Postural dizziness and transient hypotension in two healthy teenagers

Neurocardiovascular control during postural change was investigated in two teenage females with complaints of dizziness almost immediately on standing up. Blood pressure and heart rate were monitored continuously with a Finapres^TM device. On standing there was a brief but marked fall in blood pressure between 5–10 s after the onset of the manoeuvre. The maximum fall in systolic and diastolic blood pressure was 65 mmHg and 40 mmHg respectively in the first subject, and 58mmHg and 29 mmHg respectively in the second subject. In both, postural tachycardia was present after 1–2 min of standing with heart rate increasing by up to 39 beats/min in the first subject and 60 beats/min in the second subject. On a follow-up examination 3 years later these changes had disappeared in the first subject while they persisted in the second subject, when she was studied two years later. We conclude that in these patients initial postural dizziness is related to an excessive fall in blood pressure upon standing.     

Low-dose atropine amplifies cardiac vagal modulation and increases dynamic baroreflex function in humans

It has been previously known that low-dose atropine (LDA) enhances vagal outflow to the heart. To demonstrate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability, we evaluated the effect of vagal cardiac stimulation with administration of LDA on ABP fluctuation during dynamic hypertensive and hypotensive stimuli. We assessed changes in RR interval (RRI), ABP, power spectral densities of heart rate variability (HRV) and ABP variability, and spontaneous baroreflex sensitivity (BRS) in 16 healthy volunteers before and after administration of LDA (2 microg/kg). Transient hypertension was induced by phenylephrine (2 microg/kg), whereas hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. LDA elicited bradycardia and significantly increased high-frequency (HF, 0.15-0.4 Hz) power of HRV and spontaneous BRS, as determined by transfer function analysis. The increase in systolic blood pressure (SBP) after phenylephrine administration was significantly attenuated by LDA (16+/-2 to 11+/-3 mmHg, P<0.005) and was associated with the augmented reflex bradycardia, whereas the decrease in SBP after cuff deflation was not affected (14+/-5 to 13+/-5 mmHg) with the augmented reflex tachycardia. Increases of HF HRV were correlated significantly and negatively with the increased SBP induced by phenylephrine before and after LDA (r=-0.502, P<0.05). These data suggest that the increased vagal cardiac function induced by LDA augments HR buffering effects, and is important in minimizing arterial pressure fluctuation during dynamic hypertensive stimuli.     

Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury

Background

While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI.

Methods

We conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate–severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 h following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction.

Results

Thirty-two patients were included, and 7 (22 %) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p < 0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [?10.2 mmHg (95 % CI ?16.1, ?4.2)] and MAP [?9.1 mmHg (95 % CI ?13.9, ?4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p < 0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model.

Conclusions

Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.

     

Cardiovascular responses to blockade of GABA synthesis in the hypothalamus of the spontaneously hypertensive rat

Previous studies have suggested that a decreased inhibitory input onto neurons within the posterior hypothalamus (PH), a known pressor area, may contribute to hypertension in the spontaneously hypertensive rat (SHR). Recent experiments from this laboratory have shown that neurons in the PH of the SHR have an altered and elevated discharge frequency compared to those in the normotensive rat. In addition, biochemical studies have reported that there is a decreased concentration of the inhibitory neurotransmitter, GABA, in the hypothalamus of the SHR. The objective of the present study was to assess any variations in GABAergic modulation of cardiovascular activity in SHRs compared to normotensive Wistar-Kyoto (WKY) rats and Sprague-Dawley (SD) rats. Arterial pressure and heart rate responses to microinjections of the GABA synthesis inhibitor 3-mercaptopropionic acid (3-MP) into the posterior hypothalamic area of anesthetized young (6–8 weeks) and mature (11–16 weeks) hypertensive and normotensive rats were recorded. Microinjection of 3-MP elicited increases in arterial pressure of 17.4 ± 3.9 mmHg, 18.1 ± 7.8 mmHg, 16.9 ± 6.4 mmHg, and 10.4 ± 3.5 mmHg in the mature WKY, mature SD, young WKY, and young SHR, respectively. In addition, heart rate was elevated by 33.2 ± 21.9 beats/min, 70.0 ± 25.3 beats/min, 56.3 ± 15.0 beats/min and, 45.9 ± 10 beats/min in the mature WKY, adult SD, young WKY, and young SHR groups, respectively. In contrast, microinjection of 3-MP into the posterior hypothalamus of adult SHRs produced no significant change in arterial pressure (−5.0 ± 1.8 mmHg) or heart rate (+5.3 ± 6.1 beats/min). In three of the adult SHRs, cardiovascular responses to electrical stimulation in the PH were compared to responses elicited by microinjection of 3-MP into the same PH site. Electrical stimulation produced large increases in both arterial pressure and heart rate; however, microinjection of 3-MP produced no significant changes in cardiovascular activity. These results indicate that spontaneously hypertensive rats have a deficiency in the tonic GABAergic input onto posterior hypothalamic neurons. This alteration may contribute to the maintenance of the elevated blood pressure in spontaneously hypertensive rats.     

