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At least 703 records · Page 39Linked to original sources
PubMed1992

Mechanical properties of the canine mitral valve: effects of autonomic stimulation.

Experiments were designed to determine whether the canine mitral valve actively contracts and, if so, if its mechanical activity can be modulated by the autonomic nervous system. A miniature displacement gauge was sutured to the atrial (muscular) surface of the septal leaflet in 65 dogs under pentothal sodium anesthesia during total cardiopulmonary bypass. During bypass, with blood constantly drained from the left ventricle (LV), the leaflet deflected into the LV during ventricular systole as would be expected with active contraction. With blood present in the LV, leaflet deflection was reversed, indicating a passive displacement. After application of 85% phenol to the atrial surface, ventricular displacement of the leaflet was abolished, whereas the atrial displacement was significantly augmented. There was a positive inotropic effect during sympathetic stimulation and a negative inotropic effect with parasympathetic stimulation, i.e., increased and decreased ventricular deflection, respectively. These effects of autonomic stimulation were abolished by application of phenol to the leaflet muscle. During simultaneous electrical and mechanical recordings from the valve, activation appeared to originate from the atrium, before ventricular depolarization. It was concluded that the valvular muscle actively contracts to assist in bringing the valve leaflets into early apposition. This contraction imparts a measurable level of active "stiffness" to the valve, reducing atrial displacement during ventricular systole. This "stiffness" can be modified by autonomic input and may contribute to dysfunction of morphologically normal mitral valves.

Animals↗
PubMed1996

Heart rate variability during artificial ventilation and apnea in brain-damaged rabbits.

The effect of artificial ventilation, apnea, and norepinephrine administration on heart rate variability was determined in brain-damaged rabbits. Electrocardiographic R-R intervals and circulatory variables were measured for 5 min at three different ventilatory frequencies, including apnea under isoflurane general anesthesia. The same measurements were repeated after brain damage was inflicted by an inflated intracranial balloon. In control rabbits (n = 8) and in those receiving norepinephrine (n = 8), power spectral analysis of R-R intervals was repeated, and spectral components of low (LF: 0.04-0.09 Hz), mid (MF: 0.09-0.15 Hz), and high (HF: 0.15-0.40 Hz) frequency band areas were assessed. LF + MF (P < 0.05) increased during apnea, whereas HF did not change under general anesthesia. However, after brain damage in both groups LF + MF did not change, whereas HF was depressed (P < 0.05). There was no intergroup difference in decreases of HF/(LF + MF) (P < 0.05) during apnea under either condition. Norepinephrine increased heart rate and arterial pressure (P < 0.05) but did not produce any intergroup difference in the spectral components. We suggest that sympathovagal balance is apt to be sympathotonic during apnea under general anesthesia, whereas it is vagolytic with brain damage.

Animals↗
PubMed2002

Effects of sleep pressure on endogenous cardiac autonomic activity and body temperature.

This study investigated the effects of variations in sleep pressure on cardiac autonomic activity and body temperature. In a counterbalanced design, 12 healthy, young subjects (6 men and 6 women) remained recumbent during 30 h of wakefulness (high sleep pressure) and 6 h of wakefulness (low sleep pressure). Both periods of wakefulness were immediately followed by a sleep opportunity, and the first 2 h of sleep were analyzed. During extended hours of wakefulness, a reduction in heart rate was mediated by a decline in cardiac sympathetic activity (measured via preejection period) and the maintenance of cardiac parasympathetic activity (measured via respiratory sinus arrhythmia). In subsequent high-pressure sleep, parasympathetic activity was amplified and sympathetic activity was negatively associated with electroencephalographic slow-wave activity. Sleep deprivation had no impact on foot temperature, but it did alter the pattern of change in core body temperature. A downregulation of cardiac autonomic activity during both extended hours of wakefulness and subsequent sleep may respectively provide "protection" and "recovery" from the temporal extension of cardiac demand.

Adult↗
PubMed2000

Modifications of cardiac autonomic profile associated with a shift schedule of work.

BACKGROUND: Shift work is associated with an increased rate of cardiovascular diseases and accidents. Discordance between circadian rhythms of stress-related biological variables and the work-sleep schedule might explain the reduced efficiency of work. It is not clear whether a shift schedule of work may induce similar discordance in the 24-hour oscillatory pattern of the cardiac autonomic control in respect to the work-sleep periods. METHODS AND RESULTS: Twenty-two healthy male blue-collar shift workers underwent 24-hour ECG recordings during each of the 3 different shifts (first, 6 AM to 2 PM; second, 2 to 10 PM; third, 10 PM to 6 AM). Spectral analysis of heart rate variability over 24 hours provided the normalized markers of cardiac sympathetic (LF(nu)) and vagal (HF(nu)) modulation of the sinoatrial node activity and of the sympathovagal balance (LF/HF). LF(nu) and LF/HF exhibited 24-hour oscillations with different times of maximum and minimum in accordance with the working and sleeping periods, respectively. Lower values of LF(nu) and LF/HF suggestive of a reduced cardiac sympathetic modulation were present when the job task was performed at night compared with the values observed when the work was performed during morning and evening. CONCLUSIONS: Continuous weekly changes of time of maximum and minimum in the cardiac sympathetic and vagal autonomic control may play a role in the excessive rate of cardiovascular diseases in shift workers. The reduced values of the indexes of cardiac sympathetic modulation during night work might be related to the presence of sleepiness or diminished alertness, which in turn could facilitate errors and accidents.

Adult↗
PubMed1995

Acute exercise attenuates cardiac autonomic regulation in hypertensive rats.

