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At least 667 records · Page 37Linked to original sources
PubMed1981

[Experimental electrocardiographic research. Study in the rat of the cardiovascular effects of labetalol].

Electrocardiographic changes induced by Labetalol, a drug blocking alpha- and beta-adrenergic receptors, have been studied in 10 anesthetized rats. Authors observed that Labetalol has: 1) slightly negative chronotropic action; 2)slightly negative dromotropic action on both atrio-ventricular and intraventricular conduction; 3) effective antiarrhythmic and alpha-blocking action and, inconstantly, 4) the so-called "intrinsic sympathicomimetic action" (I.S.A.), typical of several beta-blocking drugs.

Animals↗
PubMed1983

Review of clinical and animal studies comparing the cardiovascular effects of doxepin and other tricyclic antidepressants.

On the basis of early reports suggesting that doxepin has fewer cardiovascular effects than do other tricyclic antidepressants, doxepin continues to be recommended for the treatment of depression in cardiac patients and in the elderly. However, these reports have been criticized, and other evidence has suggested opposite conclusions. To clarify this issue, the author reviewed clinical and animal studies and found that, in general, doxepin has an effect comparable to the effects of other tricyclic antidepressants on cardiac conduction, cardiac rhythm, heart rate, blood pressure, and cardiac mechanics.

Animals↗
PubMed1990

Histochemical studies on the conduction system of diabetic rat hearts.

We studied the metabolism of the conduction system and the working myocardium in diabetic rat hearts by enzyme histochemistry. The experiment was performed three weeks following the administration of streptozotocin (65 mg/kg) to male Wistar rats. The hearts were quickly excised and tissue was frozen immediately by immersion in isopentane at -30 degrees C and cut into 16 microns thick sections in a cryostat. The PAS positive reaction was increased in the conduction system compared to the working myocardium in control rats. In diabetic rat hearts, these reactions in the working myocardium and the conduction system were strongly increased compared to control hearts. Several enzyme activities, such as phosphofructokinase, pyruvate dehydrogenase, glucose-6-phosphate dehydrogenase, Na-K ATPase, were reduced in both the working myocardium and conduction system of diabetic rat hearts. These results suggest that the changes in metabolic condition also exist in the conduction system of the diabetic rat hearts as well as the working myocardium.

Animals↗
PubMedDate not supplied

[Experimental visualization of the ventricular conduction system of the heart intra vitam (author's transl)].

The in-vivo tolerability of an in vitro in cow, calf and sheep hearts developed method for radiologic visualization of the left ventricular conduction system is tested in four animal experiments. The clinical in-vivo tolerability could be demonstrated on principle; however, it is to accent that hypertonic X-ray contrast dyes may be the cause of morphological changes in the micro- and ultrastructures of the specialised musculature of unknown dignity.

Animals↗
PubMed2002

Circadian rhythm in the cardiovascular system: considerations in non-invasive electrophysiology.

Most cardiovascular activities show a circadian rhythm, as do electrophysiological phenomenon. Under the influence of both external stimuli and endogenous homoeostatic mechanisms, cardiac electrophysiological properties change diurnally and enable the cardiovascular system adapt to rest-exercise cycles. According to recent reports, almost all non-invasive electrophysiological phenomena, such as electrocardiographic indices, cardiac refractoriness and conduction, pacing and defibrillation threshold, heart rate variability indices, and even Q-T dispersion and T-wave alternans, show diurnal variability. Furthermore, many of these changes are clinically significant and may affect results of some diagnostic studies. These characteristics of the cardiovascular system require us keep in mind the "time" factor any time we analyze electrophysiological results and make clinical decisions.

Arrhythmias, Cardiac↗
PubMed1982

Electrophysiological effects of cardioselective and non-cardioselective beta-adrenoceptor blockers with and without ISA at rest and during exercise.

1 In 46 patients (16 female and 30 male), aged between 18 and 73 years and effect of acute beta-adrenoceptor blockade with i.v. pindolol, acebutolol and atenolol has been studied at rest and during ergometric exercise, during routine intracardiac His bundle investigations. 2 At rest the functional parameters of the sinus node were impaired most markedly by atenolol. A-V nodal conduction was more depressed with acebutolol and atenolol than with pindolol. The His-Purkinje system conduction remained unaffected by all three beta-adrenoceptor blocking agents. 3 During ergometric exercise the depressant action of beta-adrenoceptor blockade on sinus nodal function with lower heart rates and on A-V nodal conduction with slower conduction velocities was equieffective with pindolol, acebutolol and atenolol. His-Purkinje system conduction again remained unchanged with one exception that after administration of pindolol, conduction rate during exercise was faster than before beta-adrenoceptor blockade. 4 It may be concluded that, in patients with low heart rates, an antagonist such as pindolol with relatively pronounced intrinsic sympathomimetic activity can be considered to be the drug of choice. In contrast, patients with higher heart rates at rest should be treated with a cardioselective betablocker without ISA. Patients with overt Sick Sinus Syndrome should not be given beta-adrenoceptor blockers at all. 5 Physical activity may change (improve or impair) the antiarrhythmic potency of beta-adrenoceptor blockers used in the treatment of supraventricular tachycardias or tachyarrhythmias.

