(Stroke. 1997;28:2357-2362.)
© 1997 American Heart Association, Inc.
Articles |
Cardiopulmonary and Arterial Baroreflex-Mediated Control of Forearm Vasomotor Tone Is Impaired After Acute Stroke
From the University Division of Medicine for the Elderly, The Glenfield Hospital, Leicester, UK.
Correspondence to T.G. Robinson, Leicester General Hospital NHS Trust, Gwendolen Rd, Leicester LE5 4PW.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose Elevated blood pressure (BP) levels are well recognized after acute stroke and are associated with increased BP variability. The underlying mechanisms producing such changes are unclear but may include abnormalities of baroreceptor-mediated control of heart rate and vasomotor tone. Lower body negative pressure (LBNP) can be used to assess the integrity of "low-pressure" cardiopulmonary and "high-pressure" arterial baroreceptor–derived responses by inducing nonhypotensive and hypotensive stimuli.
Methods Cardiovascular responses, including BP, heart rate, forearm blood flow, and forearm vascular resistance, to nonhypotensive and hypotensive LBNP were assessed in 13 consecutive stroke patients. Patients were studied within 72 hours of stroke (acute) and again at 10 to 14 days (subacute) and were compared with 13 control subjects individually matched for age, sex, and BP.
Results At an LBNP of -10 mm Hg, BP was unchanged in all groups, but a significant increase in forearm vascular resistance occurred only in the control group (11 U [interquartile range, 7 to 15]; P<.05) compared with stroke patients in the acute (9 U [3 to 14]; P=NS) or subacute phases (7 U [2 to 12]; P=NS). After LBNP at -40 mm Hg, the reductions in systolic BP levels were similar in all groups (control: -9 mm Hg [-16 to -3]; acute stroke: -9 mm Hg [-22 to 3]; subacute stroke: -7 mm Hg [-35 to 20]), as was the associated increase in heart rate (control: 8 bpm ([4 to 11]; acute stroke: 6 bpm ([1 to 12]; subacute stroke: 9 bpm [2 to 19]). However, forearm vascular resistance increased significantly only in control subjects (20 U [9 to 30]; P<.01).
Conclusions The present study has identified abnormal vasomotor responses to LBNP after acute stroke, with an increase in FVR only being observed in control subjects in response to nonhypotensive and similar hypotensive levels of LBNP. In acute stroke patients, the stimulus of hypotensive LBNP appears to be compensated by an increase in cardiac output since there appears to be no increase in peripheral vascular resistance, unlike the changes seen in control subjects. However, the exact mechanisms for these changes are still unclear and are the subject of further study.
Key Words: baroreflex • cerebrovascular disorders • lower body negative pressure • vasomotor system
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Blood pressure levels are elevated within the first 24 hours of acute stroke and decrease spontaneously within 3 to 10 days in most patients.1 2 3 The underlying pathophysiological mechanisms producing such changes are debated but may be related to changes in sympathetic nervous system activity as reflected by increases in catecholamine and corticosteroid levels.4 5 6 7 However, impairment of the autonomic neural regulation of the cardiovascular system has also been implicated.8 9
The baroreceptor reflex arc is the principal mechanism involved in the short-term regulation of the cardiovascular system. The primary role of the arterial baroreflex is the rapid adjustment of BP around an existing mean level, which is partly accomplished by appropriate changes in HR, stroke volume, and vasomotor tone. Free and encapsulated baroreceptor nerve endings are embedded in the adventitial layer of the arterial wall in the carotid sinus and aortic arch (the carotid and aortic baroreceptors). Afferent fibers travel via the glossopharyngeal and vagal nerves to specialized nuclei within the brain stem, including the nucleus tractus solitarii, the nucleus ambiguous, and the ventrolateral nuclei of the medulla oblongata. These are influenced by central structures, including the hypothalamus and cerebral cortex, to which direct damage may occur as a consequence of stroke. Efferent discharge via the parasympathetic and sympathetic outflow tracts thereafter influences the sinoatrial node, ventricular wall, and arteriolar and capacitance vessel function.
