Der Einfluß von Infarktgröße und Spontankollateralen auf die Flimmerschwelle des Herzens nach akutem experimentellem Koronarverschluß

Schley, Gunnar; Meesmann, W.; Wild, Ursula; Wild, A.

doi:10.1007/978-3-642-85288-6_38

Cited by 5 publications

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“…Many investigations are congruous with each other in the finding that there is a rapid decrease in the ventricular fibrillation threshold (VFT) of the heart following acute coronary occlusion (3,5,6,9,10,16,27,28,34,46,48,55,58,65,70,71,76,79,92). Under constant experimental conditions the extent of decrease in VFT depends on a constellation of biological variables which, for instance, include the extent of the collateral vessels of the heart (58,70), the mass of the infarcted tissue (6, 71), the status in vagal or sympathetic tone (38,47,48) and finally the occluding mode (acute VFT is followed by a slower increase up to the pre-infarction control value within 20-30 min (3,5,10,16,27,58,65) corresponding to the end of the 1st phase of arrhythmia according to Harris (36).…”

Section: Discussionmentioning

confidence: 99%

Changes in ventricular fibrillation threshold during repeated short-term coronary occlusion and release

et al. 1977

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The time course of changes in VFT was determined during the 1st phase of arrhythmia following coronary occlusion and during consecutive reperfusion in five repeated periods of occlusion and reperfusion in 10 mongrel dogs (17--24 kg). VFT was determined using a square wave pulse series of 140 ms duration which was triggered by the R-wave of the ECG and placed into the vulnerable period of the cardiac cycle. After acute occlusion VFT decreased to a minimum level within a few minutes and then increased again slowly up to the control value which was reached about 20 min after the ligation. When the occlusions were repeated several times the extent of the decrease in VFT became increasingly less and its duration increasingly shorter until finally there was no significant decrease in VFT. Reperfusion after coronary occlusion led to an abrupt decrease in VFT within 1 min, followed by a rapid increase to the control value. This time course did not depend upon the number of prior occlusions. The results show that in the case of repeating short-term coronary occlusions one cannot expect comparable VFT time courses for the consecutive periods of occlusion except for the 1st and 2nd ones. Differing mechanisms leading to the occurrence of VF after coronary ligation and during reperfusion are discussed.

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