Cardiovascular actions of orexin-A in the rat subfornical organ

Orexin-A is a neuropeptide, primarily produced in the lateral hypothalamic/perifornical hypothalamus. Orexin receptors and immunoreactive neuronal fibres are widely distributed throughout the brain, suggesting integrative neurotransmitter roles in a variety of physiological systems. Intracerebroventricular injections of orexin-A increase blood pressure and stimulate drinking, and the subfornical organ (SFO), a circumventricular structure implicated in autonomic control, is a potential site at which orexin may act to exert these effects. We have therefore used microinjection techniques to examine the effects of orexin-A administered directly into the SFO on blood pressure and heart rate in urethane anaesthetised male Sprague-Dawley rats. Orexin-A microinjection (50 fmol) into the SFO caused site-specific decreases in blood pressure (SFO: mean area under curve (AUC) = -681.7 +/- 46.8 mmHg*s, n = 22 versus non-SFO: 63.68 +/- 54.69 mmHg*s, n = 15, P < 0.001), and heart rate (SFO: mean AUC = -26.7 +/- 2.8 beats, n = 22, versus non-SFO: mean AUC = 1.62 +/- 2.1 beats, n = 15, P < 0.001). Vagotomy did not alter the hypotensive or bradycardic responses elicited by orexin-A microinjection. Prior alpha-adrenoceptor blockade with phenoxybenzamine (1 mg/kg, i.v.) masked the orexin-A induced blood pressure (mean AUC = -122.6 +/- 17.6 mmHg*s, n = 4, P < 0.01 paired t-test) and heart rate (mean AUC = -6.7 +/- 1.7 beats, n = 4, P < 0.05, paired test) response. The orexin-A induced heart rate response was attenuated when beta-adrenoceptors were blocked with propranolol (1 mg/kg, i.v.; mean AUC = 0.6 +/- 2.8 beats, n = 5, P < 0.01 paired t-test). These studies demonstrate that microinjection of orexin-A into the SFO causes site specific decreases in blood pressure and heart rate which is mediated by a reduction in sympathetic tone.     

Is there a relationship between supine systemic blood pressure and orthostatic hypotension in the elderly?

The relationship between blood pressure and orthostatic hypotension was studied in 48 elderly patients with orthostatic hypotension and 29 healthy age-matched controls. Individuals were designated as hypertensive (systolic > 160 and or diastolic > 90 mmHg) or normotensive on the basis of supine blood pressure levels. Systolic, diastolic and mean blood pressures, heart rate, stroke volume, cardiac output, cardiac index and total peripheral resistance were measured every 5 min before, during and after 10 min head-up tilt to 70°.Eighteen orthostatic hypotension subjects and six controls were hypertensive, while 30 orthostatic hypotension subjects and 23 controls were normotensive. There were no differences between hypertensive and normotensive patients in mean age, weight, height or body surface area. Mean systolic blood pressure in orthostatic hypotension subjects was higher than in controls (148.8 ± 3.6 vs. 137.5 ± 3.34 mmHg). Mean diastolic pressure was not different (79.1 ± 2.0 vs. 79.0 ± 2.0 mmHg). There were no differences between patients with or without hypertension in the haemodynamic changes produced by head-up tilt. Heart rates in orthostatic hypotension subjects with hypertension were significantly lower throughout the study when compared with normotensive orthostatic hypotension patients. Further, the increases in heart rate on tilting were significantly smaller (8.4 ± 1.9 vs. 14.5 ± 1.8 beats/min). Control hypertensive subjects had significantly higher mean cardiac output and cardiac index compared with non-hypertensives from before and during tilt. We conclude that hypertension is not related to the development or the degree of orthostatic hypotension in the elderly. Elderly patients with orthostatic hypotension who had supine hypertension were unable to accelerate heart rate as much on tilt as normotensive patients. This may suggest cardiac impairment, failure to respond to increased sympathetic drive or a combination of these factors.     

