scholarly journals The effect of procaine amide on components of excitability in long mammalian cardiac Purkinje fibers.

1976 ◽  
Vol 38 (2) ◽  
pp. 115-122 ◽  
Author(s):  
M F Arnsdorf ◽  
J T Bigger
1994 ◽  
Vol 80 (6) ◽  
pp. 1360-1368 ◽  
Author(s):  
David F. Stowe ◽  
Juraj Sprung ◽  
Lawrence A. Turner ◽  
John P. Kampine ◽  
Zeljko J. Bosnjak

1976 ◽  
Vol 231 (5) ◽  
pp. 1415-1420 ◽  
Author(s):  
P Posner ◽  
EL Farrar ◽  
CR Lambert

The effect of catecholamines over a wide range of concentrations was studied on 42K uptake and efflux, as well as on spontaneous rate in canine cardiac Purkinje fibers. Low levels of catecholamines (less than 10(-10) M epinephrine; less than 10(-9) M norepinephrine) decreased automaticity. This negative chronotropic effect was blocked by phentolamine and mimicked by phenylephrine. These low levels of epinephrine and norepinephrine also inhibited 42K uptake by Purkinje fibers but had no effect on 42K efflux. The inhibition of 42K uptake was blocked by phentolamine and verapamil and mimicked by phenylephrine. The data indicate an alpha-receptor-mediated negative response of rate and 42K uptake to low levels of catecholamine. The end result is discussed in terms of a competitive increase in the influx of Ca2+ rather than Na+ and an indirect inhibition of the Na+-K+ pump.


1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.


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