signaling and that changes in renal vascular A1AR expression may determine the magnitude of TGF responses.


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