Changes in arterial baroreceptor activity lead to rapid alterations in HR (the arterial baroreceptor–HR reflex), mainly by variations in efferent vagal activity to the sinus node, although increased sympathetic outflow to the sinus node occurs more slowly in the response to sustained reduction in carotid baroreceptor pressure. Changes in arterial baroreceptor–HR reflex have been demonstrated in animal models of acute stroke,10 11 but human studies are limited and have been confined to patients with chronic cerebrovascular disease with the use of invasive arterial measurements.12 13 More recently, we have used noninvasive techniques of beat-to-beat BP measurement together with power spectral analysis techniques to assess the arterial baroreceptor–HR reflex in patients within 72 hours of acute stroke and demonstrated significantly impaired responses compared with a control group matched with respect to age, sex, and casual and 24-hour BP.14
Arterial baroreceptors also regulate overall systemic vascular resistance through sympathetically mediated adjustment of vasoconstrictor tone (the arterial baroreceptor–vasomotor reflex). There is limited indirect evidence of vasomotor dysfunction after acute stroke. Previous work in our department has shown an increase in short-term (beat-to-beat) systolic BP variability independent of underlying BP level in acute stroke patients compared with control subjects matched with respect to age and sex.15 This may reflect impaired arterial baroreceptor–HR reflex responses, since BP variability has been shown to be inversely related to baroreceptor sensitivity.16 17 18 19 However, we found no significant differences in pulse interval variability between acute stroke patients and control subjects, which might suggest that the increased BP variability seen could not be fully accounted for by an impairment of the arterial baroreceptor–HR reflex.15 It could be conjectured that the increased BP variability may be mediated by an impairment of vasomotor tone, although direct measurements were not made in that study, and we have previously demonstrated no change in FVR (used as a reflection of vasomotor tone) in acute stroke patients in relation to an orthostatic BP fall.20 In addition, mechanoreceptors sited in the cardiopulmonary vascular bed influence vasomotor tone (the cardiopulmonary-vasomotor reflex),21 although the integrity of this reflex arc has not been previously studied after acute stroke.
A number of techniques are available to assess the overall integrity of the autonomic control of the cardiovascular system. One such technique is LBNP, which typically involves the application of reduced atmospheric pressure to supine resting subjects from the iliac crests caudally. The technique initiates physiological changes, which at low pressures (<20 mm Hg) may selectively unload the cardiopulmonary receptors and at high pressures (>40 mm Hg) unload the arterial baroreceptors, inducing changes comparable to those observed during orthostasis or head-up tilt.22 However, the experimental method of LBNP has distinct advantages over orthostatic techniques. The subject is supine throughout the procedure, which allows the monitoring of a number of physiological variables, including FVR by mercury-in-silicone elastomer strain gauge plethysmography, without concerns regarding the effects of gravity, movement artifact, or constant position with respect to the right atrium. It was therefore proposed to use LBNP techniques to assess the cardiovascular responses including BP, HR, FBF, and FVR changes in acute stroke patients compared with control subjects and to assess changes between the acute and subacute periods after stroke.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Subjects
Thirteen consecutive stroke patients (8 men; mean age, 63.5 years; range, 45 to 85 years) were recruited after admission to the medical wards of the Leicester teaching hospitals within 24 hours of first-time acute stroke (four dominant hemispheres). Diagnosis was confirmed by head CT scanning in 10 patients (all cerebral infarction). Clinical diagnosis was made in all patients with the use of the Oxfordshire Community Stroke Project classification (6 partial anterior circulation strokes, 7 lacunar strokes). Disability was assessed by the Barthel Activities of Daily Living Index with a median score of 85 (range, 40 to 100). The following patients were excluded: unconscious or impaired conscious level, subsequent diagnosis of transient ischemic attack, CT diagnosis of cerebral hemorrhage, and other conditions associated with autonomic dysfunction.
