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Biomedical subjects

H Zieske

Publications and source records attributed to H Zieske.

At least 19 recordsLinked to original sources
PubMed1990

Insignificant bilateral convergence of preganglionic vagal fibers on postganglionic neurons to the canine heart.

We determined the extent of convergence of preganglionic fibers from the right and left vagus nerves on postganglionic neurons that supply the sinoatrial node in chloralose-anesthetized dogs. We administered hemicholinium-3 and stimulated the right vagus nerve at a high frequency to deplete acetylcholine from the postganglionic parasympathetic neurons supplied by that nerve. We compared the effects of this "depletion regimen" with the responses in two control groups: a stimulation control group, which was subjected to high-frequency right vagus stimulation only, and a drug control group, which received a hemicholinium-3 infusion only. The effects of right vagus stimulation did not differ from those of left vagus stimulation in either of the control groups. In the animals subjected to the depletion regimen, the responses to right vagus stimulation were almost abolished. However, the left vagus nerve retained its ability to prolong cardiac cycle length in these animals. Thus, our experiments indicate that left vagus preganglionic fibers do not converge with right vagus preganglionic fibers on a substantial pool of postganglionic neurons that innervate the canine sinoatrial node.

Acetylcholine↗
PubMed1982

Effects of glucagon on cardiac chronotropic response to vagal stimulation in the dog.

Glucagon accelerates the heart independent of sympathetic nervous system stimulation. The effect of glucagon on the chronotropic responses to repetitive bursts of vagal stimulation was determined in open-chest anesthesized dogs. When the cervical vagi were stimulated at constant frequencies, the change in heart rate was not affected by glucagon administration, i.e., no vagolytic effect caused by glucagon was apparent. Thus glucagon did not alter the reaction of acetylcholine with cardiac postsynaptic receptors. When the vagi were stimulated intermittently with one short burst of vagal stimuli delivered each cardiac cycle, the resultant heart period was dependent on the time of vagal stimulus delivery. Both maximum and minimum cardiac cycle lengths obtained during phasic vagal stimulation were decreased by glucagon. As it has been previously demonstrated that vagal impulses to the heart tend to be clustered during certain times of the cardiac cycle, by accelerating the heart glucagon may shift the cardiac response to vagal stimulation.

Animals↗
PubMed1981

Changes in vagal phasic chronotropic responses with sympathetic stimulation in the dog.

Sympathetic stimulation both shortens the cardiac cycle and potentiates the cardiac response to vagal stimulation. In the present study the effects of sympathetic stimulation on the chronotropic responses of the heart to brief bursts of vagal stimulation were determined in open-chest anesthetized dogs. The sinoatrial nodal pacemaker cells demonstrate a paradoxical response to repetitive bursts of vagal stimuli over a certain portion of the cardiac cycle. That is, the cardiac cycle length does not increase but actually decreases as the vagal stimulation frequency is raised. Background levels of sympathetic stimulation do not significantly alter the range over which this "paradoxical" response occurs. Sympathetic stimulation decreases the cardiac chronotropic response to short bursts of vagal stimuli regardless of the time in the cardiac cycle that the stimulus is given; however, it does not decrease the time from the minimum vagal chronotropic response to the subsequent atrial depolarization although the total cardiac cycle is shortened. Since sympathetic stimulation shifts the overall temporal relationship between vagal stimulation and pacemaker response, small changes in sympathetic tone may greatly alter the cardiac response to phasic vagal stimulation if the vagal stimulus is given at certain times in the cardiac cycle.

Animals↗
PubMed1979

Effects of repetitive bursts of vagal activity on atrioventricular junctional rate in dogs.

A stable atrioventricular (AV) junctional rhythm was produced in open-chest dogs by injecting pentobarbital into the sinus node artery. When the cervical vagus nerves were stimulated repetitively, the junctional pacemaker cells tended to become synchronized with the vagal activity. During such synchronization, the junctional rate varied directly rather than inversely with the frequency of vagal stimulation. The magnitude of the chronotropic response depended on the timing of the vagal stimuli within the cardiac cycle. In 9 dogs, when the mean heart periods were plotted as a function of the R-st intervals (i.e., the time from the beginning of ventricular depolarization to the beginning of the stimulus burst), the mean heart periods varied from a maximum of 1,815 ms to a minimum of 1,160 ms, depending on the R-st interval. A small change in the R-st interval was capable of evoking a relatively large change in cycle length. Therefore, the impulses from various efferent vagal fibers to the AV junction must arrive almost synchronously, the released acetylcholine must be removed rapidly, and the sensitivity of the pacemaker cells to acetylcholine must change rapidly at some critical time during the cardiac cycle.

Acetylcholine↗
PubMed1978

The effect of changing interpulse intervals on the negative chronotropic response to repetitive bursts of vagal stimuli in the dog.

The chronotropic responses to repetitive bursts of vagal stimulation were determined in open-chest, anesthetized dogs. Either 5 or 10 electrical pulses were included in each stimulus burst, and the interpulse interval (deltat) was varied over the range of 5 to 150 msec. As the frequency of the stimulus bursts was progressively changed, the sinoatrial (SA) nodal pacemaker cells became synchronized with the repetitive bursts of stimuli over a certain range of burst frequencies. The magnitude of this frequency range varied with deltat. For 5 and 10 pulses/burst, the values of deltat that produced the greatest magnitude of this frequency range were 30.2 and 24.3 msec, respectively. Also, over the range of values of deltat from 5 to 50 msec, the magnitude of the negative chronotropic effect of the vagal stimulus burst varied directly with deltat. It is likely that, as the interpulse interval is increased within the range of values, either more acetylcholine is released from the vagal nerve endings per pulse or there is less saturation of the receptors on the pacemaker cell membranes during each burst.

Action Potentials↗
PubMed1976

Effect of carotid sinus nerve stimulation pattern on cardiorespiratory responses.

The reflex responses to steady and intermittent stimulation of the carotid sinus nerve (CSN) were compared in anesthetized dogs. Intermittent stimulation was less effective than steady stimulation in reducing the arterial blood pressure, and the disparity was exaggerated after acute sinoaortic denervation. With the sinoaortic nerves intact, at low mean stimulation frequencies the heart rate responses were greater during intermittent than during steady CSN stimulation. At higher mean stimulation frequencies, however, steady CSN stimuli were more effective than were the intermittent type. After sinoaortic denervation, steady stimuli evoked greater heart rate responses than did intermittent stimuli over the entire mean frequency range studied. Reflex changes in respiratory depth and frequency were also greater during steady than during intermittent CSN stimulation. The greater efficacy of steady than of intermittent stimulation in evoking.the observed reflex cardiovascular and respiratory changes is probably ascribable to the pronounced frequency limitation at the first synapse of the baroreceptor reflex in the brain.

Animals↗
PubMed1975

Chronotropic response to acetylcholine injected into the sinus node artery of the isolated atrium of the dog.

Injection of a single bolus of acetylcholine into the sinus node artery of the isolated atrium of the dog produces a triphasic response similar to that previously observed after a single stimulus to the vagus nerves. There is an initial, brief but pronounced, cardiac deceleration followed by a brief, slight acceleration, which is then followed by a more prolonged deceleration which is of lesser magnitude than the initial deceleration. The most likely cause of the intermediate phase of cardiac acceleration is a direct effect of acetylcholine on the pacemaker cells, as it is also with the primary and tertiary phases of cardiac deceleration.

Acetylcholine↗