1,721,221 research outputs found
Heart rate variability as a clinical tool
No full textPower spectrum analysis of cardiovascular signal variability, and in particular of the RR period (heart rate variability), is a widely used procedure for the investigation of autonomic cardiovascular control and/or target function impairment. However, a correct methodology is essential to extract the information embedded in the frequency domain. This article has the main purpose of proposing a still wider clinical use of the spectral methodology. Indeed, with this procedure the state of the sympathovagal balance modulating the sinus node pacemaker activity can be quantified in a variety of physiological and pathophysiological conditions. Changes in the sympathovagal balance can be often detected in basal conditions; however, a reduced responsiveness to an excitatory stimulus is the most common feature that characterizes numerous pathophysiological states. Moreover, the attenuation of an oscillatory pattern or its impaired responsiveness to a given stimulus can also reflect an altered target function and thus can furnish interesting prognostic markers
Sympathetic overactivity in ischaemic heart disease.
No full textThe efficacy of pharmacological beta-blockade in decreasing cardiac death in patients after myocardial infarction suggests the existence of sympathetic overactivity and indicates the importance of assessing its magnitude. The paper by Graham and co-workers in this issue of Clinical Science has attempted to address this issue by measuring muscle sympathetic nerve activity (MSNA) in various groups of patients and control subjects. It was found that, after myocardial infarction, there was sympathetic overactivity, which was more marked and more long-lasting than after unstable angina, whereas, in the presence of simple coronary artery disease, sympathetic activity did not differ from that in control subjects. Clear signs of sympathetic overactivity lasting for months after an acute myocardial infarction have already been reported using quite different methodology, i.e. spectral analysis of heart period and systolic arterial pressure variability. The soundest hypothesis to explain such a sympathetic overactivity appears to be based on the well-demonstrated finding that the ischaemic heart is a powerful site of origin of both excitatory and/or inhibitory reflexes, which may be of paramount clinical importance
Afferent sympathetic unmyelinated fibres with left ventricular endings in cats
No full text1. We recorded the electrical impulse activity of thirty-three single afferent fibres with left ventricular endings from the third and fourth left thoracic sympathetic rami communicantes of anaesthetized cats. Their conduction velocity ranged from 0.23 to 0.98 m/sec (group C). 2. The endings of each fibre were localized to the left ventricle by mechanical probing performed at the end of the experiment on the non-beating heart. No fibre had multiple sensory fields. 3. The impulse activity (0.95 +/- 0.2 impulses/sec) was spontaneous but most often a fixed temporal correlation between impulses and ventricular dynamics was not detectable. It was increased during occlusion of the thoracic aorta, I.V. administration of isoprenaline or infusion of saline. It was unaffected by asphyxia, haemorrhage and I.V. administration of acetylcholine. It was decreased during occlusion of inferior vena cava. Therefore these ventricular receptors appeared to be mainly sensitive to mechanical events. 4. The fibres were excited during the occlusion of the left main coronary artery, after a latency of 14.5 +/- 1.3 sec. They were also excited during ventricular fibrillation, exhibiting the highest values of impulse activity (2.51 +/- 0.4 impulses/sec). The increase in impulse activity during ventricular fibrillation was sometimes immediate and extreme, with peak frequencies of about 50 impulses/sec. 5. These spontaneously active ventricular receptors with unmyelinated nerve fibres participate in the transmission of the continuous impulse activity which from the cardiovascular system reaches the spinal cord through the sympathetic nerves and which is likely to contribute to the neural control of circulation. Thus the unmyelinated cardiac sympathetic afferents should not be considered as purely nociceptive in function
From cardiac nociception to the brain : the unstable character of angina pectoris
No full textWe analyzed some particular aspects of the peripheral pathways likely to be involved in the mediation of cardiac pain. The functional characteristics and the reflex function of cardiac sympathetic afferent fibers are discussed in relation to the afferent code transmitting nociception. A modified version of the intensity theory based on the extreme excitation of a spatially restricted population of afferent sympathetic fibers is proposed as the most likely mechanism involved in the genesis of cardiac pain
Premature ventricular contractions and reflex sympathetic activation in cats
No full textIn 27 decerebrate cats under various experimental conditions, we studied the effects of programmed premature ventricular contractions on the impulse activity of preganglionic sympathetic fibres isolated from the third left thoracic ramus. Single extrastimuli increased the sympathetic discharge by 319(SEM 43)% [from 10.3(1.7) to 36(3.7) imp.s-1, p less than 0.05]. The neural response was significantly enhanced after bilateral vagotomy by 394(34)% [from 12(2.6) to 53.3(9.8) imp.s-1, p less than 0.05], but abolished when the stimuli were delivered during bilateral carotid artery occlusion. No sympathetic reflex response was observed in cats with chronic sino-aortic denervation. In eight cats, during occlusion of the left anterior descending coronary artery, the control sympathetic response was progressively and reversibly attenuated from 239(28)% to 36(14)%, at 90 s from the beginning of the occlusion. After bilateral vagotomy, this inhibitory interaction was no longer present and the sympathetic neural response to programmed stimulation was maintained throughout the occlusion period. The data indicate that the sympathetic reflex response initiated by baroreceptive deactivation could be attenuated by cardiac vagal afferent activity induced by coronary occlusion
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