Effects of Spinal Section and of Positive-Feedback Excitatory Reflex on Sympathetic and Heart Rate Variability

Montano, Nicola; Cogliati, Chiara; Silva, Valdo José Dias da; Gnecchi‐Ruscone, Tomaso; Massimini, Marcello; Porta, Alberto; Malliani, Alberto

doi:10.1161/01.hyp.36.6.1029

Cited by 37 publications

(43 citation statements)

References 40 publications

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“…[5][6][7] It is well established that afferent nerve traffic from the thorax and abdomen also provides input to central cardiovascular centers after traveling with sympathetic nerves back to the spinal cord and then to medullary cardiovascular control centers. 8 These afferents are less well understood at the level of clinical presentation and are beyond the scope of this review.…”

Section: Physiologymentioning

confidence: 98%

Four Faces of Baroreflex Failure

et al. 2002

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Background — The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. Methods and Results — Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. Conclusions — Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.

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Section: Physiologymentioning

confidence: 98%

Four Faces of Baroreflex Failure

et al. 2002

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“…A subsequent dorsal root section, by interrupting cardiovascular sympathetic afferents, abolishes this positive-feedback excitatory reflex. 60 Moreover, it is interesting to mention that propranolol, given during acute episodes in animal experiments, was capable of reducing the responsiveness of aortic and pulmonary vein sympathetic afferents to elevations in arterial pressure. 61 This effect was independent of its membranestabilizing properties because DL-propranolol was active, whereas D-propranolol, possessing only this stabilizing property, was ineffective.…”

Section: Arterial Hypertensionmentioning

confidence: 99%

Emerging Excitatory Role of Cardiovascular Sympathetic Afferents in Pathophysiological Conditions

Malliani¹,

Montano²

2002

Hypertension

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135

119

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Abstract-There is sound experimental evidence that cardiovascular sympathetic afferent fibers mediate cardiovascular reflexes largely excitatory in nature with positive-feedback characteristics. This afferent neural channel is likely to normally participate in the neural regulation of cardiovascular function. The hypothesis, which is the core of this article, is that in some pathophysiological conditions, sympathetic overactivity may be partly due to an emerging excitatory reflex action of cardiovascular sympathetic afferents. In fact, the early phase of congestive heart failure can be characterized by an increase in arterial pressure and heart rate and/or by a diastolic dysfunction, leaving unchanged the cardiac output; in these conditions, in which no baroreceptor deactivation should occur, it is possible that cardiovascular sympathetic afferents with sensory endings in the thoracic low-pressure areas, highly responsive to volume loading, are responsible for mediating the reflex sympathetic excitation. Similarly, during acute myocardial infarction, ventricular sympathetic afferents are likely to mediate a reflex sympathetic overactivity, which is known to facilitate sudden death. Finally, numerous reports have described in essential arterial hypertension an increased sympathetic activity that may be due, at least in part, to the reinforcing action of sympathosympathetic reflexes. Thus, in pathophysiological conditions, cardiovascular sympathetic afferents would mediate a reflex sympathetic overactivity independently of baroreceptive mechanisms, and such an absence of a homeostatic purpose would provide a better rationale for some beneficial effects of therapeutic correction. Key Words: heart failure Ⅲ ischemia Ⅲ hypertension, arterial Ⅲ heart rate Ⅲ reflex Ⅲ lung T he present article will attempt to support the hypothesis that in the early phase of congestive heart failure and other pathophysiological conditions, such as myocardial ischemia and arterial hypertension, sympathetic excitation seems devoid of an ultimate homeostatic purpose, and its genesis may be, in part, attributable to an enhanced peripheral excitatory function of sympathetic afferent fibers.In physiological conditions, the cardiovascular neural regulation is likely to result from a complex interaction of central integration and peripheral inhibitory and excitatory reflexes. [1][2][3] In this interplay, cardiovascular sympathetic afferent fibers mediate a reflex action that is largely excitatory in nature 1 (Figure). When a sympathetic excitation is part of an integrated physiological pattern with a clear ultimate purpose, such as emotion, the central neural and, in particular, diencephalic mechanisms 4 are likely to play a predominant role. However, the central command is also likely to be reinforced by a synergistic enhancement of peripheral excitatory reflex mechanisms, accompanied by a simultaneous attenuation of mechanisms exerting an inhibitory action. 3,4

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“…Grasso et aL [21] suggest that these are generated by baroreflex. However, previous human [10] and animal studies [10,[22][23][24] support the concept of a central oscillator. For the LF oscillations of BP, the sympathetic contribution has been convincingly shown [25].…”

mentioning

confidence: 92%

Impaired autonomic control of heart rate and blood pressure in obesity: role of age and of insulin-resistance

Quilliot

Fluckiger

Zannad

et al. 2001

Clinical Autonomic Research

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The objectives of this study were to investigate cardiac and peripheral autonomic nervous system changes in normotensive overweight or obese subjects and the possible relation between these changes and insulin resistance independent of age. The authors used spectral analysis to measure simultaneously the short-term variability of heart rate (HR) and blood pressure (BP) using a Finapres device, in 67 normotensive overweight or obese patients (age 37 +/- 12 y, body mass index [BMI] = 37 +/- 9 kg/m2) and 45 never-obese subjects (controls; age 41 +/- 13 y, BMI 22 +/- 2 kg/m2). The spectral density was determined in three situations: subjects in the supine position, spontaneously breathing; subjects in the supine with controlled breathing; and subjects standing. The insulin sensitivity of overweight and obese subjects was determined from homeostatic model assessment (HOMA). The variability of normalized low-frequency (LF) spectral analysis of both HR and BP was lower in overweight or obese subjects than in controls, in the supine and standing positions (p <0.01). Normalized LF spectral analysis was negatively correlated to BMI independent of age, whatever the position. Homeostatic model assessment values were negatively correlated to the normalized LF spectral of HR, systolic BP and diastolic BP, in the standing position independent of BMI and age (p <0.05). Normalized high frequency (HF) of HR during controlled breathing decreased with age but not with BMI. In normotensive overweight or obese subjects, changes in sympathetic nervous system modulation are strongly correlated to insulin resistance. Decreased HR and BP variability could partly account for the higher cardiovascular risk and incidence of sudden death in obese persons.

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Effects of Spinal Section and of Positive-Feedback Excitatory Reflex on Sympathetic and Heart Rate Variability

Cited by 37 publications

References 40 publications

Four Faces of Baroreflex Failure

Four Faces of Baroreflex Failure

Emerging Excitatory Role of Cardiovascular Sympathetic Afferents in Pathophysiological Conditions

Impaired autonomic control of heart rate and blood pressure in obesity: role of age and of insulin-resistance

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