Degrees Head-up Tilt Research Articles

Cross-spectral analysis of cardiovascular parameters whilst supine may identify subjects with poor orthostatic tolerance.

An easy and low-cost method for identification of subjects prone to orthostatic vasovagal syncope would be of clinical benefit. An orthostatic test with 60 degrees head-up tilt and progressive lower-body negative pressure was performed on 79 patients with histories of unexplained syncope and 26 control subjects. The test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Spectral and cross-spectral analysis was performed on the supine time series of the R-R interval (ECG) and systolic pressure (Finapres) recorded before the beginning of the test. According to reference values, 38 patients and 11 controls were classified as having poor orthostatic tolerance (PPT and CPT respectively), whereas 41 patients and 15 controls displayed normal orthostatic tolerance (PNT and CNT respectively). The central frequency of the low-frequency (LF approximately equal to 0.1 Hz.) oscillations in PNT and CNT was significantly higher than that in PPT and CPT. In addition, it was significantly linearly correlated with the time of presyncope. Using our test of orthostatic tolerance as a comparison, the LF central frequency allows the classification of subjects with poor or normal tolerance with 80% sensitivity and 82% specificity. These results suggest that the LF central frequency in the supine position may provide a useful index in the diagnosis of orthostatic intolerance.

Cerebral oxygenation monitor during head-up and -down tilt using near-infrared spatially resolved spectroscopy.

Reflectance near-infrared spectroscopy (NIRS) has become a suitable and easily manageable method to monitor cerebral oxygenation changes in presyncopal and syncopal symptoms caused by postural changing or standing. A new clinical tissue oxygenation monitor has been recently developed which measures absolute tissue haemoglobin saturation (Tissue Oxygenation Index, TOI) utilizing spatially resolved spectroscopy (SRS). The present study examined the effects of postural changes on cerebral oxygenation as reflected in SRS-NIRS findings. Cerebral oxyhaemoglobin (O2Hb), deoxyhaemoglobin (HHb), and the TOI were recorded from both sides of the forehead in five healthy male subjects (age range, 28-40 years) during 90 degrees head-up tilt (HUT) and -6 degrees head-down tilt (HDT). Three series of measurements were carried out on separate days. O2Hb was decreased during HUT. TOI was significantly lower in HUT than in the supine position (SUP). There was no significant change in TOI during HDT. A significant session effect was observed in the left forehead TOI during SUP, but not in the right. SRS-NIRS measurements confirmed sub-clinical alterations of cortical oxygenation during HUT. NIRS data from the left side of the forehead, which may vary with cognitive or emotional activation, were more variable than those from the right side.

NCPAP improves abnormal autonomic function in at-risk-for-SIDS infants with OSA

We evaluated cardiovascular autonomic control and arousability during sleep in infants with obstructive sleep apnea (OSA) before and after 10 +/- 4 (mean +/- SD) days of treatment with nasal continuous positive airway pressure (nCPAP). Six OSA infants and 12 age-matched control infants were studied with polygraphic sleep studies at the age of 13 +/- 4 wk. During the study, 45 degrees head-up tilt tests were performed in slow-wave and rapid eye movement sleep. Blood pressure (BP) and heart rate (HR) were continuously monitored. All OSA infants had decreased initial BP and HR responses, followed by hypotension in two and hypertension in two. OSA infants displayed higher arousal thresholds in response to the tilt in rapid eye movement sleep (P < 0.005) and higher baseline HR (P < 0.05) than controls. nCPAP treatment normalized BP and HR responses as well as arousal thresholds to tilting and stabilized HR levels. OSA in infants may be linked with cardiovascular autonomic control disturbances and decreased arousability during sleep. These defects are improved by control of OSA with nCPAP.

Role of the autonomic nervous system in push-pull gravitational stress in anesthetized rats.