Cardiovascular responses elicited by simulated diving and their habituation in man

The cardiovascular responses of 24 subjects were investigated under various simulated diving conditions. Muscle blood flow in forearm and calf, arterial pressure, heart rate and intrathoracic pressure were monitored. Breath holding with face immersion in water at 18°C gave a typical diving response at intrathoracic pressure of 0 and 20 mmHg, (23% bradycardia, > 60% muscle vasoconstriction). Breath holding alone at 20 mmHg intrathoracic pressure resulted in vasoconstriction (50%) and bradycardia (4%). Breath holding at 0 mmHg intrathoracic pressure induced a muscle vasoconstriction (5%). These results indicate that both increased intrathoracic pressure and facial immersion can produce a typical diving response individually but that the full diving response requires the presence of both conditions. Diving often activated two responses, the typical diving response and a superimposed defence reaction. Cardiovascular components of the defence reaction (muscle vasodilatation and tachycardia) which was elicited in some divers masked the diving response. In those subjects in whom the diving response was initially absent during repetition of diving manoeuvres the cardiovascular components of the defence reaction were habituated and the characteristic diving response gradually emerged: the initial tachycardia diminished and was replaced by bradycardia, while vasodilatation in the forearm and calf was replaced by vasoconstriction.     

Coerulear activation by crh and its role in hypertension induced by prenatal malnutrition in the rat

The effects of intracoerulear CRH and intraparaventricular prazosin on systolic pressure, diastolic pressure and heart rate were studied in prenatally malnourished hypertensive rats. At day 40 of life, (i) malnourished rats showed enhanced systolic pressure, heart rate, and plasma corticosterone; (ii) intracoerulear CRH increased systolic pressure and heart rate only in controls; (iii) intraparaventricular prazosin decreased systolic pressure and heart rate only in malnourished rats; (iv) in controls, prazosin did not prevent the stimulatory effect of CRH on the cardiovascular parameters; in malnourished rats, prazosin allowed CRH regain its stimulatory effects. Thus, coerulear activation by CRH would be involved in hypertension and tachycardia developed by prenatally malnourished animals.     

降压治疗对老年人脑梗死急性期重度高血压患者预后的影响

目的观察降压治疗对老年人脑梗死急性期重度高血压患者预后的影响。方法 2012-02-2015-02我科收住的老年人脑梗死急性期有重度高血压的(收缩压≥220mmHg或舒张压≥120mmHg)患者120例,随机分成治疗组和对照组各60例,治疗组给予硝酸甘油10 mg,1~2 mL/h泵入,根据血压调整速度,使血压下降速度20%/h,将收缩压稳定在150~160mmHg或舒张压稳定在95~100mmHg,1周后给予口服降压药,将硝酸甘油减量并停用;对照组1周内不降压,1周后给予降压药口服,观察7d、14d时2组神经功能缺损情况和心脏、肾脏受损情况。结果治疗组急性期经缓慢降压并使血压维持在150~160/95~100mmHg,和对照组1周后再降压治疗比较,7d、14d神经功能缺损程度评分均较对照组低(P0.05);治疗组诱发心律失常、心肌梗死、心脏猝死的比例较对照组低;对肾脏的损害也较对照组低。结论对重症高血压的急性期脑梗死老年患者适度降压可减轻神经功能缺损程度,减少对心脏和肾脏的损伤。     

