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Phase-Related Sensitivity of the Sinoatrial Node to Vagal Stimuli in the Isolated Rat Atrium

In isolated rat atria, endogenous neurotransmitters were released by electrical pulses that were below threshold for activation of the myocardial cells. A brief train of pulses was delivered at a specified time after each atrial activation to determine the relationship between the time of stimulus d...

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Bibliographic Details
Published in:Circulation research 1978-08, Vol.43 (2), p.217-224
Main Authors: STUESSE, SHERRY L, LEVY, MATTHEW N, ZIESKE, HARRISON
Format: Article
Language:English
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Summary:In isolated rat atria, endogenous neurotransmitters were released by electrical pulses that were below threshold for activation of the myocardial cells. A brief train of pulses was delivered at a specified time after each atrial activation to determine the relationship between the time of stimulus delivery during an atrial cycle (P-St interval) and the subsequent cardiac cycle length (P-P interval). These stimuli caused a change in P-P interval from a mean control level of 291 msec to a mean maximum P-P interval of 592 msec. This change was attributed to the release of neurotransmitters from sympathetic and parasympathetic fibers, but the effects from the parasympathetic nerve terminals predominated. Increasing the number of pulses per burst increased the atrial slowing. The extent of slowing was dependent on the time of stimulus delivery in an atrial cycle. The region of minimal effectiveness (mean P-P interval of 412 msec during stimulation) was obtained with P-St intervals that were only slightly greater (about 10 msec) than those that were maximally effective. Stimuli delivered at times in the cardiac cycle that fell between the P-St intervals that elicited maximum and minimum changes in heart rate occasionally caused profound irregularities in heart rate. These changes in cycle length do not appear to be due to pacemaker shifts, but are probably the result of the interaction between acetylcholine and the sinoatrial nodal cell membrane. The responsiveness of this membrane to acetylcholine changes with time during the cardiac cycle.
ISSN:0009-7330
1524-4571
DOI:10.1161/01.RES.43.2.217