Interacting effects of Ca2+ and hypoxia in the induction of sarcolemmal damage in mouse diaphragm in vitro

1995 ◽  
Vol 90 (4) ◽  
pp. 411-414 ◽  
Author(s):  
N. J. Bannister ◽  
S. J. Publicover



1972 ◽  
Vol 50 (3) ◽  
pp. 279-284 ◽  
Author(s):  
D. M. J. Quastel ◽  
J. T. Hackett ◽  
K. Okamoto

Chlorpromazine, like raised osmotic pressure, not only increases spontaneous miniature endplate potential frequency (F) in mouse diaphragm (in vitro) but also depresses the slope of log F versus focal presynaptic depolarization. It also depresses the slope of log F versus [Ca], in raised K+ (constant depolarization). Similar effects are seen with pentobarbital, chloral hydrate, chloroform, and lowered pH. The drugs have similar actions in locust muscle, where the transmitter is not acetylcholine.



1966 ◽  
Vol 22 (4) ◽  
pp. 241-242
Author(s):  
A. J. Moody ◽  
J. P. Felber


2008 ◽  
Vol 40 (Supplement) ◽  
pp. S76
Author(s):  
Leonardo F. Ferreira ◽  
Laura A. Ashley ◽  
Michael B. Reid


1973 ◽  
Vol 248 (18) ◽  
pp. 6450-6455
Author(s):  
Thomas R. Riggs ◽  
K. Janet McKirahan




1970 ◽  
Vol 48 (5) ◽  
pp. 291-298
Author(s):  
J. Pierluissi ◽  
J. Campbell ◽  
K. S. Rastogi ◽  
G. R. Green ◽  
V. Lazdins

The relation of insulinase activity to the biological effect of insulin on isolated tissue was studied. Rat diaphragm in vitro caused the rapid disappearance of immunoreactive insulin (IRI) in physiological concentrations. IRI loss at time intervals was exponential. The fractional rate of loss of IRI was therefore independent of IRI concentration and was also approximately constant per milligram of tissue, the value being 0.0216%/mg∙mm. The value of the Michaelis constant (Km), obtained from initial velocities at five initial concentrations of IRI, was 1.85 × 10−8M, and of the maximal velocity (Vmax) was 2.32 × 10−11 mole/g∙min, based on insulin dimer. The addition of an insulinase inhibitor (a partial hydrolysate of insulin) to hemidiaphragm in vitro reduced the fractional rate of IRI loss by 60%. The increase in Km, without appreciable change in Vmax, indicated that the inhibition was competitive. The IRI preserved by means of the inhibitor was biologically active, since it increased the glycogen accumulation and the incorporation of 14C-U-glucose into glycogen in a second, fresh hemidiaphragm. In single incubation of hemidiaphragm with insulin, the gain in glycogen was correlated with the amount of inhibitor. The biological effect of insulin on diaphragm in vitro was therefore limited by tissue insulinase activity, and insulinase inhibitor potentiated to some extent the action of insulin.



1957 ◽  
Vol 11 ◽  
pp. 1078-1079 ◽  
Author(s):  
Aa. Rye Alertsen ◽  
O. Walaas ◽  
E. Walaas ◽  
K. E. Almin ◽  
Arne Magnéli ◽  
...  


1960 ◽  
Vol 40 ◽  
pp. 562-563 ◽  
Author(s):  
Otto Walaas ◽  
Borgar Borrebæk ◽  
Tore Kristiansen ◽  
Eva Walaas


1990 ◽  
Vol 69 (4) ◽  
pp. 1390-1396 ◽  
Author(s):  
E. Derom ◽  
S. Janssens ◽  
V. De Bock ◽  
M. Decramer

We examined the effects of theophylline on contractile properties and high-frequency fatigue of canine diaphragm in vitro. Eighteen diaphragm muscle bundles were obtained from 10 anesthetized dogs and equilibrated in oxygenated Krebs solution to 100, 200, or 300 mg/l theophylline. These bundles were compared with 18 matched control bundles from the contralateral hemidiaphragm. No statistically significant differences in twitch tension, tetanic tension, twitch-to-tetanus ratio, time to peak tension, or half-relaxation time were observed. Concentrations of 300 mg/l theophylline, however, significantly (P less than 0.05) increased force production at 10 Hz by 32%. A similar tendency was present at lower concentrations and exhibited a clear dose-response behavior. High-frequency fatigue was similar in control and theophylline-treated bundles. We conclude that supratherapeutic in vitro concentrations of theophylline do not increase maximal tetanic tension and do not protect against muscle fatigue but potentiate relative force production at low stimulation frequencies. This relatively small effect cannot be explained by poor diffusion of the drug in the muscle bundle, because theophylline concentrations in the muscle bath and in the muscle bundle were virtually identical. Moreover, it remains unclear whether this potentially beneficial effect can be achieved at in vivo attainable serum concentrations.



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