Thirteen control subjects were individually matched with the acute stroke patients by age (within 5 years) (65.5 years [range, 45 to 85 years], sex (8 men), and supine BP levels (within 5 mm Hg). These subjects were recruited from among respondents to a local newspaper advertisement and had no history of cerebrovascular disease.
All subjects with a known diagnosis of ischemic heart disease, atrial fibrillation, diabetes mellitus, impaired renal function (creatinine >200 µmol/L), or other conditions associated with autonomic dysfunction were excluded. No subject received antihypertensive therapy or medication known to affect cardiovascular autonomic responses. Informed consent was obtained from subjects or their caregivers (when appropriate), and approval was given by the Leicestershire Hospital Ethics Committee.
Protocol
All studies were performed in the morning after the subjects
underwent an overnight fast, including abstaining from smoking,
alcohol, and all caffeinated products. At the time of study, stroke
patients were hemodynamically stable, did not require
intravenous fluid administration, and were not
biochemically dehydrated. Investigations took place in a quiet room
(ambient temperature, 20°C to 24°C), and the subjects were asked to
micturate before the study began. Stroke patients were studied on two
occasions: within 72 hours of acute stoke and at 10 to 14 days after
acute stroke.
Subjects were then familiarized with the protocol, including the LBNP procedure. The LBNP device was an aluminum box in which the subject rested supine on a well-padded seat. The subject wore a kayak-style skirt that was used to make an airtight seal between the subject and the box at the level of the iliac crest. Suction was produced by a commercial vacuum cleaner with a variable-speed motor and an adjustable air leak on the suction hose pipe, and box pressure (millimeters of mercury) was monitored continuously. The subject was fitted with chest leads for continuous ECG recording (model CR7, Cardiac Recorders Ltd) and the appropriately sized cuff of the 2300 Finapres noninvasive BP monitor (Ohmeda). This is a fully automated measurement that allows continuous beat-to-beat measurement of finger arterial pressure. It uses the volume clamp technique of Penaz23 and is well validated against intra-arterial BP measurements in all age groups.24 25 26 The cuff was fitted to the middle finger or thumb of the hemiparetic arm in stroke patients and the nondominant hand in control subjects and maintained heart level throughout. FBF was measured as previously described20 ; FVR was derived by dividing the MAP by the FBF.
After a 15-minute rest period, the subject underwent four consecutive periods of 10 minutes of study. Baseline recordings of HR, BP, FBF, and FVR were made over a 2-minute period. This was followed by 3 minutes of LBNP. After release of the LBNP, there was a 5-minute rest period. This process was repeated on four occasions: on two occasions at -10 mm Hg and on two additional occasions at -40 mm Hg.
Statistical Methods
Baseline values of SBP, DBP, MAP, and HR before LBNP were taken
as the mean of the 1-minute beat-to-beat ECG and BP recordings
immediately before the application of LBNP. Baseline values of FBF were
taken as the mean of the four cycles immediately before the application
of LBNP. The mean values of these variables were calculated during
3 minutes of LBNP at -10 and -40 mm Hg, and the changes with
LBNP were expressed as the absolute difference between mean baseline
values and mean values during LBNP.
Normality of the data was determined by construction of a normal probability plot with the use of the Minitab statistical package (Minitab 10 for Windows, Minitab Inc). If a value of <.05 was obtained with the Ryan-Joiner test, the data were not considered normally distributed. For normally distributed data, the results were presented as mean (SD). Statistical comparisons between paired and unpaired normally distributed data were made by Student's paired and unpaired t tests, respectively. For nonnormally distributed data, results are presented as median (interquartile range), and further statistical comparisons were made with the Mann-Whitney and Wilcoxon rank sum tests. Bonferroni's correction was applied for multiple comparisons,27 and significance was taken at the 5% level.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Stroke patients and control subjects were individually matched with respect to age (63.5 [SD 12.6] versus 65.5 [7.9[ years; P=.70) and sex (8 men versus 8 men).