Dynamic exercise may be used as a safe, therapeutic approach to reduce sympathetic nerve activity at rest and thus may be beneficial for individuals with hypertension. Therefore, we tested the hypothesis that a single bout of mild to moderate dynamic exercise would decrease cardiac sympathetic tonus at rest. We designed two experimental protocols to test this hypothesis in male spontaneously hypertensive rats. In protocol 1 (n = 6) cardiac sympathetic tonus and parasympathetic tonus were determined before and after a single bout of dynamic exercise. We developed protocol 2 (n = 5) to determine the component of the autonomic nervous system responsible for the postexercise reduction in heart rate. Rats were instrumented with catheters inserted into the descending aorta for measurements of arterial pressure, mean arterial pressure, and heart rate and into the jugular vein for infusion of drugs. A single bout of mild to moderate dynamic treadmill exercise (12 m/min, 10% grade for 42 +/- 1 minutes, representing approximately 74% to 79% of maximal heart rate) resulted in a postexercise reduction in mean arterial pressure (163 +/- 7 to 149 +/- 5 mm Hg; P < .05). Associated with the postexercise hypotension was a reduction in sympathetic and parasympathetic tonus (47 +/- 12% and 71 +/- 12%, respectively). The reduction in heart rate during the early recovery phase was due to a withdrawal of sympathetic tonus, because beta 1-adrenergic receptor blockade significantly enhanced the postexercise reduction in heart rate, and muscarinic-cholinergic receptor blockade did not affect the postexercise decrease in heart rate until 20 minutes after exercise.

Adrenergic Agents↗
PubMed1998

Cardiovascular autonomic dysfunction in parkinsonian patients.

Cardiovascular dysfunction may occur in parkinsonian patients for a variety of reasons. Patients usually are more than 50 years old and on various drugs (both antiparkinsonian and for associated medical disorders), some of which may have cardiovascular effects. Autonomic failure increases with age and also is recognized in parkinsonian patients who have the disorder multiple system atrophy, in which there is substantial cardiovascular dysfunction. Thus, recognition of cardiovascular dysfunction and its causes in parkinsonian patients is of importance in diagnosis (in separating the various parkinsonian diseases), in determining prognosis, and finally in management. This article outlines the major areas of cardiovascular dysfunction, including disorders of blood pressure control, heart rate, and regional circulation, especially to vital organs. Clinical features and evaluation are described, together with abnormalities in different parkinsonian disorders and the principles of management.

Autonomic Nervous System↗
PubMed1979

Scanning electron microscopy of Purkinje fibres of the pig heart.

Scanning electron microscopy (SEM) of Purkinje fibres (P-fibres) from the septal walls and the septomarginal trabecula was performed on deparaffinized sections, the identification in SEM made possible by comparative light microscopy. The myofibrils in P-fibres from the septal walls were arranged in a cart-wheel fashion, whereas P-fibres from the septomarginal trabecula showed a nearly parallel alignment of the contractile material. Z-line ridges resembling the T-tubules of the myocardial fibres were observed in both kinds of P-fibres. The myofibrillar arrangements are discussed in relation to the expected mechanical stress put upon P-fibres in the 2 locations during systolic-diastolic activity. An adaptive function of the contractile material to the mechanical stress is suggested and the possible need of a T-tubular system is discussed.

Animals↗
PubMed1982

Cardiovascular effects of antidepressants.

It is not the purpose of this paper to dismiss the possibility that tricyclics may somehow cause cardiac function to deteriorate, with resulting congestive heart failure. Any patient with heart disease should receive intense clinical scrutiny for the development of cardiac symptoms--dyspnea on exertion, ankle edema, orthopnea, paroxysmal nocturnal dyspnea, rales, and the presence of an S3 are never taken lightly. These parameters should be monitored because the patient has cardiac disease, not because he or she is on a tricyclic antidepressant.

Animals↗
PubMed1997

[Analysis of frequency-dependence of ventricular repolarisation by the Holter method in young adults. Influence of the autonomic nervous system on the rate-dependence of QT].

UNLABELLED: Adaptation of ventricular repolarization duration to heart rate provides additional information to the static duration of QT interval. METHODS: QT/RR relation and his slope were determined using 24-hour ECG recordings from 17 young male normal volunteers (mean age: 22 +/- 3 years). In order to determine the influence of the autonomic nervous system on the rate-dependence of QT, the authors compared the slopes obtained from recordings during the day and the night. Then, the respective rate-dependences of the entire QT interval (QTe) and its initial subdivision (QTa) and their correlations with parameters of heart rate variability were studied. RESULTS: the QTa/RR and QTe/RR relations were constantly linear, with very significant regression coefficients. The daytime QTa/RR and QTe/RR slopes were significantly steeper than the nighttime ones (0.138 +/- 0.035 vs 0.108 +/- 0.040, p < 0.05 for QTe/RR, 0.160 +/- 0.069 vs 0. 108 +/- 0.055, p < 0.01 for QTa/RR). The early part of QT showed a stronger rate-dependence than the global QT, but only at daytime (0.160 +/- 0.069 vs 0.138 +/- 0.035, p < 0.05). No correlation was found between rate dependences and heart rate variability parameters. CONCLUSION: the authors demonstrate, from ambulatory ECG recordings, the influence of the autonomic nervous system on the rate-dependence of ventricular repolarization in normal young adults, and a difference in rate-dependence between the entire QT interval and its initial part QTa, due to differences in autonomic nervous system tone. This heterogeneity should be taken to account in the study of pathological changes or drugs effects on ventricular repolarization.

Adolescent↗