Tolerance to +G(z) stress is reduced by preceding exposure to -G(z) (push-pull effect). The mechanism(s) responsible for this effect are not fully understood, although the arterial baroreceptor reflexes have been implicated. We investigated the integrative response of the autonomic nervous system by studying responses to gravitational stress before and after autonomic function was inhibited by hexamethonium in 10 isoflurane-anesthetized male and female Sprague-Dawley rats. Animals were restrained supine and subjected to two rotations imposed about the x-axis: 1) a control G profile consisting of rotation from 0 G(z) (+1 G(y)) to 90 degrees head-up tilt (+1 G(z)) for 10 s and 2) a push-pull G profile consisting of rotation from 0 G(z) to 90 degrees head-down tilt (-1 G(z)) for 2 s immediately preceding 10 s of +1 G(z) stress. Eight G profiles consisting of equal numbers of control and push-pull trials were imposed by using a counterbalanced design. We found that hexamethonium lowered baseline arterial pressure and abolished the push-pull effect. The lack of a push-pull effect after autonomic blockade persisted when arterial pressure was restored to baseline levels by phenylephrine infusion. Lowering baseline arterial pressure by sodium nitroprusside infusion or by hemorrhage when autonomic function was intact also abolished the push-pull effect. We conclude that intact autonomic function and a normal baseline arterial pressure are needed for expression of the push-pull effect in anesthetized rats subjected to tilting.

Changes in the transthoracic impedance signal predict the outcome of a 70 degrees head-up tilt test.

We determined whether early changes in central haemodynamics, as determined by transthoracic impedance, induced by a 70 degrees head-up tilt (HUT) test could predict syncope. Heart rate, arterial blood pressure and central haemodynamics [pre-ejection period and rapid left ventricular ejection time ( T (1)), slow ejection time ( T (2)) and d Z /d t (max) (where Z is thoracic impedance), assessed by the transthoracic impedance technique], were recorded during supine rest and during a 45 min 70 degrees HUT test in 68 patients (40+/-2 years) with a history of unexplained recurrent syncope. We found that 38 patients (42+/-3 years) had a symptomatic outcome to 70 degrees HUT (fainters) and 30 (39+/-2 years) had a negative outcome (non-fainters). When measured between 5 and 10 min of 70 degrees HUT, T (2) had increased significantly only in the fainters, and a change in T (2) of >40 ms from baseline predicted a positive outcome with a sensitivity of 68% and a specificity of 70%. During supine rest prior to 70 degrees HUT, the fainters exhibited a shorter T (2) than non-fainters (183+/-10 compared with 233+/-14 ms; P <0.01), and a T (2) of <199 ms predicted a positive outcome to 70 degrees HUT with a sensitivity of 68% and a specificity of 63%. Incorporation of the changes that occurred from rest to 70 degrees HUT in other haemodynamic variables (heart rate >11 beats/min, systolic pressure <2 mmHg, diastolic pressure <7 mmHg and pulse pressure <-3 mmHg) increased the specificity to 97% and the positive predictive value to 93%. Thus transthoracic impedance could detect differences in central haemodynamics between fainters and non-fainters during supine rest and during the initial period of 70 degrees HUT with a consistent sensitivity and specificity when combined with peripheral haemodynamic variables.

Serum prolactin levels in Parkinson's disease and multiple system atrophy.

The hypothalamic-pituitary axis (HPA) may be involved early in multiple system atrophy (MSA), whereas in idiopathic Parkinson's disease (IPD) its impairment seems to be correlated with motor disability. The release of prolactin (PRL) is mediated through the HPA and an increase in PRL levels is documented during stress. In this study, we investigated basal and erect PRL levels to assess whether basal PRL or changes in PRL levels after 60 degrees head-up tilt (HUT; orthostatic stress) could distinguish between MSA and IPD patients. We studied five patients with MSA on levodopa treatment, five levodopa-naive MSA patients, nine IPD patients on dopaminergic treatment, six drug-naive IPD patients and six normal individuals. PRL levels were measured in the supine position after 30 minutes rest and during 60 degrees HUT after 5 and 15 minutes. Baseline PRL values were significantly lower for patients with IPD than for those with MSA, both for levodopa-treated and naive patients ( p < 0.004, estimated decrease 55.1 %, 95 % CI from 29.4 % to 71.52 %). After orthostatic stress PRL levels were increased in healthy individuals after 15 minutes of HUT ( p = 0.044, estimated increase 11.5 %, 95 % CI from 0.4 % to 23.8 %), whereas there was no evidence for a change of PRL levels in patients with MSA or IPD after 5 and 15 minutes of HUT. We also did not find any evidence for a difference in PRL change after HUT between MSA and IPD patients. Baseline PRL levels might differentiate between early MSA and IPD, being higher in MSA. However, orthostatic stress using HUT appears unable to differentiate between MSA and IPD.