Differentialdiagnose der orthostatischen Dysregulationen

Orthostatic circulatory disorders are frequently the cause of orthostatic intolerance, syncope or dangerous falls. A sufficient therapy should be based on a differential diagnosis by means of an active standing test or a tilt-table test. Three typical pathological reactions of blood pressure and heart rate can be differentiated. The hypoadrenergic orthostatic hypotension is characterised by an immediate drop in blood pressure (systolic drop > 20 mmHg below base line within 3 min) with or without compensatory tachycardia. It is caused by peripheral or central sympathetic dysfunction. Tachycardia (> 30 beats per minute above base line within 10 min) without significant blood pressure drop but with a fall of cerebral blood flow indicates a postural tachycardia syndrome. In general, there is no further somatic dysfunction. Increased venous pooling is thought to be the assumed pathomechanism. A reflex mechanism evokes the neurocardiogenic syncope after a certain time of standing: sympathetic inhibition yields a strong blood pressure drop and vagal activation bradycardia. Proved therapies include use of the mineralocorticoide fludrocortison (hypoadrenergic orthostatic hypotension), of the alpha-agonist midodrin (postural tachycardia syndrome) and of beta-blockers (neurocardiogenic syncope).     

Neurogenic cardiac arrhythmias in acute intracranial increase in pressure (recurrent hemorrhage in subarachnoid hemorrhages)

Neurogenic cardiac arrhythmias during 5 cases of subarachnoid rebleeding in 4 patients were analyzed by using long-term ECG (Holter). The initial onset of rebleeding was characterized by an abrupt decrease of heart rate from 93.3 +/- 7.85 (beats/min) to 63.3 +/- 14.6 (beats/min). This was immediately followed by pronounced tachycardia of 163.0 +/- 20.9 (beats/min) and subsequently, alterations of the P wave, ST depression with an increase in T wave amplitude. Frequent premature ventricular contractions, couplets, and self-terminating episodes of ventricular tachycardia for 2-8 minutes were observed during 2 episodes of rebleeding, an idioventricular rhythm in one case. The ECG returned to normal in the 3 non-lethal cases. Pathogenetically, the initial heart rate decrease with varying P wave configuration can be explained through activation of the baroreceptor reflex. Elevated intracranial pressure causes a blood pressure increase thus stimulating the baroreceptors and consequently, the afferent and efferent tracts of the vagus nerve. The sympathicotonus appears to have a modulating effect.     

Baroreflex control of heart rate and renal sympathetic nerve activity in rats with low brain angiotensinogen

The main objective of the present study was to evaluate baroreceptor control of heart rate (HR) and renal sympathetic nerve activity (RSNA) in transgenic rats (TG) with low angiotensinogen production in glial cells, TGR(ASrAogen)-680. In addition, the sympathetic and vagal autonomic tonus to the heart was investigated. As previously shown, TG rats presented a lower arterial pressure (AP) and HR. However, TG rats had decreased AP variability during the night (8.9+/-0.4 mmHg vs 9.8+/-0.3 mmHg, in SD) accompanied by an increase in HR variability (39+/-1 beats/min vs 35+/-1 beats/min, in SD) and augmented locomotor activity during the night (3.5+/-0.3 counts/min vs 2.5+/-0.2 counts/min, in SD). In addition, TG rats presented increased baroreflex sensitivity for the RSNA (slope of line that correlates decreases in RSNA and increases in AP=1.36+/-0.18 vs 0.77+/-0.1, in SD) and an increased sensitivity for both the baroreflex bradycardia (0.79+/-0.04 ms/mmHg vs 0.52+/-0.04 ms/mmHg, in SD) and tachycardia (1.46+/-0.1 ms/mmHg vs 0.93+/-0.01 ms/mmHg, in SD). Further, TG rats had increased vagal tonus (25+/-3 beats/min vs 11+/-4 beats/min in SD) without significant change in the sympathetic tonus to the heart. These results confirm and extend previous observations showing that glial angiotensinogen, the main source of brain RAS peptides, importantly modulates sympathetic tonus, at least to the renal nerve, and vagal tonus to the heart.     

