Hepatosplanchnic Vasoregulation and Oxygen Consumption During Selective Aortic Blood Flow Reduction and Reperfusion

2011 ◽  
Vol 171 (2) ◽  
pp. 532-539 ◽  
Author(s):  
Ruy J. Cruz ◽  
Alejandra G. Garrido ◽  
Décio de Natale Caly ◽  
Mauricio Rocha-e-Silva
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Aortic Blood Flow ◽  
Flow Reduction ◽  
Aortic Blood ◽  
Blood Flow Reduction

scholarly journals Changes in regional blood flow and pCO2 gradients during isolated abdominal aortic blood flow reduction

2003 ◽  
Vol 29 (12) ◽  
pp. 2255-2265 ◽  
Author(s):  
Rafael Knuesel ◽  
Stephan M. Jakob ◽  
Lukas Brander ◽  
Hendrik Bracht ◽  
Andreas Siegenthaler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Aortic Blood Flow ◽  
Flow Reduction ◽  
Aortic Blood ◽  
Blood Flow Reduction ◽  
Abdominal Aortic

Failure of acute saralasin to reverse chronic hypertension in fetal lambs

1991 ◽  
Vol 260 (4) ◽  
pp. R811-R816
Author(s):  
D. F. Anderson ◽  
N. D. Binder
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Upper Body ◽  
Chronic Hypertension ◽  
Aortic Blood Flow ◽  
Flow Reduction ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Blood Flow Reduction

Upper body arterial hypertension developed in 12 fetal lambs after chronic suprarenal aortic blood flow reduction. Sixty minutes after blood flow reduction, intravenous saralasin infusion was able to reduce upper body mean arterial blood pressure to control levels. Although saralasin infusion was able to decrease upper body arterial blood pressure after 1 day of hypertension, it was not able to return blood pressure to control levels. Three or more days later, saralasin was unable to cause a significant reduction in upper body arterial blood pressure. We conclude that, although the renin-angiotensin system has a role in maintaining the elevated blood pressure after greater than or equal to 1 day of suprarenal aortic blood flow reduction, some other mechanism also participates. We have ruled out a role for changing blood volume, and our results suggest that an elevation of plasma catecholamines is not responsible. Some other pathway for fluid regulation available to the fetus may be responsible.

scholarly journals Famotidine prevents canine gastric blood flow reduction by NSAIDs

2005 ◽  
Vol 21 (s2) ◽  
pp. 55-59 ◽  
Author(s):  
J. Hata ◽  
T. Kamada ◽  
N. Manabe ◽  
H. Kusunoki ◽  
D. Kamino ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gastric Blood Flow ◽  
Flow Reduction ◽  
Blood Flow Reduction

COMPUTATIONS OF PULSATILE AORTIC BLOOD FLOW PROBLEMS ON PARALLEL COMPUTERS

2003 ◽  
Vol 15 (03) ◽  
pp. 109-114
Author(s):  
YANG-YAO NIU ◽  
SHOU-CHENG TCHENG
Keyword(s):  
Blood Flow ◽  
Stokes Equations ◽  
Computing Time ◽  
Time Integration ◽  
Parallel Computer ◽  
Aortic Blood Flow ◽  
Pc Cluster ◽  
Flow Problems ◽  
Aortic Blood ◽  
Speed Up

In this study, a parallel computing technology is applied on the simulation of aortic blood flow problems. A third-order upwind flux extrapolation with a dual-time integration method based on artificial compressibility solver is used to solve the Navier-Stokes equations. The original FORTRAN code is converted to the MPI code and tested on a 64-CPU IBM SP2 parallel computer and a 32-node PC Cluster. The test results show that a significant reduction of computing time in running the model and a super-linear speed up rate is achieved up to 32 CPUs at PC cluster. The speed up rate is as high as 49 for using IBM SP2 64 processors. The test shows very promising potential of parallel processing to provide prompt simulation of the current aortic flow problems.

S-nitroso-albumin carries a thiol-labile pool of nitric oxide, which causes venodilation in the rat

2005 ◽  
Vol 289 (2) ◽  
pp. H916-H923 ◽  
Author(s):  
Nelson N. Orie ◽  
Patrick Vallance ◽  
Dean P. Jones ◽  
Kevin P. Moore
Keyword(s):  
Nitric Oxide ◽  
Molecular Weight ◽  
Blood Flow ◽  
Vascular Function ◽  
Low Molecular Weight ◽  
Aortic Blood Flow ◽  
Hemodynamic Effects ◽  
Rapid Decomposition ◽  
Aortic Blood

It is now established that S-nitroso-albumin (SNO-albumin) circulates at low nanomolar concentrations under physiological conditions, but concentrations may increase to micromolar levels during disease states (e.g., cirrhosis or endotoxemia). This study tested the hypothesis that high concentrations of SNO-albumin observed in some diseases modulate vascular function and that it acts as a stable reservoir of nitric oxide (NO), releasing this molecule when the concentrations of low-molecular-weight thiols are increased. SNO-albumin was infused into rats to increase the plasma concentration from <50 nmol/l to ∼4 μmol/l. This caused a 29 ± 6% drop in blood pressure, 20 ± 4% decrease in aortic blood flow, and a 25 ± 14% reduction of renal blood flow within 10 min. These observations were in striking contrast to those of an infused arterial vasodilator (hydralazine), which increased aortic blood flow, and suggested that SNO-albumin acts primarily as a venodilator in vivo. This was confirmed by the observations that glyceryl trinitrate (a venodilator) led to similar hemodynamic changes and that the hemodynamic effects of SNO-albumin are reversed by infusion of colloid. Infusion of N-acetylcysteine into animals with artificially elevated plasma SNO-albumin concentrations led to the rapid decomposition of SNO-albumin in vivo and reproduced the hemodynamic effects of SNO-albumin infusion. These data demonstrate that SNO-albumin acts primarily as a venodilator in vivo and represents a stable reservoir of NO that can release NO when the concentrations of low-molecular-weight thiols are elevated.

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