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Probing the arterial baroreflex: is there a 'spontaneous' baroreflex?

The arterial baroreflex is important for beat-to-beat arterial pressure control and its sensitivity has predictive value for clinical outcomes in a myriad of cardiovascular conditions. Given this, researchers have sought approaches for baroreflex assessment that are not invasive and easily obtained. These techniques have exploited the beat-by-beat parallel changes in arterial pressure and heart period to produce estimates that have been termed 'spontaneous' baroreflex indices. The two most commonly used analyses--frequency domain or spectral analyses and sequence analysis have been evaluated in both animals and humans. The animal data suggests an important baroreflex role in linking spontaneous heart period and pressure variabilities, but do not resolve the extent to which these fluctuations reflect baroreflex gain. The human data suggest a high correlation between spontaneous indices and pharmacologically derived baroreflex gain, but also indicate a poor correspondence between them. This may be due to the fact that short-term fluctuations in RR interval are not intimately and always linked to those in pressure via the baroreflex and thus simple observation of arterial pressure and heart period alone may not reveal the extent of arterial baroreflex involvement. If baroreflex function is to be assessed with the fewest and safest assumptions, the input to the system should be driven externally to create large and apparent responses. Nonetheless, spontaneous baroreflex indices may have predictive power; although it remains unknown whether spontaneous indices provide predictive power beyond that provided by heart rate variability indices alone.

Animals↗

Bionic technology revitalizes native baroreflex function in rats with baroreflex failure.

BACKGROUND: We developed a bionic technology for the treatment of baroreflex failure and tested its efficacy in restoration of arterial pressure against head-up tilt (HUT) in rats with baroreflex failure. METHODS AND RESULTS: The bionic baroreflex system (BBS) was a negative feedback system controlled by a computer, the artificial vasomotor center. It sensed systemic arterial pressure (SAP) through a micromanometer placed in the aortic arch and automatically computed the frequency of a pulse train to stimulate sympathetic efferent nerves. We selected the celiac ganglion as the sympathetic vasomotor interface. To make this system bionic, the operational rule of the artificial vasomotor center (H(BRP-->STM); BRP indicates baroreceptor pressure; STM, electrical stimulation) was actively matched to that of the native center. First, we identified the open-loop transfer functions of the native baroreflex control of SAP (H(Native)) and the response of SAP to electrical stimulation of the celiac ganglion (H(STM-->SAP)). We computed H(BRP-->STM) from H(Native)/H(STM-->SAP) and transplanted the operational rule into the computer. In 10 rats with baroreflex failure, we evaluated the performance of the BBS during rapid hypotension induced by HUT. Abrupt HUT dropped SAP by 34+/-6 mm Hg in 2 seconds and by 52+/-5 mm Hg in 10 seconds. During real-time execution of the BBS, on the other hand, the fall in SAP was 21+/-5 mm Hg at 2 seconds and 15+/-6 mm Hg at 10 seconds after HUT. These arterial responses controlled by the BBS were indistinguishable from those by the native baroreflex. CONCLUSIONS: We concluded that the BBS revitalized the native baroreflex function in rats with baroreflex failure.

Animals↗

Novel therapeutic strategy against central baroreflex failure: a bionic baroreflex system.

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.

Animals↗

Does halothane really preserve cardiac baroreflex better than sevoflurane? A noninvasive study of spontaneous baroreflex in children anesthetized with sevoflurane versus halothane.