Acute effects of L- and T-type calcium channel antagonists on cardiovascular reflexes in conscious rabbits.

1. The effects of the relatively selective T-type voltage- operated calcium channel (VOCC) antagonist mibefradil were compared with verapamil, an L-type VOCC antagonist, on a range of autonomic reflexes in conscious rabbits. 2. Mean arterial pressure (MAP), heart rate (HR), the baroreceptor-HR reflex, postural adaptation reflex (90 degrees head-up tilt), Bezold-Jarisch-like reflex and the vasoconstrictor component of the nasopharyngeal reflex were assessed before and during i.v. infusion of vehicle (saline), mibefradil or verapamil. Doses of mibefradil that gave low (M1; 0.45 +/- 0.02 microg/mL) and high (M2; 0.93 +/- 0.05 microg/mL) plasma concentrations, or verapamil (0.059 +/- 0.004 microg/mL; n = 6 each) were chosen to mimic clinically observed therapeutic levels. 3. At steady state infusion over 30-90 min, MAP was significantly lower in M2 (- 7 mmHg) and verapamil (- 6 mm Hg) treatments, but only verapamil caused a significant tachycardia (+ 31 b.p.m.) compared with vehicle. Mibefradil (M2) and verapamil decreased the HR range of the baroreflex by 27 and 29%, respectively, but neither treatment affected the vagal or sympathetic constrictor components of the Bezold-Jarisch-like and nasopharyngeal reflexes, respectively. 4. In response to 90 degrees tilt, vehicle- and verapamil-treated rabbits responded with small rises in MAP of 4 +/- 2 and 8 +/- 2 mm Hg, respectively, 5 s into the upright posture, while M1 and M2 caused falls in MAP of 6 +/- 4 and 9 +/- 3 mm Hg, respectively, at 5 s. 5. Thus, both L- and T-type VOCC antagonists, at plasma concentrations in the clinical range, lowered MAP in the conscious rabbit, but only mibefradil caused postural hypotension. We conclude that T-type VOCC may play an important role in the venoconstrictor reflex in response to tilt in the rabbit.

Altered autonomic function and reduced arousability in apparent life-threatening event infants with obstructive sleep apnea.

The aim of this study was to examine cardiorespiratory control in infants presenting with an apparent life-threatening event (ALTE). We performed six to eight 45 degrees head-up tilts in 10 ALTE infants (age, 14 +/- 3 weeks) and 12 age-matched control subjects during slow wave sleep and rapid eye movement sleep (REM). All infants underwent full overnight polygraphic sleep recordings with noninvasive measurement of beat-to-beat blood pressure. All control infants had normal sleep breathing. In contrast, 5 of the 10 ALTE infants had more than two obstructive apneas per hour of sleep, with short hypoxic episodes (obstructive sleep apnea [OSA]). In slow wave sleep, in response to the tilt, the ALTE infants with OSA showed a reduced heart rate response, and three of the five showed a marked postural hypotension. The ALTE infants with OSA also had altered heart rate and blood pressure variability and an increased arousal threshold in REM (p = 0.0002). By contrast, those ALTE infants with normal sleep breathing had cardiovascular and arousal responses similar to those of the control infants. We conclude that a number of ALTE infants with OSA have abnormal cardiovascular autonomic control that, combined with their decreased arousability in REM, may provide an explanation for the ALTE episodes.

Syncope - a systematic overview of classification, pathogenesis, diagnosis and management

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.

