scholarly journals Change in heart period: A function of sensorimotor event timing within the cardiac cycle

1977 ◽  
Vol 5 (3) ◽  
pp. 383-393 ◽  
Author(s):  
Beatrice C. Lacey ◽  
John I. Lacey
1982 ◽  
Vol 242 (1) ◽  
pp. H7-H12 ◽  
Author(s):  
S. L. Stuesse ◽  
M. N. Levy ◽  
H. Zieske

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.


1987 ◽  
Vol 252 (2) ◽  
pp. H360-H367
Author(s):  
P. Martin ◽  
S. Ishikawa

We studied the dynamic interaction between the independent effects of sympathetic stimuli and heart period on atrial contractile force with three experiments: 1) we measured the inotropic response to brief sympathetic stimuli when the heart was paced; this represented the pure sympathetic effect on contractile force. 2) We measured the responses to identical stimuli when the heart was not paced; this represented the effect of the combined influences. 3) We measured the contractile responses to the identical sequences of changing cycle lengths that were recorded (expt 2) but in the absence of sympathetic activity; this represented the pure effect of changing cardiac cycle length on contractile force. We subtracted the paced from the unpaced responses. This difference represented the linear elimination of the pure sympathetic effect from the combined responses. We then compared this difference with the responses to changing cycle lengths that were measured in the absence of sympathetic activity (expt 3). The values were not equal from 2.5 through 22.5 s after the stimulus of experiment 1 of the protocol above. We performed a similar comparison after expressing the results in the frequency domain. The values were significantly different for most of the frequency spectrum where the greatest power was concentrated. We therefore conclude that there is a significant interaction between the effects of sympathetic activity and changing heart periods, and this interaction determines the resultant inotropic state on any specific beat.


1980 ◽  
Vol 239 (4) ◽  
pp. H494-H494
Author(s):  
Paul Martin

The vagosympathetic trunks of anesthetized propranolized dogs were stimulated with brief electrical bursts, and heart period (P-P interval), atrioventricular conduction (P-R interval), and pressure generated on a balloon anchored in the atrium (AP) were measured. Two vagal stimulus bursts were given separated by an integral number of cardiac cycles but with each placed at the same relative time in the cardiac cycle. The time between stimulus bursts ( T) varied from 2 to 60 s. For all cardiac variables over this time span, the peak response to the second stimulus (P2) was less than that of the first (P1) i.e., the ratio P2/P1 was less than unity. The maximum depression of P2/P1 for all variables occurred at a T of about 5 s. The effect of changing the time in the cardiac cycle at which the stimulus was given, and the effect of stimulus intensity on the P2/P1 ratio was also measured. Previous experiments observing the P-R interval alone suggested that synthesis and release of acetylcholine were not involved in the time dependent P2/P1 effect. The present results suggest that neuroeffector mechanisms at the target cellular level are also not involved in the depression of P2/P1. A time-dependent increase in acetylcholine inactivation is consistent with the present results, but an antagonism between primary and secondary inhibitory effects also cannot be ruled out.


2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.


1999 ◽  
Vol 13 (1) ◽  
pp. 18-26 ◽  
Author(s):  
Rudolf Stark ◽  
Alfons Hamm ◽  
Anne Schienle ◽  
Bertram Walter ◽  
Dieter Vaitl

Abstract The present study investigated the influence of contextual fear in comparison to relaxation on heart period variability (HPV), and analyzed differences in HPV between low and high anxious, nonclinical subjects. Fifty-three women participated in the study. Each subject underwent four experimental conditions (control, fear, relaxation, and a combined fear-relaxation condition), lasting 10 min each. Fear was provoked by an unpredictable aversive human scream. Relaxation should be induced with the aid of verbal instructions. To control for respiratory effects on HPV, breathing was paced at 0.2 Hz using an indirect light source. Besides physiological measures (HPV measures, ECG, respiration, forearm EMG, blood pressure), emotional states (pleasure, arousal, dominance, state anxiety) were assessed by subjects' self-reports. Since relaxation instructions did not have any effect neither on the subjective nor on the physiological variables, the present paper focuses on the comparison of the control and the fear condition. The scream reliably induced changes in both physiological and self-report measures. During the fear condition, subjects reported more arousal and state anxiety as well as less pleasure and dominance. Heart period decreased, while EMG and diastolic blood pressure showed a tendency to increase. HPV remained largely unaltered with the exception of the LF component, which slightly decreased under fear induction. Replicating previous findings, trait anxiety was negatively associated with HPV, but there were no treatment-specific differences between subjects with low and high trait anxiety.


Author(s):  
Marci Sammons ◽  
Sharon Mutter ◽  
Leslie Plumlee ◽  
Laura Strain

1996 ◽  
Vol 35 (05) ◽  
pp. 146-152 ◽  
Author(s):  
A. Kögler ◽  
H.-A. Schmitt ◽  
D. Emrich ◽  
H. Kreuzer ◽  
D. L. Munz ◽  
...  

SummaryThis prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (± SD) was 11.5 ± 2.7 mm and 5.8 ± 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 ± 3.4 mm and 3.7 ± 3.1 mm in 31 with reversible lesions, 11.3 ± 2.8 mm and 3.3 ± 1.9 mm in 10 with mild persistent defects, 9.2 ± 2.9 mm and 3.2 ±2.2 mm in 15 with moderate persistent defects, 5.8 ± 1.7 mm and 1.3 ± 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p <0.0005) and systolic wall thickening (p <0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.


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