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At least 145 records · Page 8Linked to original sources
PubMed1995

Effect of autonomic blockade on heart rate and blood pressure in sleep apnea syndrome.

To determine the impact of the autonomic nervous system on hemodynamic responses to sleep apnea we studied 7 male patients (48 +/- 6 years, BMI = 29.7 +/- 2.9 kg/m2) with an apnea index = 33 + 11/h. In two hypertensives, therapy was withdrawn 2 weeks before the study. During a full night polysomnography EEG, EOG, EMG, respiration, oximetry, heart rate (HR) and blood pressure (BP) (Finapres 23OOE) were recorded. Placebo and 3 short-acting autonomic blockers were randomly i.v. administered: antimuscarinic (atropine 1 mg, A), beta 1 blocker (esmolol 40 mg, E), alpha blocker (nicergoline 2.5 mg, N). A total of 367 obstructive apneas in NREM sleep were studied. With atropine, HR was increased at the beginning of apnea (P1)(74.5 +/- 2 bpm vs 65.4 +/- 2 bpm with placebo) and at the end apnea (P3) (76.6 +/- 1.9 bpm vs 67.1 +/- 1.76 bpm). At the resumption of breathing (RB), HR still increased (83.5 +/- 1.5 bpm vs 80.1 +/- bpm). Nicergoline had no significant effect on HR but significantly decreased SBP (117.8 +/- 1.4 mmHg vs 127 +/- 1.6 with placebo, p < 0.001). Nevertheless, the rise in BP from P3 to RB remained significant (p < 0.001). Esmolol significantly decreased HR at P1 (68.1 +/- 1.9 bpm vs 73.9 +/- 1.9 bpm) and at RB (75.9 +/- 1.9 vs 81.6 +/- 1.8). With A, the rise in HR at end-apnea (P3) suggests a vagal hyperactivity during this phase which is blunted at resumption when HR is unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1979

Lack of cardiovascular effects of delta-9-tetrahydrocannabinol in chemically denervated men.

We have previously reported that 25 micrograms/kg of intravenous (i.v.) delta-9-tetrahydrocannabinol (delta-9-THC) produces marked increases in heart rate, prolongation of left ventricular ejection time corrected for heart rate (LVETc), and a shortening of the pre-ejection period in normal volunteers. Beta-adrenergic blockade partially attenuates these responses. To elucidate further the mechanism of action of delta-9-THC, we gave 10 normal volunteers 0.1 mg/kg of i.v. propranolol and 2 mg of i.v. atropine before they received 25 micrograms/kg of i.v. delta-9-THC. Systolic time intervals were compared in the denervated subjects before and after delta-9-THC. Post delta-9-THC responses were measured at a time approximating peak psychologic high. Mean +/- SEM heart rate before and after delta-9-THC was 89 +/- 4 and 87 +/- 3 beats/min (NS); mean +/- SEM pre-ejection period before and after delta-9-TCH was 107 +/- 5 and 109 +/- 4 ms (NS); and mean +/- SEM LVETc before and after delta-9-THC was 433 +/- 6 and 429 +/- 6 ms (NS). Since previous denervation of our subjects with atropine and propranolol totally abolished changes in heart rate and systolic time intervals, the cardiac effects of delta-9-THC appear to be mediated totally via the autonomic nervous system, probably reflecting direct central nervous system stimulation.

Adult↗
PubMed1992

Some aspects of vascular pharmacology of frog (Rana tigrina).

Vascular autonomic receptors in amphibians exhibit difference from more evolved mammalian species. Vascular perfusion studies in frog indicate constrictions by prominent muscarinic but rudimentary nicotinic constrictive regulation by cholinergic systems. Difference from classical effect-patterns of pharmacological interventions, observed in the study, make room to visualise complexity of additional regulatory mechanisms.

Adrenergic alpha-Antagonists↗
PubMed1992

[Mitral valve prolapse. Atrial stimulation, ajmaline test and "pharmacological denervation" in the evaluation of ventricular repolarization].

In patients with mitral valve prolapse syndrome (MVP) various electrophysiological abnormalities occur. There are convergent opinions concerning QT distance variability and the influence of autonomic nervous system on ventricular repolarization in this syndrome. In 38 MVP patients (group I) and 24 subjects without this abnormality (group II) ecg was recorded during transvenous right atrial pacing at baseline, after ajmaline administration and after pharmacological autonomic blockade (atropine + propranolol). The following ventricular repolarization parameters were analysed: QTe (distance to the end of T wave), JTe (distance between J point and the end of T wave--so called "pure repolarization"), QTdys (repolarization dispersion) and the corrected QTc.QTe during 90/min right atrial pacing was significantly shorter than QTc in both groups. QTc was abnormally prolonged (above 440 msec) in MVP group. Ajmaline administration prolonged QTe in group II only, whereas autonomic blockade resulted in marked shortening of QTe in MVP group. QTdys was significantly prolonged only after ajmaline administration in group II. Based on above results, the following conclusions are made: 1) Right atrial pacing technique may be used for calculating standardized QT distance, an alternative to corrected QT. 2) Ajmaline test is useless in ventricular repolarization estimations in MVP patients. 3) In MVP patients the influence of adrenergic system on ventricular repolarization at rest appears to be greater than in non-MVP subjects.

