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At least 721 records · Page 40Linked to original sources
PubMedDate not supplied

Modulation of cardiac impulse generation and conduction by nifedipine and verapamil analyzed by a refined surface ECG technique in Langendorff perfused guinea pig hearts.

Using a modified Langendorff system, a special ECG recording technique and appropriate placement of two silver wire electrodes, early atrial and His bundle activity can be detected continuously from the surface of intact and spontaneously beating guinea pig hearts. This new method was applied to measure the direct and inhibitory effects of nifedipine and verapamil on impulse generation and conduction in isolated and perfused guinea pig hearts. Depression of sinoatrial conduction was the most prominent effect of nifedipine. In all concentrations applied (10(-7) M, 10(-6) M, 10(-5) M) nifedipine predominantly led to sinoatrial blocks of different degrees. Heart rate decreased slightly in a dose-dependent manner. PQ and HV duration remained essentially constant. In the highest concentration of nifedipine (10-5) M), sinus node activity was so depressed that AV dissociation or ventricular rhythm developed. Only in one out of eight experiments with cumulative increase of nifedipine concentrations to 10(-5) M was the AV node affected by nifedipine and a second-degree AV block developed (10(-6) M). Verapamil's inhibitory effects on the rate of impulse initiation in the sinus node were more pronounced than those of nifedipine, but the inhibition of sinoatrial conduction by verapamil was less marked. At 10(-6) M verapamil, the incidence of sinoatrial blocks and of ventricular rhythm was similar to the incidence of first degree AV blocks. PQ time (+14%) but also HV time (+12%) were prolonged under the influence of this concentration of verapamil. At the highest concentration of verapamil (10(-5) M) applied for 10 min, ventricular rhythm developed in five out of eight experiments, as well as one second and two third-degree AV blocks. The results confirm that the simultaneous measurements of sinus node activity of sinoatrial and atrioventricular conduction and of HV duration is feasible with this ECG technique, to evaluate the inhibitory effects of Ca-antagonists on sinus and AV node activity in the intact heart.

Animals↗
PubMed1986

Effects of sympathetic tone on vagally induced phasic changes in heart rate and atrioventricular node conduction in the anesthetized dog.

We examined the effects of stellate ganglia stimulation on the phase-dependent chronotropic and dromotropic responses to brief vagal bursts in open-chest anesthetized dogs. Stellate stimulation affected the phasic vagal effects on heart rate by shortening the latent period, shifting the phase at which maximum decrease in heart rate occurred to earlier phases, and reducing the maximum decrease in heart rate. These effects were due primarily to an increase in the basic heart rate. No significant sympathetic-parasympathetic interaction occurred for heart rate, indicating that accentuated antagonism did not occur with brief vagal bursts. Stellate stimulation primarily decreased the amplitude of the phasic vagal effects on atrioventricular nodal conduction, regardless of the underlying heart rate, and a significant sympathetic-parasympathetic interaction was associated with this effect. The peak of the phase-dependent vagal effects on heart rate and atrioventricular nodal conduction were phase-shifted with one another. From these findings, we postulate the small changes in sympathetic tone might shift the predominant phase-dependent vagal effect from one on heart rate to one on atrioventricular nodal conduction. Furthermore, our results suggest that dynamic vagal control of heart rate and atrioventricular node conduction involves both phase-dependent and phase-independent factors. Sympathetic activity appears to affect only the phase-independent factor(s) in the control of heart rate, whereas it affects both phase-dependent and phase-independent factors in the control of atrioventricular node conduction.

Animals↗
PubMed2005

Functional properties of mouse connexin30.2 expressed in the conduction system of the heart.