Effects of KMD-3213, a Uroselective α1A-Adrenoceptor Antagonist, on the Tilt-Induced Blood Pressure Response in Normotensive Rats

KMD-3213 ((-)-1-(3-hydroxypropyl)-5-((2R)-2-[[2-([2-[(2,2,2-trifluoroethyl)oxy]phenyl]oxy)ethyl]amino]propyl)-2,3-dihydro-1H-indole-7-carboxamide), an alpha(1A)-adrenoceptor antagonist with potency similar to that of tamsulosin, is under development for the treatment of bladder outlet obstruction in patients with benign prostatic hypertrophy. In the present study, we investigated the effects of KMD-3213 on the tilt-induced blood pressure response in anesthetized normotensive rats. Male normotensive Sprague-Dawley rats were placed in the supine position on a board under cocktail anesthetization (alpha-chloralose, urethane and sodium pentobarbital). The arterial blood pressure was measured from the carotid artery. The animals were given consistent 45 degrees head-up tilt from the horizontal position, following the transient decrease in the blood pressure, and then recovery of the blood pressure to the normal level. Significant orthostatic hypotension was seen with intravenous administration of both prazosin and tamsulosin at doses over 3 micro g/kg, and these drugs completely blocked the tilt-induced blood pressure responses at 30 micro g/kg. On the other hand, these responses were still retained when KMD-3213 was administered intravenously at a dose up to 75 micro g/kg of KMD-3213. Moreover, KMD-3213 showed the highest uroselectivity of the test drugs. These results indicate that KMD-3213 is not likely to induce orthostatic hypotension and would be a useful compound for the treatment of urinary outlet obstruction in patients with benign prostatic hyperplasia.

Evidence for central venous pressure resetting during initial exposure to microgravity.

We measured central venous pressure (CVP); plasma volume (PV); urine volume rate (UVR); renal excretion of sodium (UNa); and renal clearances of creatinine, sodium, and osmolality before and after acute volume infusion to test the hypothesis that exposure to microgravity causes resetting of the CVP operating point. Six rhesus monkeys underwent two experimental conditions in a crossover counterbalance design: 1) continuous exposure to 10 degrees head-down tilt (HDT) and 2) a control, defined as 16 h/day of 80 degrees head-up tilt and 8 h prone. After 48 h of exposure to either test condition, a 120-min course of continuous infusion of isotonic saline (0.4 ml. kg(-1). min(-1) iv) was administered. Baseline CVP was lower (P = 0.011) in HDT (2.3 +/- 0.3 mmHg) compared with the control (4.5 +/- 1.4 mmHg) condition. After 2 h of saline infusion, CVP was elevated (P = 0.002) to a similar magnitude (P = 0.485) in HDT (DeltaCVP = 2.7 +/- 0.8 mmHg) and control (DeltaCVP = 2.3 +/- 0.8 mmHg) conditions and returned to preinfusion levels 18 h postinfusion in both treatments. PV followed the same pattern as CVP. The response relationships between CVP and UVR and between CVP and UNa shifted to the left with HDT. The restoration of CVP and PV to lower preinfusion levels after volume loading in HDT compared with control supports the notion that lower CVP during HDT may reflect a new operating point about which vascular volume is regulated. These results may explain the ineffective fluid intake procedures currently employed to treat patients and astronauts.

Spontaneous baroreflex modulation of heart rate and heart rate variability during orthostatic stress in tetraplegics and healthy subjects.

This study was addressed to investigate the contribution of vagal and sympathetic mechanisms to the genesis of low-frequency (LF) oscillations of RR-interval. To this aim, we utilized the pathophysiological model of tetraplegics, who have intact vagal afferent and efferent pathways of the baroreceptor reflex arc but interrupted medullary-spinal sympathetic pathways. We studied nine complete, traumatic, tetraplegics (C4-C7, TET) and 10 normally healthy subjects (NR) at rest and during physiological baroreceptors unloading induced by 70 degrees head-up tilt. Autoregressive power spectral analysis was used to investigate RR-interval and systolic arterial pressure (SAP) variabilities. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. Both at-rest and during-tilt LF and high frequency (HF) components were detected in RR-interval of NR, whereas in TET only the HF component was observed in both conditions (with one exception). Baroreflex sensitivity (BRS) did not significantly differ between TET and NR at rest, and underwent a significant and similar decrease during tilt in both groups, being accompanied in NR by a significant increase in LF relative power. Spectral analysis of SAP provided results similar to RR-interval. Tilt also slowed the centre frequency of the LF components of RR-interval and SAP. During unperturbed physiological conditions, a change in efferent vagal activity to the heart from baroreflex stimulation by spontaneous arterial pressure changes, is unlikely to contribute on its own to the genesis of LF heart period oscillations in humans who lack the ability to modulate sympathetic nerve traffic to the heart. However, the possibility that a baroreflex modulation of LF oscillations require an intact sympathetic control should be carefully considered.