No significant differences were seen before LBNP at -10 mm Hg in
baseline SBP, DBP, MAP, HR, FBF, or FVR between control subjects and
acute stroke patients (Table 1
). There
was no significant change from baseline in SBP, DBP, MAP, or HR in
either control subjects or acute stroke patients during LBNP at
-10 mm Hg (Table 2). However,
there was a significant fall in FBF, associated with a significant
increase in FVR in control subjects only (Table 2). A nonsignificant BP
reduction was seen in stroke patients before LBNP at -10 mm Hg
between acute and subacute study periods, and there were no
significant changes in the other baseline variables (Table 1). In
addition, no significant changes were seen from baseline in any of the
variables during LBNP at -10 mm Hg in stroke patients
studied during the subacute period (Table 2), and there was no
difference between values for the control and subacute stroke
groups.
|
|
SBP, DBP, MAP, HR, FBF, and FVR values were similar before -40
mm Hg LBNP in control subjects and for both phases in the stroke
patients (Table 1
). The median hypotensive SBP stimulus was not
significantly different between groups (control: -9 mm Hg
[interquartile range, -16 to -3]; acute stroke: -9 [-22 to 3];
subacute stroke: -7 [-35 to 20]) (Table 2, Figure
). No significant changes were seen from
baseline in any group, although a significant reduction was seen in MAP
in the control group only (-4 mm Hg [-8 to -2],
P
.01) (Table 2). FBF fell significantly in all groups
(control: -0.7 mL/min per 100 mL forearm [-1.0 to -0.3],
P<.01; acute stroke: -0.5 [-1.2 to -0.2],
P<.05; subacute stroke: -1.0 [-1.8 to -0.2],
P<.01) (Table 2, Figure), although FVR increased
significantly from baseline in the control group only (control: 20 U
[9 to 30], P<.01; acute stroke: 5 [-12 to 23];
subacute stroke: 16 [-9 to 27]) (Table 2, Figure). There was an
associated significant rise in HR in all groups (control: 8 bpm [4 to
11], P<.01; acute stroke: 6 [1 to 12],
P<.01; subacute stroke: 9 [2 to 19],
P<.05) (Table 2, Figure).
|
) and -40 (
) mm Hg LBNP for 3
minutes in control subjects (CON) and stroke patients studied during
the acute and subacute phases. Values are expressed as mean (SEM)
increases (+) or decreases (-) from baseline. *P<.05,
**P<.01 for changes compared with baseline. CVA
indicates cerebrovascular accident. |
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
In the present study, in response to -10 mm Hg LBNP, stroke patients in the acute and subacute phases showed no significant increase in FVR, although in an age-, sex-, and BP-matched control group FVR did increase to this nonhypotensive stimulus. No other significant differences in the hemodynamic responses assessed were observed between control subjects and stroke patients. At levels of LBNP (-40 mm Hg) that induced a fall in SBP, no significant increase in FVR was observed in stroke patients despite the BP decrease, but control subjects showed the expected increase in FVR. HR increased to a similar degree in both control subjects and stroke patients studied in the acute and subacute periods. In the poststroke follow-up period, no differences were found in any of the cardiovascular parameters measured in response to nonhypotensive and hypotensive LBNP between stroke patients and control subjects.