Twenty-four-hour blood pressure profile,orthostatic hypotension,and cardiac dysautonomia in elderly type 2 diabetic hypertensive patients

Purpose

The aim of this study was to evaluate the relationship between orthostatic hypotension (OH), defined as a decrease in systolic blood pressure (SBP) ≥20 mmHg and/or a decrease in diastolic blood pressure (DBP) ≥10 mmHg, and 24-h ambulatory BP profile in elderly hypertensive type 2 diabetic patients.

Methods

After a 2-week antihypertensive wash-out period, 200 hypertensive well-controlled diabetic outpatients, aged 65–75 years, underwent a clinical examination, including BP measurements, ECG, 24-h ABP monitoring (ABPM), an orthostatic test, and three tests for cardiovascular autonomic function assessment [deep breathing, heart rate (HR) variability, resting HR].

Results

According to their nighttime BP profile, patients were divided into three groups: dippers (n = 86) (BP fall during nighttime ≥10 %), non-dippers (n = 80) (BP fall during nighttime 0–10 %), and reverse dippers (n = 34) (nighttime BP > daytime BP). Orthostatic test produced a significantly greater orthostatic SBP fall in dippers and even more in reverse dippers. In these latter, a significant fall was observed also in DBP. Prevalence of OH was 9.3 % in dippers, 30 % in non-dippers, and 79.4 % in reverse dippers.

Conclusions

In elderly hypertensive type 2 diabetics, a blunted nocturnal BP fall is associated with OH and autonomic dysfunction. These data suggest that ABPM should be performed in the assessment of hypertensive diabetic patients in whom the cardiovascular dysautonomia is suspected or the signs of it are present (such as OH).

     

Effect of pentobarbital anesthesia on renal sympathetic nerve activity in the rabbit

The effects of pentobarbital (PB) anesthesia on arterial pressure, heart rate, and renal nerve activity (RNA) were studied in chronically instrumented intact rabbits and rabbits with sinoaortic baroreceptor denervation (SAD). In intact rabbits, PB caused an initial decrease in mean arterial pressure from 82 +/- 2 to 42 +/- 5 mm Hg, which then returned to the control level within 5 min. RNA increased by 144 +/- 19% in response to hypotension induced by PB then also returned to the control level within 5 min. Heart rate increased by 56 +/- 10 from 244 +/- 11 beats/min and remained elevated for 60 min. Sensitivities of baroreflex control of heart rate and RNA were markedly impaired by PB anesthesia. In SAD rabbits, PB caused hypotension (-46 +/- 5 mm Hg), which lasted for 15 min. RNA decreased initially by 80 +/- 5%, then gradually returned toward the control level. However, at 45 min after injection of PB, RNA was still depressed significantly. Tachycardia induced by PB was abolished by SAD, i.e. heart rate actually decreased by 53 +/- 10 beats/min. These results suggest that in intact rabbits steady-state effects of PB were: no change in mean arterial pressure or RNA, and tachycardia, all due to baroreflex compensation. However, in the absence of baroreflex compensation, PB elicited hypotension, bradycardia, and a decrease in RNA.     

Effects of the converting enzyme inhibitor trandolapril on short-term variability of blood pressure in essential hypertension

Short-term fluctuations in blood pressure and heart rate were analysed in a group of eight males with essential hypertension. Indirect finger blood pressure was measured by a non-invasive device (Finapres). Analogue-to-digital conversion of the blood pressure was used to determine systolic and diastolic blood pressure and heart rate every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transformation algorithm. The effect of 7-day administration of the angiotensin converting enzyme inhibitor, trandolapril (2 mg/day), was assessed in a double-blind, randomized, placebo-con-trolled cross-over study. After trandolapril there was a significant reduction in systolic blood pressure levels (- 15 mmHg). The reduction in diastolic blood pressure did not reach significance. The standard deviation of systolic and diastolic blood pressure levels were significantly reduced (–20% and –22% for systolic and diastolic respectively). Neither average heart rate nor standard deviations of heart rate time series was affected by the angiotensin converting enzyme inhibitor. Spectral analysis of fluctuation in blood pressure showed a reduction in the variability underlying the standard deviation changes of systolic and diastolic blood pressure. Trandolapril selectively reduced the amplitude of systolic and diastolic oscillations in the 66–129 mHz region, corresponding to Mayer waves. The significant decrease in the 10 s period oscillations of blood pressure after chronic angiotensin converting enzyme blockade with trandolapril could reflect reduced sympathetic outflow to vascular smooth muscle.     