Carbon dioxide, critical closing pressure and cerebral haemodynamics prior to vasovagal syncope in humans

The cerebrovascular changes that occur prior to vasovagal syncope (VVS) are unclear, with both increases and decreases in cerebrovascular resistance being reported during pre-syncope. This study assessed the cerebrovascular responses, and their potential underlying mechanisms, that occurred before VVS induced by head-up tilt (HUT). Groups of 65 normal subjects with no previous history of syncope and of 16 patients with recurrent VVS were subjected to 70 degrees HUT for up to 30 min. Bilateral middle cerebral artery (MCA) cerebral blood flow velocities (CBFVs) were measured using transcranial Doppler ultrasound, along with simultaneous measures of MCA blood pressure, heart rate, and end-tidal and transcutaneous carbon dioxide concentrations. All 16 patients and 14 of the control subjects developed VVS during HUT. During pre-syncope, mean CBFV declined, due predominantly to a decrease in diastolic rather than systolic CBFV (decreases of 44.5+/-19.8% and 6.3+/-12.9% respectively; P<0.0001). CO(2) levels and indices of cerebrovascular resistance decreased during pre-syncope, while critical closing pressure (CrCP) increased to levels approaching MCA diastolic blood pressure before decreasing precipitously on syncope. Pre-syncopal changes were similar in syncopal patients and syncopal controls. CrCP, therefore, rises during pre-syncope, possibly related to progressive hypocapnia, and may account for the relatively greater fall in diastolic CBFV. Falls in cerebrovascular resistance, therefore, may be offset by rises in CrCP due to hypocapnia, leading to diminished cerebral blood flow during pre-syncope.

Time delay of vagally mediated cardiac baroreflex response varies with autonomic cardiovascular control.

To examine whether changes in autonomic activity have an effect on the latency of the vagally mediated cardiac baroreflex response in humans, we investigated the effects of neck suction fluctuating sinusoidally at 0.2 Hz on R-R intervals (known to be mediated mainly by vagal activity) in the supine position, during 15 degrees head-down tilt and 60 degrees head-up tilt, and during vagotonic (2 microg/kg) and vagolytic (10 microg/kg) doses of atropine while the subjects breathed at 0.25 Hz. The phase shift between fluctuations in neck chamber pressure and in R-R interval was calculated by complex transfer function analysis and was used as a measure of the time delay between carotid baroreceptor stimulation and cardiac effector response. Cardiac baroreflex responsiveness increased significantly during low-dose atropine and decreased during head-up tilt or 10 microg/kg atropine. With increasing tilt angle, the time delay between cyclic baroreceptor stimulation and oscillations in R-R interval increased from 0.32 +/- 0.27 s (head down), to 0.59 +/- 0.25 s (supine position, P < 0.05 vs. head down), and to 0.86 +/- 0.27 s (head up, P < 0.01 vs. supine). Low-dose atropine had a similar effect to head-down tilt on baroreflex latency, whereas 10 microg/kg atropine increased the time delay markedly to 1.24 +/- 0.30 s. Our results demonstrate that changes in autonomic activity, generated either by gravitational stimulus or by atropine, not only affect baroreflex responsiveness but also have a major influence on the latency of the vagally mediated carotid baroreceptor-heart rate reflex. The prolonged baroreflex latency during decreased parasympathetic function may contribute to an unstable regulation of heart rate in patients with cardiac disease.

