THE EFFECT OF ACETYLCHOLINE ON ADRENALINE-INDUCED SUBATRIAL RHYTHMS IN THE SENSITIZED CAT HEART

1964 ◽  
Vol 42 (4) ◽  
pp. 431-445 ◽  
Author(s):  
Don P. MacLeod ◽  
A. K. Reynolds

Acetylcholine has been shown to be an effective antiarrhythmic agent against arrhythmias induced by adrenaline in combination with the myocardial sensitizers petroleum ether, halothane, and harman methosulphate. It has also been shown that acetylcholine will reduce or prevent the increase in ventricular automaticity produced by adrenaline in the intact cat and in the isolated papillary muscle of the cat. All of these actions of acetylcholine can be blocked by atropine. Evidence from experiments in which petroleum ether inhalation was begun after an arrhythmia had been induced by adrenaline indicated that petroleum ether was causing an increase in ventricular automaticity. The results appear to support the idea that petroleum ether and possibly other sensitizers interfere with the stabilizing action of endogenous acetylcholine on the ventricle and allow the stimulating action of adrenaline to produce severe prefibrillatory rhythms by an increase in ventricular automaticity.

1997 ◽  
Vol 29 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Csaba Pankucsi ◽  
Tamás Bányász ◽  
János Magyar ◽  
Ildikó Gyönös ◽  
Anikó Kovács ◽  
...  

1949 ◽  
Vol 156 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Solomon Garb ◽  
Maynard B. Chenoweth
Keyword(s):  

1965 ◽  
Vol 48 (5) ◽  
pp. 933-948 ◽  
Author(s):  
Jon Goerke ◽  
Ernest Page

The exchange of cell K with K42, JK, has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. JK increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, PK, calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. JK is not affected by replacement of O2 by N2, or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10-5 M and 10-8 M ouabain.


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