Gap junction channels composed of connexin (Cx) 40, Cx43, and Cx45 proteins are known to be necessary for impulse propagation through the heart. Here, we report mouse connexin30.2 (mCx30.2) to be a new cardiac connexin that is expressed mainly in the conduction system of the heart. Antibodies raised to the cytoplasmic loop or the C-terminal regions of mCx30.2 recognized this protein in mouse heart as well as in HeLa cells transfected with wild-type mCx30.2 or mCx30.2 fused with enhanced green fluorescent protein (mCx30.2-EGFP). Immunofluorescence analyses of adult hearts yielded positive signals within the sinoatrial node, atrioventricular node, and A-V bundle of the cardiac conduction system. Dye transfer studies demonstrated that mCx30.2 and mCx30.2-EGFP channels discriminate poorly on the basis of charge, but do not allow permeation of tracers >400 Da. Both mCx30.2 and mCx30.2-EGFP gap junctional channels exhibited weak sensitivity to transjunctional voltage (Vj) and a single channel conductance of approximately 9 pS, which is the lowest among all members of the connexin family measured in HeLa cell transfectants. HeLa mCx30.2-EGFP transfectants when paired with cells expressing Cx40, Cx43, or Cx45 formed functional heterotypic gap junction channels that exhibited low unitary conductances (15 to 18 pS), rectifying open channel I-V relations and asymmetric Vj dependence. The electrical properties of homo- and hetero-typic junctions involving mCx30.2 may contribute to slow propagation velocity in nodal tissues and directional asymmetry of excitation spread in the AV nodal region.

Animals↗
PubMedDate not supplied

[Adriamycin induced chronic cardiotoxicity: a morphological ultrastructural study on ventricular myocardium and conducting system of rabbit heart (author's transl)].

The administration of high doses of adriamycin in rabbits causes morphologically evident alterations of cardiac myocites, such as cellular structure disorganization, myofilaments disappearance and vacuolar degeneration through the cytoplasm. The less damaged myocites show protein synthesis activation with newly produced myofilaments. Macrophages and fibroblasts are seen in the interstitium among markedly injured cells. As a response to the toxic damage induced by adriamycin, it would be seen an hypertrophic compensatory response in the well preserved cells and interstitial fibrosis. The conducting system shows similar but less extensive lesions as the ventricular myocardium.

Animals↗
PubMed1991

[The pathomorphology of the intra- and extraorganic neural apparatus of the heart in congenital defects].

Different components of the heart sympathetic and parasympathetic innervation were studied in 22 autopsy cases of congenital heart defects. Central efferent neurons in the lateral horns of the upper thoracic segments of the spinal cord and in the dorsal nucleus of the medulla oblongata are damaged stronger than the neurons of the upper neck and stellate sympathetic nodes and the heart intramural ganglia this resulting in the selective destruction of the preganglionic nervous conducting elements. It is suggested that the disturbance of the connection between the heart nervous structures and the central nervous system exerts a negative influence on its function.

Autopsy↗
PubMed1986

Effect of sudden rate acceleration on the human His-Purkinje system: adaptation of refractoriness in a dampened oscillatory pattern.

Although the refractoriness of the human His-Purkinje system (HPS) during constant-cycle length pacing appears to be closely related to the cycle length of the stimulation, the mode of adaptation of this refractoriness with sudden rate acceleration is not well understood. A systematic evaluation of this adaptation was performed in 14 patients with normal QRS durations and HV intervals referred for electrophysiologic evaluation. The relative refractory period of the HPS (HPS-RRP) was evaluated by the extrastimulus (S2) method during a constant ventricular drive (S1) having a cycle length as close to sinus rhythm as possible. An accelerated train of 6 ventricular beats (S1') was then added to the constant drive and the HPS-RRP of each successive beat of this train was similarly determined. Mean S1 cycle length was 750 +/- 164 msec (range 600 to 1000). Mean S1' cycle length was 475 +/- 55 msec (range 400 to 600). The HPS-RRP of each successive beat of the accelerated train was significantly shorter than that during the S1 drive and behaved in a dampened oscillatory fashion alternating from a lower value on the odd-numbered beats to a higher value on the even-numbered beats. In contrast, the effective and relative refractory periods of the ventricular myocardium during the accelerated train behaved in a cumulative manner, decreasing progressively with the first 2 beats of the train before reaching a plateau value. In conclusion, the data reported here present a new and intriguing picture of the mode of adaptation of the HPS refractoriness to sudden rate acceleration. At least in the range of the cycle lengths used in this study, the refractoriness of the HPS behaves in a dampened oscillatory manner that is radically different from the behavior of the ventricular myocardial refractoriness.