Heart rate and arterial pressure variability in the experimental renovascular hypertension model in rats

This study was conducted in one kidney, one clip (1K1C) Goldblatt hypertensive rats to evaluate vascular and cardiac autonomic control using different approaches: 1) evaluation of the autonomic modulation of heart rate (HR) and systolic arterial pressure (SAP) by means of autoregressive power spectral analysis 2) assessment of the cardiac baroreflex sensitivity; and 3) double blockade with methylatropine and propranolol. The 1K1C group developed hypertension and tachycardia. The 1K1C group also presented reduction in variance as well as in LF (0.23+/-0.1 vs. 1.32+/-0.2 ms2) and HF (6.6+/-0.49 vs. 15.1+/-0.61 ms2) oscillations of pulse interval. Autoregressive spectral analysis of SAP showed that 1K1C rats had an increase in variance and LF band (13.3+/-2.7 vs. 7.4+/-1.01 mmHg2) in comparison with the sham group. The baroreflex gain was attenuated in the hypertensive 1K1C (-1.83+/-0.05 bpm/mmHg) rats in comparison with normotensive sham (-3.23+/-0.06 bpm/mmHg) rats. The autonomic blockade caused an increase in the intrinsic HR and sympathetic predominance on the basal HR of 1K1C rats. Overall, these data indicate that the tachycardia observed in the 1K1C group may be attributed to intrinsic cardiac mechanisms (increased intrinsic heart rate) and to a shift in the sympathovagal balance towards cardiac sympathetic over-activity and vagal suppression associated to depressed baroreflex sensitivity. Finally, the increase in the LF components of SAP also suggests an increase in sympathetic activity to peripheral vessels.     

Effects of tyramine administration in Parkinson's disease patients treated with selective MAO-B inhibitor rasagiline.

Rasagiline is a novel, potent, and selective MAO-B inhibitor shown to be effective for Parkinson's disease. Traditional nonselective MAO inhibitors have been associated with dietary tyramine interactions that can induce hypertensive reactions. To test safety, tyramine challenges (50-75 mg) were performed in 72 rasagiline-treated and 38 placebo-treated Parkinson's disease (PD) patients at the end of two double-blind placebo-controlled trials of rasagiline. An abnormal pressor response was prespecified as three consecutive measurements of systolic blood pressure (BP) increases of >or= 30 mm Hg and/or bradycardia of < 40 beats/min. In the first study involving 55 patients with early PD on rasagiline monotherapy, no patients randomized to rasagiline (1 mg/2 mg; n = 38) or placebo (n = 17) developed systolic BP (SBP) or heart rate changes indicative of a tyramine reaction. In the second trial involving 55 levodopa-treated patients, 3 of 22 subjects on rasagiline 0.5 mg/day and 1 of 21 subjects on placebo developed asymptomatic, self-limiting SBP elevations >or= 30 mm Hg on three measurements. No subject on 1 mg/day rasagiline (0/12) experienced significant BP or heart rate changes following tyramine ingestion. These data demonstrate that rasagiline 0.5 to 2 mg daily is not associated with clinically significant tyramine reactions and can be used as monotherapy or adjunct to levodopa in PD patients without specific dietary tyramine restriction.     

Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

Introduction

Hemorrhage is accompanied by baroreflex-mediated tachycardia and vasoconstriction. The difference between baseline and maximum responses is defined as the heart rate (HR) and vasoconstrictor ??reserve??.

Objective

To test the hypothesis that higher HR and vasoconstrictor reserves in subjects with high tolerance (HT) to central hypovolemia is associated with greater reserve for sympathoexcitation and vagal withdrawal compared with low tolerant (LT) subjects.