Acebutolol↗
PubMed2006

Autonomic regulation of calcium cycling in developing embryonic mouse hearts.

In the present study, we combined optical Ca(2+) imaging with immunocytochemistry studies to characterize autonomic regulation of Ca(2+) cycling during early development in isolated embryonic mouse hearts. At embryonic days 9.5-11.5 (E9.5-E11.5), the Ca(2+) transient originated in the superior portion of the right atrium, propagated rapidly through both atria, slowly through the atrio-ventricular (AV) ring, and rapidly through both ventricles. Isoproterenol (ISO) significantly increased heart rate, increased Ca(2+) transient amplitude, rate of rise (RR) and a rate of decay, and shortened AV conduction time, indicating the presence of functional beta-adrenergic receptors. The muscarinic agonist carbachol (CCh) had no effects until 1 day later at E10.5. Both beta1-adrenergic and M2 muscarinic receptors were detected in ventricular muscle sections by immunochemistry at E10.5. Growing nerves, labeled using growth-associated protein 43 antibodies, were detected at the E14.5 stage, but not at E10.5, whereas mature sympathetic nerves, detected by tyrosine hydroxylase (TH) labeling, were not yet present at E14.5. These results demonstrate that functional regulation of Ca(2+) cycling by beta-adrenergic receptors occurs earliest in developing embryonic mouse hearts, followed a day later by muscarinic receptor responsiveness, with autonomic innervation developing later. These results define the functional and structural sequence of autonomic regulation of Ca(2+) transient in the embryonic mouse heart.

Age Factors↗
PubMed1997

Comparative direct electrophysiological effects of propofol on the conduction system and ionic channels of rabbit hearts.

1. Propofol, an intravenous anaesthetic agent, can affect cardiac conduction but the ionic mechanisms have not been well defined. 2. This study measured the direct effects of propofol on the cardiac conduction system by using intracardiac recording/stimulation in Langendorff-perfused rabbit hearts. The underlying ionic mechanism was elucidated by using the whole-cell voltage clamp on rabbit isolated atrial and ventricular myocytes. 3. Propofol prolonged significantly the AV conduction (AH) interval at a clinically relevant concentration (3 microM). This AH interval prolongation was dose-dependent (3 to 100 microM). At higher concentrations, the AV nodal Wenckebach cycle length and its refractory period were also prolonged (10 to 100 microM). In addition, the conduction through the His-Purkinje system (HV interval) and the atrial tissue (SA interval), as well as the spontaneous cycle length, were lengthened dose-dependently (30 to 100 microM). 4. In isolated ventricular myocytes, Na current was decreased dose-dependently by propofol. In part this was due to a negative-shift of the steady-state voltage-dependent inactivation and a slowed rate of recovery from inactivation. The INa suppression by propofol was frequency-dependent. Propofol also blocked the ICa. The ED50 for peak current inhibition was 6.9 +/- 0.9 (n = 6) and 8.3 +/- 1.5 microM (n = 7) for INa and ICa, respectively. 5. The transient outward potassium current (Ito) of atrial myocytes was suppressed with an ED50 of 5.7 +/- 0.8 microM (n = 11), which was only partly caused by a left-shift of the steady-state inactivation. The inward rectifier K current (IK1) of the ventricular cells was reduced somewhat by propofol. 6. In summary, propofol can cause direct dromotropic and chronotropic effects on the cardiac conduction system, especially the atrioventricular node. These changes can be attributed, at least in part, to its direct dose-dependent suppression of the cardiac ICa, INa and Ito. Special concerns in the use of propofol anaesthesia for cardiac patients and the therapeutic antiarrythmic potential of propofol-like compounds are addressed.

Analgesia↗
PubMedDate not supplied

Magnetism and cardiac arrhythmias.

Low-level electromagnetic fields (EMFs) have been used to treat various neurologic disorders. In the present study, we applied micro Gauss (microG) levels of EMFs either to the vagosympathetic nerve trunks, dissected in the neck, or across the chest in anesthetized dogs. Based on theoretical and empiric grounds, we compared EMFs (2.87 microG at 0.043 Hz) delivered to the vagosympathetic trunks in an experimental set (n = 5) with a sham control group (n = 6). Over a period of 2 to 3 hours, heart rate decreased after an initial 5-minute EMF exposure. The maximal heart rate changes in the experimental versus control groups was 29% versus 12% (P = 0.03). The voltage applied to the autonomic nerves required to induce atrioventricular (AV) conduction block decreased by 60% in the experimental group versus a 5% increase in the control group (P = 0.005). This effect also lasted 2 to 3 hours. Another EMF setting (amplitude 0.34 microG, frequency 2 kHz) applied for 5 minutes to the vagosympathetic trunks was associated with a significant increase in the occurrence of atrial premature depolarizations (APDs), atrial tachycardia (AT), and atrial fibrillation (AF) in response to autonomic nerve stimulation compared with control states before EMF exposure. No atrial arrhythmias could be induced after propranolol and atropine, even at the highest voltage used to stimulate the autonomic nervous input to the heart (n = 11). Only 2 dogs showed no response to this EMF application. In 3 dogs in whom atrial pacing (cycle length = 250 ms) and autonomic nerve stimulation induced AF, an EMF (2.87 microG at 0.043 Hz) delivered for 35 minutes across the chest suppressed AF for up to 3 to 4 hours, after which the same protocol again induced AF. We conclude that in these preliminary experiments, specific low-level EMFs alter heart rate, AV conduction, and heart rhythm. These effects were mediated through the autonomic nervous system inputs to the heart based on adjunctive effect of autonomic nerve stimulation and the inhibitory action of autonomic blockers.

