Novel therapeutic strategy against central baroreflex failure: a bionic baroreflex system.
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BACKGROUND: Central baroreflex failure in Shy-Drager syndrome and traumatic spinal cord injuries results in severe orthostatic hypotension and often confines the patient to the bed. We proposed a novel therapeutic strategy against central baroreflex failure: implementation of an artificial feedback control system able automatically to regulate sympathetic vasomotor tone, that is, a bionic baroreflex system (BBS). With the use of a rat model of central baroreflex failure, we developed the BBS and tested its efficacy. METHODS AND RESULTS: Our prototype BBS for the rat consisted of a pressure sensor placed into the aortic arch, stimulation electrodes implanted into the greater splanchnic nerve, and a computer-driven neural stimulator. By a white noise approach for system identification, we first estimated the dynamic properties underlying the normal baroreflex control of systemic arterial pressure (SAP) and then determined how the BBS computer should operate in real time as the artificial vasomotor center to mimic the dynamic properties of the native baroreflex. The open-loop transfer function of the artificial vasomotor center was identified as a high-pass filter with a corner frequency of 0.1 Hz. We evaluated the performance of the BBS in response to rapid-progressive hypotension secondary to sudden sympathetic withdrawal evoked by the local imposition of a pressure step on carotid sinus baroreceptors in 16 anesthetized rats. Without the BBS, SAP rapidly fell by 49+/-8 mm Hg in 10 seconds. With the BBS placed on-line with real-time execution, the SAP fall was suppressed by 22+/-6 mm Hg at the nadir and by 16+/-5 mm Hg at the plateau. These effects were statistically indistinguishable from those of the native baroreflex system. CONCLUSIONS: These results suggest the feasibility of a BBS approach for central baroreflex failure. (+info)
Abnormal autonomic cardiovascular control in ankylosing spondylitis.
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OBJECTIVE: This study was aimed at assessing the contribution of the autonomic nervous system to adjustments of cardiovascular function in patients with ankylosing spondylitis (AS). METHODS: In 18 AS patients (mean age: 34.9; mean disease duration: 6.4 years) and 13 healthy controls (mean age: 31.7) the changes of heart rate (HR) with deep breathing (E/I ratio) and standing up (30/15 ratio) were recorded. The slope of cardiac baroreflex, the times series of blood pressure and HR values upon lying and standing, and venous plasma concentrations of catecholamines were also analysed. Erythrocyte sedimentation rate (ESR), plasma C reactive protein (CRP) concentration and a clinical index (BASDAI score) were used to assess the degree of disease activity in patients. RESULTS: In the standing patients, blood pressure was found to decrease progressively (p< 0.001). Furthermore, the patients with a BASDAI score > 5 had a higher heart rate than patients with a BASDAI score < 5 (p<0.02), and there was a trend for a similar difference when patients were classified according to their ESR and CRP. Plasma catecholamine concentrations and the E/I ratio were not different in patients from controls. The 30/15 ratio and the slope of the spontaneous baroreflex during standing were both lower in AS patients than controls (p< 0.01). CONCLUSIONS: This study demonstrated a change in autonomic nervous system function of AS patients, with a decreased parasympathetic activity, as evidenced by higher HR and lower baroreflex slope. As these significant deviances were mainly observed in patients with more active (or more inflammatory) disease, the autonomic nervous system involvement could be related to the inflammatory process. This autonomic strain may be related to the cardiac involvement in AS patients. (+info)
Baroreflex gain predicts blood pressure recovery during simulated ventricular tachycardia in humans.
(35/1596)
BACKGROUND: Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. METHODS AND RESULTS: We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (n=12) or 120 (n=2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP (r=0.57, P=0.034). No significant correlation between ejection fraction and baroreflex gain (r=0.48, P=0.08) or BP recovery (r=0.41, P=0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. CONCLUSIONS: These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT. (+info)
Arterial baroreflex function in humans anaesthetized with sevoflurane.
