scholarly journals Effects of Temperature on the Action Potential of Toad Ventricular Muscle Fiber and on Its Recovery Process

1960 ◽  
Vol 24 (1) ◽  
pp. 1-10
Author(s):  
BUNJIRO ONO ◽  
KEITA SUEKANE ◽  
FUYUO MAEKAWA
Author(s):  
Joachim R. Sommer ◽  
Teresa High ◽  
Betty Scherer ◽  
Isaiah Taylor ◽  
Rashid Nassar

We have developed a model that allows the quick-freezing at known time intervals following electrical field stimulation of a single, intact frog skeletal muscle fiber isolated by sharp dissection. The preparation is used for studying high resolution morphology by freeze-substitution and freeze-fracture and for electron probe x-ray microanlysis of sudden calcium displacement from intracellular stores in freeze-dried cryosections, all in the same fiber. We now show the feasibility and instrumentation of new methodology for stimulating a single, intact skeletal muscle fiber at a point resulting in the propagation of an action potential, followed by quick-freezing with sub-millisecond temporal resolution after electrical stimulation, followed by multiple sampling of the frozen muscle fiber for freeze-substitution, freeze-fracture (not shown) and cryosectionmg. This model, at once serving as its own control and obviating consideration of variances between different fibers, frogs etc., is useful to investigate structural and topochemical alterations occurring in the wake of an action potential.


1960 ◽  
Vol 198 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
Chandler McC. Brooks ◽  
Jerome L. Gilbert ◽  
Martin E. Greenspan ◽  
Gertrude Lange ◽  
Hector M. Mazzella

Measurements were made of the changes in the monophasic action potential, excitability, durations of the refractory periods and conduction times in an area of left ventricular muscle during the development of ischemia subsequent to ligation of the ramus descendens anterior. The degree and duration of the ischemia produced varied greatly and effects were related thereto. It was found that action potentials shortened as did the refractory periods; thresholds fell momentarily and then rose progressively as tissue responsiveness failed due to continuing ischemia. Latency of responses increased, the action potentials decreased in amplitude and alternation occurred before the tissue became completely unresponsive. Early re-establishment of a blood supply caused a reversal of the abnormalities. The significance of these changes to the origin of arrhythmias is discussed.


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