Animals↗
PubMed1999

Relation of ventricular repolarization to cardiac cycle length in normal subjects, hypertrophic cardiomyopathy, and patients with myocardial infarction.

BACKGROUND: Prolonged QT interval and QT dispersion have been reported to reflect an increased inhomogeneity of ventricular repolarization, which is believed to be responsible for the development of arrhythmic events in patients with long QT syndrome, coronary heart disease, and myocardial infarction, congestive heart failure, and hypertrophic cardiomyopathy (HC). HYPOTHESIS: This study was undertaken to determine whether an abnormal QT/RR dynamicity may reflect autonomic imbalance and may contribute to arrhythmogenesis in patients with heart disease. METHODS: The relation between QT, QTpeak (QTp), Tpeak-Tend (TpTe) intervals and cardiac cycle length was assessed in 70 normal subjects, 37 patients with HC, and 48 survivors of myocardial infarction (MI). A set of 10 consecutive electrocardiograms was evaluated automatically in each subject using QT Guard software (Marquette Medical Systems, Milwaukee, Wisc.). RESULTS: In patients with HC, all intervals were significantly prolonged compared with normals (p < 0.001 for QT and QTp; p < 0.04 for TpTc); in survivors of MI, this was true for the maximum QT and QTp intervals (p < 0.05). A strong linear correlation between QT, QTp, and RR intervals was observed in normals and in patients with MI and HC (r = 0.65-0.59, 0.82-0.77, 0.79-0.74, respectively, p < 0.0001). TpTe interval only showed a weak correlation with heart rate in normals (r = 0.24, p < 0.05) and was rate-independent in both patient groups (p = NS). Compared with normals, the slopes of QT/RR and QTp/RR regression lines were significantly steeper in patients with MI and HC (0.0990-0.0883, 0.1597-0.1551, 0.1653-0.1486, respectively). Regression lines were neither parallel nor identical between normals and patients (T > 1.96, Z > 3.07). There was no difference in steepness for TpTeR/RR lines between groups (0.0110, 0.0076, 0.0163, respectively). TpTe/QTp ratio was similar in normals and in patients with MI and HC (0.30 +/- 0.03, 0.31 +/- 0.07, 0.30 +/- 0.04, respectively), in the absence of any correlation between QTp and TpTe intervals, suggesting disproportional prolongation of both components of QT interval. CONCLUSION: Compared with normals, a progressive increase in QT and QTp intervals at slower heart rates in patients with MI and HC may indicate an enhanced variability of the early ventricular repolarization and may be one of the mechanisms of arrhythmogenesis.

Adolescent↗
PubMed1995

Differential effects of ketamine and midazolam on heart rate variability.

Alterations in autonomic activity caused by anaesthesia can be assessed by spectral analysis of heart rate variability (HRV). This study examined the effects of ketamine and midazolam on HRV. Thirty patients of ASA PS 1 were studied. Fifteen were given ketamine (2 mg.kg-1) and 15 received midazolam (0.3 mg.kg-1), iv. The RR intervals of ECG were measured before and after induction of anaesthesia for ten minutes during spontaneous respiration. Power spectral density of the data was computed using fast Fourier transform. The spectral peaks within each measurement were calculated: low frequency area (LF, 0.04-0.15 Hz), high frequency area (HF, 0.15-0.5 Hz), and total power (TP, 0.04-0.5 Hz). Normalized unit power was derived as follows: low frequency area (nuLF): LF/TP x 100%, high frequency area (nuHF): HF/TP x 100%. Both ketamine and midazolam caused reductions in all measurements of HRV power (P < 0.05). However, ketamine increased nuLF from 64 +/- 14% to 75 +/- 13% (P < 0.05) and decreased nuHF from 36 +/- 14% to 25 +/- 13% (P < 0.05), while midazolam decreased nuLF from 66 +/- 15% to 54 +/- 14% (P < 0.05) and increased nuHF from 34 +/- 15% to 46 +/- 14% (P < 0.05). These results documented that both ketamine and midazolam reduced the total power and all frequency components of power in spite of their opposing effects on autonomic nervous activity. However, normalized unit power showed the expected sympathetic activation with ketamine and sympathetic depression with midazolam since ketamine increased nuLF and midazolam decreased nuLF.

Adult↗