Heart rate profiles during the induction of anesthesia differ markedly between the administration of sevoflurane and halothane. Previous investigations have shown that halothane preserves cardiac parasympathetic activity more than sevoflurane. Because vagal drive to the sinus node is the main effector of arterial baroreflex control of heart rate, halothane may preserve cardiac baroreflex better than sevoflurane. To investigate cardiac baroreflex in anesthetized children, we used two noninvasive methods providing different approaches to the arterial blood pressure (BP) and R-R interval (RRI) relationship: the sequence methods investigating beat-to-beat changes in BP and RRI (time domain) and the cross-spectral analysis investigating relationships between oscillations of BP and RRI (frequency domain). Children were randomly assigned to mask induction with sevoflurane in 100% oxygen, sevoflurane in 50% nitrous oxide/50% oxygen, or halothane in 50% nitrous oxide/50% oxygen. After tracheal intubation, the inspired fraction of volatile anesthetic was reduced to 1 minimum alveolar anesthetic concentration (MAC). The spontaneous baroreflex (SBR) sensitivity was calculated with the sequence method at baseline, during induction, and after intubation. The cardiac baroreflex was also estimated with cross-spectral analysis at baseline and at 1 MAC (stationary conditions). In the three groups, the induction of anesthesia was associated with a marked decrease of SBR sensitivity, which occurred earlier with sevoflurane than with halothane. Five minutes after intubation (1 MAC), the sequence method showed a similar decrease of the SBR sensitivity in the three groups. Similarly, the cross-spectral analysis between systolic blood pressure and RRI showed a decrease of the gain calculated in the low-frequency band, but the gain in the respiratory band was higher with halothane compared with sevoflurane. In children, the induction of anesthesia with halothane and sevoflurane is associated with a marked decrease of cardiac baroreflex activity. The persistence of respiratory RRI fluctuations under halothane might reflect reflex respiratory arrhythmia rather than efficient parasympathetic baroreflex activity.

Anesthetics, Inhalation↗

Baroreflex effectiveness index: an additional measure of baroreflex control of heart rate in daily life.

In healthy subjects, progressive beat-to-beat increases or decreases in systolic blood pressure (SBP) ramps are not always accompanied by baroreflex-driven lengthening or shortening in pulse interval (PI) ramps, respectively. This phenomenon has been quantified by a new index, the baroreflex effectiveness index (BEI), defined as the ratio between the number of SBP ramps followed by the respective reflex PI ramps and the total number of SBP ramps observed in a given time window. Specificity of BEI was shown in eight cats by a -89% reduction of BEI after sinoaortic denervation. In 14 healthy humans, the 24-h average BEI value was 0.21, with a marked day-night modulation ( approximately 0.25 day, approximately 0.15 night) in counterphase with modulation of baroreflex sensitivity (BRS). Our analysis indicates that 1) in normal subjects, arterial baroreflex can induce beat-by-beat PI changes in response to only 21% of all SBP ramps, possibly because of central inhibitory influences or of interferences at sinus node level by nonbaroreflex mechanisms and 2) BEI provides information on the baroreflex function that is complementary to BRS.

Adult↗

Counteraction of aortic baroreflex to carotid sinus baroreflex in a neck suction model.

Although neck suction has been widely used in the evaluation of carotid sinus baroreflex function in humans, counteraction of the aortic baroreflex tends to complicate any interpretation of observed arterial pressure (AP) response. To determine whether a simple linear model can account for the AP response during neck suction, we developed an animal model of the neck suction procedure in which changes in carotid distension pressure during neck suction were directly imposed on the isolated carotid sinus. In six anesthetized rabbits, a 50-mmHg pressure perturbation on the carotid sinus decreased AP by -27.4+/-4.8 mmHg when the aortic baroreflex was disabled. Enabling the aortic baroreflex significantly attenuated the AP response (-21.5+/-3.8 mmHg, P<0.01). The observed closed-loop gain during simulated neck suction was well predicted by the open-loop gains of the carotid sinus and aortic baroreflexes using the linear model (-0.43+/-0.13 predicted vs. -0.41 +/-0.10 measured). We conclude that the linear model can be used as the first approximation to interpret AP response during neck suction.

Animals↗

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗

Artificial baroreflex: clinical application of a bionic baroreflex system.

