Characteristics of reactivity change as fuel debris falls in water

2021 ◽  
Vol 139 ◽  
pp. 103857
Author(s):  
Takeshi Muramoto ◽  
Jun Nishiyama ◽  
Toru Obara
Keyword(s):  
2004 ◽  
Vol 287 (6) ◽  
pp. H2510-H2517 ◽  
Author(s):  
S. Krishnamurthy ◽  
X. Wang ◽  
D. Bhakta ◽  
E. Bruce ◽  
J. Evans ◽  
...  

In 28 healthy adults, we compared the dynamic interaction between respiration and cerebral autoregulation in 2 groups of subjects: those who did and did not develop presyncopal symptoms during 70° passive head-up tilt (HUT), i.e., nonpresyncopal (23 subjects) and presyncopal (5 subjects). Airflow, CO2, cerebral blood flow velocity (CBF), ECG, and blood pressure (BP) were recorded. To determine whether influences of mean BP (MBP) and systolic SP (SBP) on CBF were altered in presyncopal subjects, coherencies and transfer functions between these variables and mean and peak CBF (CBFm and CBFp) were estimated. To determine the influence of end-tidal CO2 (ETco2) on CBF, the relative CO2 reactivity (%change in CBFm per mmHg change in ETco2) was calculated. We found that in presyncopal subjects before symptoms during HUT, coherence between SBP and CBFp was higher ( P = 0.02) and gains of transfer functions between BP (MBP and SBP) and CBFm were larger (MBP, P = 0.01; SBP, P = 0.01) in the respiratory frequency region. In the last 3 min before presyncope, presyncopals had a reduced relative CO2 reactivity ( P = 0.005), likely a consequence of the larger decrease in ETco2. We hypothesize that the CO2-mediated increase in resistance attenuates autoregulation such that the relationship between systemic and cerebral hemodynamics is enhanced. Our results suggest that an altered cardiorespiratory interaction involving cerebral hemodynamics may contribute in the cascade of events during tilt that culminate in unexplained syncope.


Author(s):  
S. Lu

As the result of the advancing TCP/IP based inter-process communication technology, more and more legacy thermal-hydraulic codes have been coupled with neutronics codes to provide best-estimate capabilities for reactivity related reactor transient analysis. Most of the coupling schemes are based on closely coupled serial or parallel approaches. Therefore, the execution of the coupled codes usually requires significant CPU time, when a complicated system is analyzed. Leap Frog scheme has been used to reduce the run time. The extent of the decoupling is usually determined based on a trial and error process for a specific analysis. It is the intent of this paper to develop a set of general criteria, which can be used to invoke the automatic Leap Frog algorithm. The algorithm will not only provide the run time reduction but also preserve the accuracy. The criteria will also serve as the base of an automatic time step sub-cycle scheme when a sudden reactivity change is introduced and the thermal-hydraulic code is marching with a relatively large time step.


2013 ◽  
Vol 125 (45) ◽  
pp. 12091-12094 ◽  
Author(s):  
Naoki Ishida ◽  
Yuuta Nakanishi ◽  
Masahiro Murakami
Keyword(s):  

1991 ◽  
Vol 11 (4) ◽  
pp. 661-666 ◽  
Author(s):  
R. J. Nelson ◽  
S. Perry ◽  
A. C. R. Burns ◽  
J. Roberts ◽  
J. D. Pickard

Impairment of cerebral autoregulation and development of hyponatraemia are both implicated in the pathogenesis of delayed cerebral ischaemia and infarction following subarachnoid haemorrhage (SAH) but the pathophysiology and interactions involved are not fully understood. We have studied the effects of hyponatraemia and SAH on the cerebral vasomotor responses of the rabbit. Cerebrovascular reactivity to hypercapnia and cerebral autoregulation to trimetaphan-induced hypotension were determined in normal and hyponatraemic rabbits before and 6 days after experimental SAH produced by two intracisternal injections of autologous blood. Hyponatraemia (mean plasma sodium of 119 m M) was induced gradually over 48 h by administration of Desmopressin and intraperitoneal 5% dextrose. Sham animals received normal saline. The cerebrovascular reactivity (% change ±SD in cortical CBF/mm Hg PaCO2, measured by hydrogen clearance) of hyponatraemic (4.8 ± 3.0%) and SAH (1.3 ± 2.0%) animals was significantly less ( p < 0.05) than control (11.6 ± 4.0%) and sham (8 ± 2.0%) animals, whereas the reactivity of hyponatraemic-SAH animals was preserved (9.8 ± 6.0%). Hyponatraemia and SAH alone each significantly impaired CBF autoregulation but their combined effects were not additive. Systemic hyponatraemia impairs normal cerebral vasomotor responses but does not augment the effects of experimental SAH in the rabbit.


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