Adolescent↗
PubMed1987

[Neuroautonomic organization of cardiac rhythm and of nonrhythmic oscillations in the frequency of cardiac contractions and respiration].

In 25 chronic adult rabbits, the functional organization of neurally mediated short-term rhythms and patterns of the heart rate (HR) were investigated. The respiration-unrelated arrhythmia seems to be vagally mediated only, being abolished with atropine. The respiration-related arrhythmia exists not only within the range of respiratory frequency but also in lower frequencies as discovered by spectral and coherence analysis. During motor activity, there is a systematic correlation among increasing premotor, motor and amygdaloid multispike activities, increasing HR and depressed HR-rhythms with limbic initiation of motor and concomitant autonomic patterns, "Immobile confrontations" alone produces vagally induced HR-decrease and increased amplitudes of vagal HR-rhythms with a concomitant cortical multispike depression, a mirror image of the autonomic patterns after nociceptive stimulation.

Action Potentials↗
PubMed1987

[Role of the autonomic nervous system in the genesis of the electrophysiologic pattern of the double nodal pathway].

Thirty-five patients (age: 53 +/- 13 years) with dual A-V nodal pathways pattern were studied following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Six of them had "idionodal" paroxysmal reentrant supraventricular tachycardia. After autonomic blockade the dual A-V nodal pathways pattern remained in 20 patients (57%) and disappeared in 15; however, in the latter, the effective refractory period of the fast pathway decreased significantly and the disappearance of the slow pathway conduction may not have been real since the marked shortening of the fast pathway refractory period may have masked the slow pathway conduction. The longest A2-H2 interval, the effective and functional refractory periods of the fast pathway did not change significantly after autonomic blockade. Even the electrophysiological measures of the slow pathway in the 20 patients in whom they were comparable did not change significantly. The behaviour of the fast and slow pathways measures varied from patient to patient after autonomic blockade. In the 6 patients with idionodal reentrant tachycardia a discrepancy between jump persistence after autonomic blockade and tachycardia induction was observed. These data suggest that: 1) the dual A-V nodal pathways pattern is mainly related to the anatomic structure of the A-V node; 2) the autonomic system affects in a variable way the conduction velocity and the refractoriness of the fast and slow pathways; 3) the dual A-V nodal pathways pattern and the reentry circuit of idional tachycardia imply two different electrophysiological substrata.

Atrioventricular Node↗
PubMed1985

Effects of fentanyl and diazepam in dogs deprived of autonomic tone.

In contrast to reports of the untoward hemodynamic effects of fentanyl and diazepam in intact organisms, we found that neither a bolus of 100 micrograms/kg fentanyl nor the addition of intravenous doses of diazepam, up to and including 1 mg/kg (cumulative dose 2 mg/kg) caused cardiovascular depression in 13 anesthetized dogs after elimination of their sympathetic and parasympathetic tone. There were no significant changes in mean arterial blood pressure, cardiac output, heart rate, peak left ventricular dP/dt, cardiac filling pressures, or systemic vascular resistance. Rapid bolus injection of 3 mg/kg diazepam (cumulative dose 5 mg/kg) caused a significant (P less than 0.05) but transient (time to 50% recovery less than 2 min) decrease in systemic vascular resistance, blood pressure, and dP/dt. When corrected for pressure changed (dP/dt divided by simultaneous left ventricular pressure), the decrease in dP/dt did not attain statistical significance, nor did changes in cardiac output or filling pressures, even after this large dose of diazepam. We conclude that previously reported decreases in hemodynamic function in subjects with intact autonomic function after fentanyl alone, or after the combination of fentanyl and diazepam, are indirect in nature, that is, are caused by a centrally mediated decrease in vasoregulatory (mainly sympathetic) outflow from the central nervous system.

Animals↗
PubMed1982

Chagas' heart disease as an experimental model for studies of cardiac autonomic function in man.

Patients presented here include apparently healthy persons who had diagnostic evidence of chronic cardiac Chagas' disease in the form of a positive complement-fixation test and an abnormal electrocardiogram. They had never been in heart failure. All were examined for autonomic cardiac function. Normal persons served as controls. Patients with Chagas' disease with sole involvement of hollow viscera were also included. In patients with cardiac Chagas' disease, failure of the heart rate to increase after administration of atropine and greatly reduced reflex changes in cardiac rate are believed to be a functional disorder related to degeneration of the neuronal supply to the sinoatrial region of the heart. It is concluded that Chagas' disease is a model of spontaneous denervation of the heart which may be used for the assessment of autonomic control of cardiac function in man.

Adult↗