BACKGROUND: We proposed a novel therapeutic strategy against central baroreflex failure: implementation of an artificial baroreflex system to automatically regulate sympathetic vasomotor tone, ie, a bionic baroreflex system (BBS), and we tested its efficacy in a model of sudden hypotension during surgery. METHODS AND RESULTS: The BBS consisted of a computer-controlled negative-feedback circuit that sensed arterial pressure (AP) and automatically computed the frequency (STM) of a pulse train required to stimulate sympathetic nerves via an epidural catheter placed at the level of the lower thoracic spinal cord. An operation rule was subsequently designed for the BBS using a feedback correction with proportional and integral gain factors. The transfer function from STM to AP was identified by a white noise system identification method in 12 sevoflurane-anesthetized patients undergoing orthopedic surgery involving the cervical vertebrae, and the feedback correction factors were determined with a numerical simulation to enable the BBS to quickly and stably attenuate an external disturbance on AP. The performance of the designed BBS was then examined in a model of orthostatic hypotension during knee joint surgery (n=21). Without the implementation of the BBS, a sudden deflation of a thigh tourniquet resulted in a 17+/-3 mm Hg decrease in AP within 10 seconds and a 25+/-2 mm Hg decrease in AP within 50 seconds. By contrast, during real-time execution of the BBS, the decrease in AP was 9+/-2 mm Hg at 10 seconds and 1+/-2 mm Hg at 50 seconds after the deflation. CONCLUSIONS: These results suggest the feasibility of a BBS approach for central baroreflex failure.

Aged↗

Baroreflex effectiveness index and baroreflex sensitivity predict all-cause mortality and sudden death in hypertensive patients with chronic renal failure.

OBJECTIVES: Impaired arterial baroreflex sensitivity (BRS) has been associated with cardiac mortality and non-fatal cardiac arrests after a myocardial infarction. Patients with chronic renal failure (CRF) have a poor prognosis because of cardiovascular diseases, and sudden death is common. The aim of this study was to assess whether BRS or the baroreflex effectiveness index (BEI), a novel index reflecting the number of times the baroreflex is active in controlling the heart rate in response to blood pressure fluctuations, is associated with prognosis in CRF. METHODS: Hypertensive patients with CRF who were treated conservatively, by haemodialysis or peritoneal dialysis were studied. Electrocardiogram and beat-to-beat blood pressures were recorded continuously and BRS and BEI were calculated. Patients were then followed prospectively for 41 +/- 15 months (range 1-64). RESULTS: During follow-up 69 patients died. Cardiovascular diseases and uraemia accounted for the majority of deaths (60 and 20%, respectively), whereas sudden death occurred in 15 patients. In adjunct with established risk factors such as age, diabetes, congestive heart failure and diastolic blood pressure, reduced BEI was an independent predictor of all-cause mortality among CRF patients [relative risk (RR) 0.50, 95% confidence interval (CI) 0.33-0.71 for an increase of one standard deviation in BEI, P < 0.001]. Diabetes and reduced BRS were independent predictors of sudden death (RR 0.29, 95% CI 0.09-0.86 for an increase of one standard deviation in BRS, P=0.022). CONCLUSIONS: Both BEI and BRS convey prognostic information that may have clinical implications for patients with cardiovascular diseases in general.

Baroreflex↗

High-cut characteristics of the baroreflex neural arc preserve baroreflex gain against pulsatile pressure.

A transfer function from baroreceptor pressure input to sympathetic nerve activity (SNA) shows derivative characteristics in the frequency range below 0.8 Hz in rabbits. These derivative characteristics contribute to a quick and stable arterial pressure (AP) regulation. However, if the derivative characteristics hold up to heart rate frequency, the pulsatile pressure input will yield a markedly augmented SNA signal. Such a signal would saturate the baroreflex signal transduction, thereby disabling the baroreflex regulation of AP. We hypothesized that the transfer gain at heart rate frequency would be much smaller than that predicted from extrapolating the derivative characteristics. In anesthetized rabbits (n = 6), we estimated the neural arc transfer function in the frequency range up to 10 Hz. The transfer gain was lost at a rate of -20 dB/decade when the input frequency exceeded 0.8 Hz. A numerical simulation indicated that the high-cut characteristics above 0.8 Hz were effective to attenuate the pulsatile signal and preserve the open-loop gain when the baroreflex dynamic range was finite.