THE EFFECT OF AGE AND GENDER ON HEART RATE VARIABILITY FOLLOWING ENDURANCE TRAINING

This research investigated the effect of standardized/quantified endurance training on autonomic nervous system control of the heart. The latter was analyzed from spectral analysis of electrocardiogram records of heart rate variability (HRV) during both rest and sub-maximum exercise in groups of older (40–45yrs) and younger (19–21yrs), mixed gender groups (6 males and 6 females), pre and post standardized training. All subjects were recreational runners who completed the same 12 week running program. Previously and subsequent to training, heart rate variability (HRV) was measured during supine rest, 70 degree head-up tilt, and standardized sub-maximum cycling. There was a significant group mean decrease in heart rate both at rest (5%), and during sub-maximum exercise (6%), in both age groups after training. Total spectral power increased (59%), and high frequency power (HFP) (0.15–0.5Hz) increased 166% in both age groups at rest. The younger group showed a greater increase in total power (73%) and young females increased most in total power (112%). There was a significant increase in heart rate response (6%) to 5 minutes of 70 degree head-up tilt in both groups following training. It is concluded that the significant increase in HRV, total power and HFP following training are better indicators of improved cardiovascular condition than a resting heart rate index. HRV measurement provides and effective, non-invasive assessment of cardiovascular adaptation to aerobic training. Supported by The Heart and Stroke Foundation of B.C. & Yukon

Cardiovascular reflex testing contributes to clinical evaluation and differential diagnosis of Parkinsonian syndromes

The differentiation between Parkinson's disease (PD), progressive supranuclear palsy (PSP), and multiple system atrophy (MSA) may be difficult but is important for prognostic and therapeutic purposes. Varying degrees of autonomic failure have been described in PD and MSA, whereas its involvement in PSP remains controversial. The aim of this study was to investigate autonomic function in patients fulfilling strict clinical diagnostic criteria for the disorders above, to evaluate the diagnostic capacity of laboratory autonomic tests. The study group was consecutively recruited among patients referred to a movement disorder unit. Thirty-four patients with PD, 15 patients with PSP, and 47 patients with MSA were compared with 18 healthy age-matched controls. Autonomic tests included analysis of heart rate variability (HRV) in temporal domain, at rest and during forced respiration, as well as blood pressure (BP) changes during 75 degrees head-up tilt. HRV did not differ between groups during quiet breathing but was significantly reduced during forced respiration in MSA (P < 0.01), while PD and PSP groups did not differ from controls. Hypotensive responses during orthostatic provocation were seen in PD (P < 0.01) and MSA (P < 0.001), whereas BP remained stable in most PSP patients, not differing from the healthy control group. On an individual basis, decreased HRV and severe hypotensive responses were seen in MSA patients regardless of age and disease duration, whereas PD patients showed this combination only at high age and long duration. In PSP, only a few cases with decreased HRV and limited hypotensive responses were found. We conclude that cardiovascular reflex tests can supplement the clinical differentiation of Parkinsonian syndromes.

Thermal stress modulates arterial pressure variability and arterial baroreflex response of heart rate during head-up tilt in humans.

To examine the effects of thermal stress on the blood pressure variability and the arterial baroreceptor-cardiac reflex during orthostatic stress, 11 male volunteers underwent whole body thermal stress using a cool or hot water-perfused suit during 5 min of 70 degrees head-up tilt (HUT). The spontaneous variability in arterial pressure was quantified by power spectrum analysis. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and heart rate (fc). During supine rest the variability of arterial pressure decreased during cooling, while it remained unchanged during heating. The variability increased with HUT; it was greater (P < 0.05) with heating than with cooling. In the supine condition, the arterial baroreflex sensitivity of fc increased during cooling, while it did not change during heating. The sensitivities decreased (P < 0.05) with HUT during both thermal stresses; the decreased rate of sensitivity from the pre-tilt value was greater during heating [mean 63 (SEM 4)%] and smaller during cooling [mean 11 (SEM 24)%] than during normothermia [mean 47 (SEM 4)%] (both, P < 0.05). There were significant negative correlations between the sensitivities and the amplitude of the arterial pressure variability during normothermia and heating (P < 0.0001). The results suggest that the spontaneous baroreflex response of fc is a modulatory factor for the changes of arterial pressure variability brought about by thermal stress during orthostatic stress.

Central and peripheral adverse hemodynamic changes during laparoscopic surgery and their reversal with a novel intermittent sequential pneumatic compression device.