Methods

R?CR intervals (RRI), systolic arterial pressure (SAP), estimated stroke volume, and muscle sympathetic nerve activity (MSNA) were measured during lower body negative pressure (LBNP) designed to induce pre-syncope. Subjects with tolerance ??60?mmHg LBNP were classified as LT (n?=?22) while subjects who tolerated LBNP levels >60?mmHg were classified as HT (n?=?56). Spontaneous cardiac baroreflex sensitivity (BRS) was assessed via RRI-SAP down?Cdown sequences.

Results

HR reserve in HT subjects (+52?±?2?bpm) was twofold greater (P?P?=?0.04) than that of the LT group (+1.9?±?0.3?pru). HT subjects demonstrated greater (P????0.03) BRS reserve (?14.2?±?1.8?ms/mmHg) and MSNA reserve (+41?±?2 bursts/min) compared with LT subjects (?7.4?±?1.7?ms/mmHg and +26?±?7?bursts/min).

Interpretation

Our data support the hypothesis that greater physiological reserve capacity for tachycardia and vasoconstriction related to high tolerance to central hypovolemia is associated with greater reserves for sympathoexcitation and cardiac vagal withdrawal.     

Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome

A variety of approaches have been used to alleviate symptoms in postural tachycardia syndrome (POTS). Drugs reported to be of benefit include midodrine, propranolol, clonidine, and phenobarbital. Other measures used include volume expansion and physical countermaneuvers. These treatments may influence pathophysiologic mechanisms of POTS such as -receptor dysfunction, -receptor supersensitivity, venous pooling, and brainstem center dysfunction. The authors prospectively studied hemodynamic indices and symptom scores in patients with POTS who were acutely treated with a variety of interventions. Twenty-one subjects who met the criteria for POTS were studied (20 women, 1 man; mean age, 28.7±6.8 y; age range, 14–39 y). Patients were studied with a 5-minute headup tilt protocol, ECG monitoring, and noninvasive beat-to-beat blood pressure monitoring, all before and after the administration of an intervention (intravenous saline, midodrine, propranolol, clonidine, or phenobarbital). The hemodynamic indices studied were heart rate (ECG) and systolic, mean, and diastolic blood pressure. Patients used a balanced verbal scale to record any change in their symptoms between the tilts. Symptom scores improved significantly after the patients received midodrine and saline. Midodrine and propranolol reduced the resting heart rate response to tilt (p<0.005) and the immediate and 5-minute heart rate responses to tilt (p<0.002). Clonidine accentuated the immediate decrease in blood pressure on tilt up (p<0.05). It was concluded that midodrine and intravenous saline are effective in decreasing symptoms on tilt in patients with POTS when given acutely. Effects of treatments on heart rate and blood pressure responses generally reflected the known pharmacologic mechanisms of the agents.     

Ambulatory blood pressure in patients with Parkinson's disease without and with orthostatic hypotension

Non-invasive ambulatory recordings of blood pressure and heart rate were performed using a Spacelabs device during day and night periods in patients with Parkinson's disease with (n = 19) or without orthostatic hypotension (n = 19). In patients with orthostatic hypotension, the average systolic and diastolic blood pressure during the night (137 ± 5/80 ± 3 mmHg) was higher (p < 0.05) than during the day period (121 ± 3/76 ± 2 mmHg). In patients without orthostatic hypotension, a decrease in blood pressure was recorded during the nocturnal period. In patients with orthostatic hypotension, the blood pressure variability was higher (p < 0.05) during the day (systolic: 14.6 ± 1.3%; diastolic: 16.5 ± 1.0%) than during the night (systolic: 9.1 ± 0.8%; diastolic: 10.8 ± 1.1%). The blood pressure load (percentage of values above 140/90 mmHg) during the night was significantly higher than during the day for both systolic (41.2 ± 8.1 vs. 19.6 ± 4.7%) and diastolic blood pressure (24.9 ± 6.9 vs. 16.3 ± 4.9%). There was a decrease in heart rate in both groups during the night. A fall of 25 mmHg or more in systolic blood pressure after meals occurred in ten patients with orthostatic hypotension and in one patient without orthostatic hypotension. These results indicate that orthostatic hypotension in Parkinson's disease is associated with specific modifications of ambulatory blood pressure including loss of circadian rhythm of blood pressure, increased diurnal blood pressure variability and post-prandial hypotension.