Animals↗

Estimation of baroreflex gain using a baroreflex equilibrium diagram.

Two types of closed-loop perturbations can be applied to the arterial baroreflex system. The first (P(D1)) is introduced into the baroreceptors without a direct effect on arterial pressure (AP), whereas the second (P(D2)) initially affects AP. Neck suction and hemorrhage are examples of P(D1) and P(D2), respectively. To estimate the baroreflex open-loop gain (G(Baro)) without knowing the absolute magnitudes of P(D1) and P(D2), we explored a new strategy to estimate G(Baro) by combining P(D1) and P(D2) in a baroreflex equilibrium diagram. In this diagram, the neural arc presents the input-output relationship between baroreceptor pressure input and sympathetic nerve activity (SNA). The peripheral arc presents the input-output relationship between SNA and AP. In 8 anesthetized rabbits, we estimated G(Baro) by multiplying the slopes of the peripheral arc determined from P(D1) and the neural arc determined from P(D2). We also estimated G(Baro) by a conventional open-loop analysis. The G(Baro) values estimated by the equilibrium diagram and the open-loop analysis showed a positive correlation (y = 0.80x + 0.22, r(2) = 0.95) and a standard error of estimate of 0.21 across the animals. We conclude that G(Baro) was estimated well by combining P(D1) and P(D2) in the equilibrium diagram.

Animals↗

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits.

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90-100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5-16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Baroreflex and non-baroreflex modulation of vagal cardiac control after myocardial infarction.

Vagal control of sinus node exerted by arterial baroreceptors is markedly impaired 48 hours after acute myocardial infarction (AMI), but it recovers 10 days later. However, it is unknown whether this recovery is peculiar to baroreceptor vagal control or reflects normalization of the overall vagal modulation of heart rate. In 21 untreated patients (aged 51+/-3 years, mean +/- SEM) studied 10+/-1 and 21+/-1 days after an AMI and in 13 healthy controls (aged 47+/-2 years), we examined the increases in RR interval (electrocardiogram) induced by carotid baroreceptor stimulation via a neck chamber and by immersion of the face in iced water for 15 seconds (diving reflex). Both 10 and 21 days after AMI, baseline blood pressure and RR interval values were superimposable to those obtained in controls. Ten days after AMI, the bradycardic responses to carotid baroreceptor stimulation were similar to those seen in controls (maximal RR interval lengthenings: 248+/-34 vs 270+/-31 ms, respectively, p = NS) and remained virtually unchanged later. In contrast, the bradycardic response to diving was reduced in patients after AMI compared with controls (maximal RR interval lengthenings: 203+/-43 vs 325+/-52 ms, respectively, p <0.05) and did not improve later. Thus, in AMI recovery of the early impairment of baroreceptor-heart rate control does not reflect normalization of vagal cardiac control, which remains lower than normal values at a time when the baroreflex is restored.

Blood Pressure↗

Baroreflexes and cardiovascular regulation in hypertension.

