Spatial and Temporal Inhomogeneity of Adenosine's Effect on Atrial Refractoriness in Humans:.

1994 ◽  
Vol 5 (6) ◽  
pp. 477-484 ◽  
Author(s):  
GREGORY W. BOTTERON ◽  
JOSEPH M. SMITH
2021 ◽  
Vol 13 (13) ◽  
pp. 2489
Author(s):  
Lanlan Rao ◽  
Jian Xu ◽  
Dmitry S. Efremenko ◽  
Diego G. Loyola ◽  
Adrian Doicu

To retrieve aerosol properties from satellite measurements, micro-physical aerosol models have to be assumed. Due to the spatial and temporal inhomogeneity of aerosols, choosing an appropriate aerosol model is an important task. In this paper, we use a Bayesian algorithm that takes into account model uncertainties to retrieve the aerosol optical depth and layer height from synthetic and real TROPOMI O2A band measurements. The results show that in case of insufficient information for an appropriate micro-physical model selection, the Bayesian algorithm improves the accuracy of the solution.


Circulation ◽  
2002 ◽  
Vol 106 (11) ◽  
pp. 1410-1419 ◽  
Author(s):  
Akira Miyata ◽  
Douglas P. Zipes ◽  
Stephen Hall ◽  
Michael Rubart

1988 ◽  
Vol 233 (1273) ◽  
pp. 461-475 ◽  

The question is raised as to whether competitive inhibitors should block responses of tissue to nerve-released neurotransmitter to the same extent as they block equivalent responses to exogenous agonist. From a simple dynamic model of synaptic events, which takes into account non-constancy of transmitter concentration in space and time, it is deduced that equal blockade of responses to nerve-released and exogenous transmitter substance will occur if: (i) there are locally many more receptor molecules than transmitter molecules; (ii) the active agonist–receptor complex, A n R, has n = 1 ; and (iii) tissue response is insensitive to spatial or temporal inhomogeneity of AR. In such a case there will also be equal sensitivity of responses to other modes of inhibition: irreversible competitive, uncompetitive, and non-competitive. Equal blockade of responses to equi-effective endogenous and exogenous agonist will also occur if nerve stimulation gives rise to a steady uniform concentration of agonist, so that equilibrium kinetics are applicable. When n > 1 and/or when tissue responses reflect local peak A n R, response to nerve-released transmitter will be relatively insensitive to receptor blockade by a competitive inhibitor. The same is true for irreversible competitive blockade or for modulation of receptor density. However, an uncompetitive inhibitor (e. g. a ‘channel blocker’) may be more effective against nerve-released agonist than against exogenous agonist.


2002 ◽  
Vol 13 (2) ◽  
pp. 151-157 ◽  
Author(s):  
CHRISTIAN STICHERLING ◽  
WILLIAM HSU ◽  
HIROSHI TADA ◽  
ANTON C. BARES ◽  
HAKAN ORAL ◽  
...  

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S80-S80
Author(s):  
O J Arias-Mutis ◽  
C J Calvo ◽  
A Bizy ◽  
L Such-Miquel ◽  
C Soler ◽  
...  

1977 ◽  
Vol 233 (1) ◽  
pp. H44-H49
Author(s):  
S. Teague ◽  
P. Denes ◽  
F. Amat-y-Leon ◽  
K. M. Rosen

The effect of anomalous pathway (AP) location and conduction time on the cycle length (CL) and sustainability of paroxysmal A-V reentrant tachycardia was studied in 15 dogs, using an anomalous pathway simulator (APS). The APS was a programmable digital electronic circuit with ability for unidirectional conduction, ventricular sensing, adjustable delay, and atrial stimulation. Contiguous pairs of ventricular sensing electrodes were placed along the A-V ring in each dog at the following sites: anterior, posterior, and lateral right (AR, PR, and LR) and anterior, posterior, and lateral left (AL, PL, and LL) and septal (S). There were significant differences in the CL of tachycardias among the tested sites (P less than 0.01). The CL of tachycardias from the LL site was significantly longer and from the PR site significantly shorter than that from the other sites (P less than 0.05). These differences in CL of tachycardias in relation to the AP location were explicable in terms of corresponding variation in conduction times of the various components of the tachycardia circuit (e.g., intra-atrial, A-V nodal, intraventricular conduction times). The differences in magnitude of the CL of tachycardias, although significant, were small. It was also found that all sites allowed maintenance of tachycardias up to an AP conduction time of 10 ms. In 27% of experiments, atrial refractoriness prevented sustained tachycardias at pathway delays of 1 ms. The relationship between AP conduction time and CL of tachycardias was exponential.


2011 ◽  
Vol 57 (3) ◽  
pp. 302-307 ◽  
Author(s):  
Jeff Bechard ◽  
John Ken Gibson ◽  
Cheryl R Killingsworth ◽  
Jeffery J Wheeler ◽  
Marlowe J Schneidkraut ◽  
...  

1995 ◽  
Vol 25 (2) ◽  
pp. 64A-65A
Author(s):  
Duane P. Pool ◽  
Harvey L. Leo ◽  
George Nadzam ◽  
Patrick J. Tchou ◽  
Patrick M. McCarthy ◽  
...  

1981 ◽  
Vol 47 ◽  
pp. 496 ◽  
Author(s):  
Eric N. Prystowsky ◽  
Gerald V. Naccarelli ◽  
Warren M. Jackman ◽  
Robert L. Rinkenberger ◽  
James J. Heger ◽  
...  

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