LBNP initiates cardiovascular changes comparable to those observed during active standing and passive head-up tilt to 70°22 and allows an assessment of the integrity of the physiological responses to hemodynamic stress. At negative pressures of <20 mm Hg, approximately 500 to 1000 mL of blood pools in the lower body.22 This reduces central venous return with a consequent reduction in central venous pressure and right ventricular filling and output. This initiates compensatory vasomotor changes, including a reduction in FBF resulting in increased FVR, as reported in this study and in other studies including healthy control subjects.28 29 30 These changes were not associated with a fall in BP in the present study, also in agreement with other reports.22 28 29 31 The cardiovascular changes initiated by low-level LBNP are probably a consequence of selective unloading of the cardiopulmonary receptors,22 28 31 32 although animal studies suggest that arterial baroreceptors may also be involved in the initiation of reflex vasoconstriction.33 34 However, no significant HR changes were observed in the present study, in agreement with the findings of others.28 29 30 31
At higher levels of LBNP (
-40 mm Hg), significant reductions
in SBP were seen in control subjects, again in agreement with other
studies.29 35 This triggers sympathetic nervous
system–mediated adjustments in vasomotor activity and
HR.21 Vasomotor changes are predominantly mediated by the
cardiopulmonary receptor vasomotor reflexes in skeletal muscle
vascular beds36 and arterial
baroreceptor–vasomotor reflexes in splanchnic vascular
beds.37 The present study only assessed changes in the
forearm vascular bed and reported significant increases in FVR, similar
to those found in other healthy control studies.29 30
In the present study control subjects were individually matched with acute stroke patients with particular respect to age and BP because of the effect of these variables on the physiological parameters studied.21 However, compared with control subjects, acute and subacute stroke patients (individually matched with respect to age, sex, and BP) demonstrated a failure to increase FVR from baseline in response to the nonhypotensive and hypotensive LBNP. This impairment is most marked in the acute period, with gradual improvement over the 2 weeks after acute stroke. There are a number of possible explanations for impaired vasomotor responses after acute stroke. First, this may represent abnormalities of cardiopulmonary and/or arterial baroreceptor–mediated changes in vasomotor tone. To the authors' knowledge, changes in cardiopulmonary receptor–mediated reflexes have not been previously assessed after acute stroke. Certainly, impaired arterial baroreceptor–mediated reflexes to the Valsalva maneuver are well documented in patients with chronic cerebrovascular disease.12 13 We have also previously demonstrated an absence of significant change in FVR despite hypotensive responses to orthostasis after stroke.20
Second, this may reflect impairment of the efferent pathway, ie, impaired vasoconstrictor responses in skeletal muscle. This cannot be excluded because the present study did not use other techniques to assess the integrity of this response, such as the cold pressor test. Equally, forearm vasoconstriction may already be maximal in the stroke patients, thereby limiting further vasoconstriction. The assessment of forearm vasodilator responses after release of LBNP would have allowed a further measurement of the integrity of reflex responses but was not performed in the present study. Therefore, it is unclear whether impaired vasoconstriction is related to a generalized alteration of autonomic vascular control or specific volume and pressure stretch receptor influences. Also, the present study only assessed vasoconstriction in the forearm, although other vascular beds, such as the splanchnic circulation, may have exhibited vasoconstrictor responses.
However, although vascular responses were studied in the nonhemiparetic forearm in the present study, vasomotor changes have been previously described in hemiplegic limbs,38 39 40 and some information can be derived from these studies. Wanklyn and colleagues39 reported a significant reduction in hand blood flow in a group of chronic stroke patients with symptomatic coldness of the hemiplegic limb. This may simply reflect muscle disuse but may also be related to alterations in vasomotor tone and reactivity. A spinally mediated vasoconstriction response to deep inspiration or coughing is increased in tetraplegic patients, indicating the loss of a descending inhibitory influence.41 Equally, a descending inhibitory response may be interrupted after stroke, resulting in abnormal persistent vasoconstriction secondary to a spinal reflex with consequent reduced blood flow and absence of further vasoconstriction.39
Finally, there are problems related to technical aspects of the study. There was marked interpatient variability in forearm vascular responses, particularly in the stroke patients, which may explain a lack of statistical significance between the control and stroke groups. It could be argued that a more appropriate control would be to compare vasomotor responses between the hemiparetic and nonhemiparetic arms in stroke patients. This was not performed to limit the duration of the study in acutely ill patients and because of previous reports of impaired blood flow in hemiparetic limbs, possibly related to changes other than vasomotor activity.39 40 41 Also, it cannot be stated with absolute confidence that the stimulus of central blood volume reduction was identical between control subjects and stroke patients. The cardiopulmonary receptor–vasomotor reflex initiates a response to changes in central venous pressure,22 but for ethical reasons central venous cannulation and the recording of pressure changes were not performed in the present study. Equally, the present study did not utilize echocardiographic techniques to assess the effects of LBNP on cardiac volumes. However, a hypotensive stimulus detected by the arterial baroreceptors also initiates forearm vasoconstriction (the arterial baroreceptor–vasomotor reflex), and despite a similar hypotensive stimulus, no significant changes in FVR were seen in stroke patients.