Adaptation, Physiological↗
PubMed1982

[Clinico-electrocardiographic criteria of heart rhythm disorders in the sick sinus syndrome].

A total of 75 patients with proved weak sinus node syndrome (WSNS) were examined. In many cases, WSNS was found to accompany cardiovascular diseases, such a coronary disease, myocarditic cardiosclerosis and essential hypertension. Sinus node dysfunction is often combined with signs of disorder in other departments of the hearts conductive system. A screening for WSNS should incorporate a combination of diagnostic procedures, of which Holter's ECG monitoring and electrophysiological investigation of the heart's conductivity are the most reliable and informative.

Adult↗
PubMed1994

Character of the effect of microwave on conduction velocity of frog ventricular muscle.

Thirty-two frog hearts were divided into four groups and placed individually in temperature-controlled waveguides filled with Ringer's solution. The pacemaker was removed, and stimulation was provided at 0.3 Hz by three carbon-loaded Teflon electrodes located on the aorta and the ventricular muscle. Conduction velocity was measured from the difference between two action potentials. One group served as control; the three other groups were exposed for 2 h to pulsed 2,450 MHz microwave fields (10 microseconds, 0.001 duty cycle, 16 Hz modulation) at specific absorption rates (SARs) of 0.003, 2, and 6 W/kg, respectively. No significant difference in conduction velocity was found between the control and the exposed groups.

Animals↗
PubMed1994

Cardiovascular autonomic dysfunction in normotensive awake subjects with obstructive sleep apnoea syndrome.

Cardiovascular autonomic function in normotensive awake patients with obstructive sleep apnoea syndrome was studied in 21 normotensive (mean age 48 +/- 14 years), drug-free men with obstructive sleep apnoea syndrome. Cardiovascular reflex tests with continuous blood pressure monitoring and biochemical indices were performed the morning after a standard polygraphic sleep recording. A group of 20 age-matched (mean age 49 +/- 19 years) normal subjects was used as controls. The obstructive sleep apnoea syndrome patients showed higher heart rate and noradrenaline plasma levels (p < 0.05) at rest and a higher blood pressure response to head-up tilt (p < 0.01), suggesting sympathetic overactivity. Respiratory arrhythmia, baroreflex sensitivity index and Valsalva ratio were significantly lower in the obstructive sleep apnoea syndrome group (p < 0.01) whereas the decrease in heart rate induced by the cold face test was significantly higher (p < 0.05) showing a blunting of reflexes dependent on baroreceptor or pulmonary afferents with normal or increased cardiac vagal efferent activity. These abnormalities in autonomic regulation may predispose obstructive sleep apnoea syndrome patients to cardiovascular complications like hypertension and cardiac arrhythmias.

Adult↗
PubMedDate not supplied

Bedside diagnosis of cardiac autonomic damage by computerized analysis of heart rate-respiration relationship.

In this study we propose a method for the analysis of the relationship between heart rate changes and respiration as a possible diagnostic tool for cardiac autonomic damage. The method consists in recording R-R intervals and respiratory amplitude by a suitably equipped personal computer, and by evaluating the cross-correlation peak between the two signals. This mathematical function appeared to be more sensitive to the degree of concordance between the two signals, rather than their absolute amplitude. The cross-correlation appeared to be lower in diabetics with autonomic dysfunction, markedly decreased after injection of atropine (only in normals), slightly increased after propranolol. Hyperpnea increased the cross-correlation peak between 3-18 breaths/min in normals, but only at lower frequencies, if at all, in diabetic subjects with various degrees of autonomic dysfunction. The cross-correlation showed the best reproducibility among R-R change tests. These preliminary results suggest that this method may provide new information on autonomic integrity and a substantial advantage in terms of reproducibility.

Adult↗