The primary purpose of the arterial baroreflex is to keep blood pressure close to a particular set point over a relatively short period of time. The rapid resetting of arterial baroreceptor afferents toward any sustained new level of blood pressure ensures that the reflex acts as an effective buffer of short-term blood pressure fluctuations that accompany daily life but also ensures that arterial baroreflexes play little role in setting the long-term level of blood pressure. Nevertheless, the minimization of blood pressure variability by baroreflex mechanisms is important as studies suggest that a diminished baroreflex is an independent risk factor or sudden death after myocardial infarction. In hypertensive humans and animals, the baroreflex control of heart rate is diminished. Using the steady-state method for assessment of the cardiac baroreflex in rats, we have shown that the change in baroreflex sensitivity is due to a reduction in the vagal range. Although the cardiac sympathetic component of the baroreflex is normal, the level of cardiac sympathetic activity is enhanced, particularly in young hypertensive rats. We have shown that there is a stronger inverse relationship between vagal heart rate range and levels of cardiac hypertrophy than with other variables, such as blood pressure, hypertension, or indexes of vascular hypertrophy. Treatments that reduce cardiac hypertrophy restore cardiac vagal function. Centrally acting antihypertensive agents increase the sensitivity of vagal baroreceptor heart rate reflexes, mainly through an action on central alpha 2-adrenoceptors. They also reduce cardiac sympathetic activity and diminish cardiac sympathetic baroreflexes through a non-alpha 2-adrenoceptor, possibly an imidazoline receptor mechanism. Both of these effects are beneficial in hypertension, where cardiac sympathetic function is enhanced and vagal activity is reduced. Thus, these actions would be expected to cause a desirable reduction in blood pressure variability. The effect of hypertension on baroreflex control of sympathetic vasomotor function is less clear. Studies have shown diminished, normal, and enhanced sympathetic vasomotor baroreflex control. Basal renal sympathetic drive, however, appears to be increased in human essential hypertension. Our studies in conscious rabbits have shown that rilmenidine reduces renal sympathetic baroreflex function. Rilmenidine acts principally at the level of the rostral ventrolateral medullary imidazoline receptors to markedly reduce the basal renal sympathetic nerve activity and the maximum response to transient fluctuations in blood pressure. Thus, in addition to their antihypertensive actions, centrally acting agents, such as rilmenidine, reduce cardiac and renal sympathetic baroreflex responses and increase cardiac vagal baroreflex sensitivity. This provides an ideal profile of action for the restoration of baroreflex function in addition to reversal of cardiac and vascular hypertrophy in hypertension.

Animals↗

Muscle sympathetic baroreflex sensitivity is different at rest and during evoked hypotension.

Arterial muscle sympathetic baroreflexes are frequently assessed using pharmacologically evoked decrements in arterial blood pressure. Since drugs administered for baroreflex tests may themselves alter the sympathetic response to evoked pressure variations we proposed a method to determine sympathetic baroreflex gain during spontaneous fluctuations in arterial pressure at rest and tested the null hypothesis that baroreflex gain assessed during spontaneous fluctuations in arterial pressure equals baroreflex gain determined during evoked hypotension. Muscle sympathetic nerve activity (MSA), arterial blood pressure, and heart rate were assessed at rest in 15 healthy volunteers (age: 29 years +/- 5, mean +/- SD). All diastolic pressures sampled during a 5 min period were grouped in intervals of 1 mmHg and the burst incidence per interval was calculated. The slope of the regression line of burst incidence and diastolic pressure represents baroreflex gain during spontaneous fluctuations in arterial pressure. In the same volunteers, burst incidence was also determined over 30 s periods before and after a decrease in arterial pressure evoked by nitroprusside (SNP, 2-3 micro g kg(-1) i. v.). The relationship between mean MSA burst incidence and diastolic arterial pressure was compared before and after the pressure decrease yielding an average baroreflex "gain" during evoked hypotension. Average baroreflex "gain" assessed by this conventional method was compared to baroreflex gain assessed during spontaneous arterial pressure fluctuations by Bland-Altman analysis and correlation analysis. Resting MSA was 28 bursts/100 heart beats +/- 10 at a diastolic pressure of 71 mmHg +/- 11. Baroreflex gain during spontaneous arterial pressure fluctuations was 4.0% mmHg(-1) +/- 1.9 and was significantly greater than the average "gain" assessed during evoked hypotension (2.1% mmHg(-1) +/- 1.6). Individual values for baroreflex gain determined with both methods did not correlate (r = 0.1, p = 0.8). Baroreflex gain as determined during spontaneous arterial pressure fluctuations differs from that assessed during SNP-evoked hypotension, possibly due to intrinsic effects of SNP on the baroreflex. Thus, caution should be exercised when interpreting baroreflex gain derived during SNP-evoked hypotension.

Adult↗