To study the influence of a novel intermittent sequential pneumatic compression device (Lympha-press) on the adverse cardiac and peripheral hemodynamic changes induced by positive-pressure pneumoperitoneum (PPPn) in laparoscopic surgery. Creation of PPPn is known to cause adverse central and peripheral hemodynamic changes. An intrasubject observational study was undertaken to quantitate these adverse changes and to assess the influence of an intermittent sequential pneumatic compression system on these adverse hemodynamic changes during laparoscopic surgery with PPPn. The study involved 16 consecutive patients undergoing laparoscopic surgery with PPPn of 12 mmHg and 30 degrees head-up tilt position. The following peripheral hemodynamic recordings were made using Doppler ultrasound: peak systolic velocity (PSV), end diastolic velocity (EDV), and cross-sectional area of the femoral vein. Central monitoring included cardiac output and stroke volume by transesophageal Doppler, blood pressure, and pulse. The hemodynamic state based on these parameters was assessed before induction of PPPn with the anesthetized patient in the supine position, after induction of PPPn and head-up tilt position with Lympha-press off, and during PPPn and head-up tilt position with Lympha-press on, and after desufflation with the patient in the supine position under general anesthesia. Positive-pressure pneumoperitoneum and the head-up tilt position resulted in a 33% reduction in PSV, a 21% reduction in EDV, and a 29% increase in cross-sectional area of the femoral vein. This was associated with a 20% reduction in cardiac output and an 18% reduction in stroke volume. Activation of Lympha-press during PPPn and the head-up tilt position resulted in a 129% increase in PSV and a 55% increase in EDV by 55%. It also increased the cardiac output by 27% and stroke volume by 16%, with no effect on cross-sectional area. Compared with the pre-PPPn stage, there was no difference in cardiac output or stroke volume, but the PSV was higher by 78% and the EDV by 32%. After abdominal desufflation in the supine position, the cardiac output and stroke volume were restored to the pre-PPPn level, but persistent and significant elevations were observed during the period of study in PSV, EDV, and cross-sectional area. Significant and individually variable central and peripheral hemodynamic changes are encountered during laparoscopic surgery with PPPn and the head-up tilt position. These are reversed by intermittent sequential pneumatic compression using Lympha-press.

The effect of systemic blood pressure on cardio-vascular reflexes in elderly subjects.

The evidence for impairment of cardiovascular reflexes by hypertension in elderly subjects is mixed. This study tested the hypothesis that baroreceptor- and non-baroreceptor-mediated responses in elderly subjects differed with hypertension. 54 elderly subjects were studied: 16 with combined hypertension (CT) (blood pressure 184 +/- 4/102 +/- 2 mmHg), 16 with isolated systolic hypertension (180 +/- 3/85 +/- 1 mmHg) and 22 normotensives (NT) (138 +/- 2/76 +/- 1 mmHg). All subjects performed isometric exercise with a handgrip dynamometer. Heart rate (HR), blood pressure and forearm vascular resistance (FVR) responses were then studied to 60 degrees head-up tilt and the cold face stimulus. Baseline FVR, and the response to isometric handgrip, were similar in all groups. Subjects with isolated systolic hypertension manifested greater increases in FVR with tilt (P<0.001), whilst the HR increment was greater in the NT group (P<0.001). Blood pressure changes with tilt were similar in the three groups. With the cold face stimulus (CFS) a rise in FVR of approximately 30% was seen in all groups and blood pressure rose modestly, with the largest increases being seen in the combined hypertensives. This study in elderly subjects indicates significant differences with hypertension in the response to tilt, with an impaired baroreceptor-cardiac reflex being compensated by an augmented baroreceptor-vascular response.

Infant autonomic function is altered by maternal smoking during pregnancy.

Sudden infant death syndrome (SIDS) is more prevalent in infants of smokers and may involve subtle alterations in autonomic control mechanisms. Autonomic function can be assessed using blood pressure responses to a passive head-up tilt and power spectral analysis of heart rate variability. This study aimed to determine if maternal smoking altered infants' responses to head-up tilt. Blood pressure and heart rate responses to a passive 70 degrees head-up tilt were compared in infants of smokers and non-smokers at 2-3 days and 3 months of age. There were no significant differences between groups in power spectral indices. At 2-3 days, the systolic pressure response to tilt was significantly different between groups (P<0.01). In infants of smokers, systolic pressure decreased by a mean (S.E.) of 7.7(1.1) mmHg, whereas in control infants it remained unchanged. At 3 months, systolic pressure in infants of smokers remained unchanged but increased in control infants by 6.2(2.1) mmHg (P<0.05). These results indicate that maternal smoking alters autonomically mediated cardiovascular responses in the infant.