(36/1596)
Volatile anaesthetic agents attenuate arterial baroreflex function, while noxious stimuli may modify baroreflex-induced circulatory responses during anaesthesia. We have examined baroreflex control of heart rate during the entire course of sevoflurane anaesthesia in adult patients undergoing surgical procedures. Baroreflex sensitivity was assessed in nine healthy patients undergoing general anaesthesia with sevoflurane. After an 8-10-h fast and no premedication, measurements of R-R intervals were made at conscious baseline (awake), during 2% end-tidal sevoflurane and 67% nitrous oxide before incision (anaesthesia), during surgery at 2% end-tidal sevoflurane and 67% nitrous oxide (surgery) and 20 min after extubation (recovery). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine 50-100 micrograms and nitroprusside 100-200 micrograms to increase and decrease systolic arterial pressure by 20-30 mm Hg, respectively. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during anaesthesia, surgery and the recovery periods compared with awake values. Pressor test sensitivity during recovery increased significantly from that during surgery (mean 6.16 (SD 2.95) vs 4.42 (3.19) ms mm Hg-1; P < 0.05), but was still significantly less than the awake value (22.50 (17.02) ms mm Hg-1). No improvement in the depressor test sensitivity was seen during the recovery period. (+info)
Reflex control of sympathetic activity during simulated ventricular tachycardia in humans.
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BACKGROUND: Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. METHODS AND RESULTS: Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (-4.7+/-1.4 U/mm Hg) than during ventricular pacing (-3.4+/-1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (P=0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (P<0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212+/-35% versus 189+/-37%, P=0. 04). Conclusions--These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation. (+info)
A five-parameter logistic equation for investigating asymmetry of curvature in baroreflex studies.
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Baroreceptor reflex curves are usually analyzed using a symmetric four-parameter function. We wished to ascertain the validity of assuming symmetry in the baroreflex curve and also of constraining the curves to pass through the resting blood pressure and heart rate (HR) values. Therefore, we have investigated the suitability of a new five-parameter asymmetric logistic model for analysis of baroreflex curves from rabbits and dogs. The five-parameter model is an extension of the usual four-parameter model and reduces to that model when the fitted data are symmetrical. Using 30 data sets of blood pressure versus renal sympathetic nerve activity (RSNA) and HR from six conscious rabbits, we compared the five-parameter curves with the four-parameter model. We also tested the effect of forcing these baroreflex curves through the resting point. We found that the five-parameter model reduced the unexplained variation and gave small but important improvements to the estimates of plateaus for RSNA and HR and the HR gain. Although forcing the HR curves through the resting values had little effect, this procedure, when applied to RSNA, produced a worse curve fit by increasing the unexplained variation with alteration to most of the estimated curve parameters. The mean arterial pressure-HR baroreflex relationship from six conscious dogs was also analyzed and showed clear evidence of systematic asymmetry. We conclude that the asymmetric model is a valuable extension to the symmetric logistic model when examining baroreceptor reflexes, giving improved estimates of the parameters and a new approach to examining the mechanisms contributing to baroreflex curve asymmetry. Furthermore, forcing the curves through the resting value is a statistically questionable practice when analyzing RSNA, because it affects the parameter estimates. (+info)
Effects of 17beta-estradiol on the baroreflex control of sympathetic activity in conscious ovariectomized rats.
(39/1596)
The effects of chronic treatment with 17beta-estradiol on baroreflex control of sympathetic activity were examined in conscious unrestrained ovariectomized rats. Baroreflex function was evaluated by logistic sigmoidal analysis of the relationships between changes in mean arterial pressure (MABP) and changes in heart rate (HR) and splanchnic nerve activity (SNA) when MABP was rapidly increased to 150 mmHg by intravenous phenylephrine after its reduction to 50 mmHg by intravenous nitroprusside. These baroreflex function curves were similar in vehicle- and estradiol-treated rats. However, after a 30-min infusion of vasopressin in vehicle-treated rats, the curve for HR was shifted downward, and the upper plateau and maximum gain for the SNA curve were reduced. These effects were abolished by estradiol. A 30-min phenylephrine infusion had no effect on the baroreflex curves. Thus estrogen can modulate the action of vasopressin on baroreflex control of sympathetic outflow and thereby participate in cardiovascular regulation. (+info)
Slowing and attenuation of baroreflex heart rate control with nitrous oxide in exercising men.
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The objective of the present study was to determine whether mild inert-gas narcosis impairs cardiovascular control mechanisms and contributes to the relative bradycardia that occurs in humans exercising in a hyperbaric environment. Eight healthy subjects were exposed to a normoxic 30% nitrous oxide (N(2)O) mixture and an air control during dynamic exercise of 100-W intensity. Beat-by-beat heart rate (HR) and invasive arterial blood pressure measurements were made. The sensitivity and the response latency of the arterial-cardiac-chronotropic baroreflex were determined from repeated blood pressure and HR transients induced by rapid tilts between the upright and supine posture. A significant increase (37%, P +info)