Kinetics of Almitrine Bismesylate and its Metabolites in the Carotid Body and Other Tissues of the Rat

Author(s):  
B. H. Gordon ◽  
D. J. Pallot ◽  
A. Mir ◽  
R. M. J. Ings ◽  
Y. Evrard ◽  
...  
1990 ◽  
pp. 199-206 ◽  
Author(s):  
P. C. G. Nye ◽  
D. L. Maxwell ◽  
P. G. Quirk ◽  
C. Cook

1998 ◽  
Vol 53 (2) ◽  
pp. 330-339 ◽  
Author(s):  
J. R. López-López ◽  
M. T. Pérez-García ◽  
E. Canet ◽  
C. Gonzalez

1997 ◽  
Vol 78 (5) ◽  
pp. 2388-2395 ◽  
Author(s):  
Machiko Shirahata ◽  
Robert S. Fitzgerald ◽  
James S. K. Sham

Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham. Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]i was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]i in ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]i was dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]i in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]i of cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+ influx via nicotinic channels. In addition, other pathways such as Ca2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+ release from intracellular stores may participate in increasing [Ca2+]i in response to ACh. Muscarinic receptors appear to play only a small role, if any.


Author(s):  
R. G. O’Regan ◽  
M. Kennedy ◽  
A. W. Przybyszewski

1990 ◽  
pp. 207-211
Author(s):  
M. Kennedy ◽  
S. Ennis ◽  
R. G. O’Regan ◽  
Y. Evrard

Author(s):  
J. F. DeNatale ◽  
D. G. Howitt

The electron irradiation of silicate glasses containing metal cations produces various types of phase separation and decomposition which includes oxygen bubble formation at intermediate temperatures figure I. The kinetics of bubble formation are too rapid to be accounted for by oxygen diffusion but the behavior is consistent with a cation diffusion mechanism if the amount of oxygen in the bubble is not significantly different from that in the same volume of silicate glass. The formation of oxygen bubbles is often accompanied by precipitation of crystalline phases and/or amorphous phase decomposition in the regions between the bubbles and the detection of differences in oxygen concentration between the bubble and matrix by electron energy loss spectroscopy cannot be discerned (figure 2) even when the bubble occupies the majority of the foil depth.The oxygen bubbles are stable, even in the thin foils, months after irradiation and if van der Waals behavior of the interior gas is assumed an oxygen pressure of about 4000 atmospheres must be sustained for a 100 bubble if the surface tension with the glass matrix is to balance against it at intermediate temperatures.


Author(s):  
R. J. Lauf

Fuel particles for the High-Temperature Gas-Cooled Reactor (HTGR) contain a layer of pyrolytic silicon carbide to act as a miniature pressure vessel and primary fission product barrier. Optimization of the SiC with respect to fuel performance involves four areas of study: (a) characterization of as-deposited SiC coatings; (b) thermodynamics and kinetics of chemical reactions between SiC and fission products; (c) irradiation behavior of SiC in the absence of fission products; and (d) combined effects of irradiation and fission products. This paper reports the behavior of SiC deposited on inert microspheres and irradiated to fast neutron fluences typical of HTGR fuel at end-of-life.


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