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January 1, 1977Circulation Research241 citationsOpen Access

Alterations in canine myocardial excitability during ischemia.

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VEVictor ElharrarPFPeter R. FosterTJT L Jirak

Key Points

  • To evaluate temporal changes in ventricular diastolic excitability thresholds and regional activation conduction patterns during acute coronary artery occlusion.
  • Assessed open-chest anesthetized dogs (N=16) using an automatic threshold-following pacemaker following left anterior descending coronary artery occlusion.

Structured PICO

P
Population
Open-chest anesthetized dogs (n=16)
I
Intervention
Occlusion of the left anterior descending coronary artery (LAD)
C
Comparator
Control conditions (pre-occlusion)
O
Outcome
Changes in ventricular diastolic excitability threshold measured by an automatic threshold-following pacemaker (ATFP)surrogate

During acute myocardial ischemia in a canine model, the ventricular diastolic excitability threshold exhibits a biphasic response, initially decreasing before rapidly increasing, which creates a gradient that influences refractory periods and conduction times.

Abstract

Changes in the ventricular diastolic excitability threshold following occlusion of the left anterior descending coronary artery (LAD) were studied in open-chest anesthetized dogs by using a new automatic threshold-following pacemaker (ATFP). The ATFP measures the diastolic excitability threshold by successively decreasing the duration of regularly occurring pacing stimuli until the ventricle fails to respond. Under control conditions, the threshold stimulus duration was 60 +/- 4 (mean +/- SEM) musec. In the first 1-3 minutes following occlusion of the LAD, the diastolic excitability threshold in the ischemic zone (IZ) decreased to 51 +/- 5 musec and then rapidly increased to 600 musec at 5 minutes. The initial decrease in excitability threshold at IZ could be abolished by elevating the serum K+ concentration prior to the LAD occlusion. These changes in excitability threshold at IZ could be prevented by infusing nonoxygenated solutions into the LAD at a site distal to the occlusion. As the excitability threshold increased in IZ during ischemia, the earliest time at which IZ could be reactivated by a stimulus with a voltage equal to twice the preligation diastolic voltage threshold was increased. In nine of 16 dogs, after 5 minutes of LAD ligation, the IZ to normal zone (NZ( activation time (when stimulating at IZ) exceeded the NZ to IZ activation time (when stimulating at NZ) by an average of 9 msec. We also found that in four dogs the NZ to IZ activation time exceeded the IZ to NZ activation time by an average of 10 msec. We conclude from these findings that a gradient of increasing excitability threshold exists as one moves from normally perfused toward more ischemic tissue, passing through a heterogenous border zone that manifests some areas which have a decreased excitability threshold and other areas which have an increased excitability threshold, and that these changes in excitability importantly influence the determination of refractory period durations and conduction times.

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Cite This Study

Elharrar et al. (1977) studied this question.

synapsesocial.com/papers/6a0fa3f42badbc352afe784fhttps://doi.org/10.1161/01.res.40.1.98
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