The integrity of the arterial baroreceptor–HR reflex was also assessed in the present study. Significant HR increases were seen in control subjects, in agreement with other studies,22 37 42 and in both acute and subacute stroke patients. This is in contrast to the abnormalities in vasomotor reflexes discussed previously and to our previous reports of impaired arterial baroreceptor–HR reflex sensitivity with the use of power spectral analysis techniques in patients studied within 72 hours of acute stroke.14 Abnormalities of cardiovascular reflexes after stroke are probably a result of damage to the sites of central integration of reflex responses. However, the present study was too small to correlate CT findings, and in particular the site of stroke, with specific abnormalities of cardiovascular response, although no patient had evidence of brain stem disease.
In summary, the present study has demonstrated abnormalities of vasomotor tone after acute stroke in response to stimulation of both cardiopulmonary receptors and arterial baroreceptors, assessed by LBNP at -10 and -40 mm Hg, which persist in the subacute period. This may be related to stroke-related damage to the central connections of the cardiovascular reflex arcs or to impaired vasoconstrictor responses in skeletal muscle. Such abnormalities of cardiovascular autonomic control may have implications in the BP changes after acute stroke and in the acute management of BP after stroke.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was supported by a grant from the Stroke Association of the United Kingdom (Dr Robinson).
Received July 11, 1997; revision received August 21, 1997; accepted September 10, 1997.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Britton M, Carlsson A, de Faire U. Blood pressure course in patients with acute stroke and matched controls. Stroke. 1986;17:861–864.
2. Jansen P, Schulte B, Poels E, Gribanu F. Course of blood pressure after cerebral infarction and transient attack. Clin Neurol Neurosurg. 1987;89:243–246.[Medline] [Order article via Infotrieve]
3. Harper G, Castleden C, Potter J. When can we diagnose hypertension after stroke?. Age Ageing. 1991;20(suppl 1):P23. Abstract.
4.
Meyer J, Stoica E, Pascu I, Shimazu K, Hartmann A.
Catecholamine concentrations in CSF and plasma of patients
with cerebral infarction and haemorrhage. Brain. 1973;96:277–288.
5. Feibel J, Baldwin C, Joynt R. Catecholamine-associated refractory hypertension following acute intracranial haemorrhage: control with propranolol. Ann Neurol. 1981;9:340–343.[Medline] [Order article via Infotrieve]
6.
Myers M, Norris J, Hachinski V, Sole M. Plasma
norepinephrine in stroke. Stroke. 1981;12:200–204.
7. Olsson T. Urinary free cortisol excretion shortly after ischaemic stroke. J Intern Med. 1990;228:177–181.[Medline] [Order article via Infotrieve]
8.
Natelson B. Neurocardiology: an
interdisciplinary area for the 80s. Arch Neurol. 1985;42:178–184.
9. Talman W. Cardiovascular regulation and lesions of the central nervous system. Ann Neurol. 1985;18:1–12.[Medline] [Order article via Infotrieve]
10.
Doba N, Reis D. Role of the cerebellum and the
vestibular apparatus in regulation of
orthostatic reflexes in the cat. Circ Res. 1974;34:9–18.
11. Cechetto D, Wilson J, Smith K, Wolski D, Silver M, Hachinski V. Autonomic and myocardial changes in middle cerebral artery occlusion: stroke models in the rat. Brain Res. 1989;502:296–305.[Medline] [Order article via Infotrieve]
12. Appenzeller 0, Descarries L. Circulatory reflexes in patients with cerebrovascular disease. N Engl J Med. 1964;217:820–823.
13. Gross M. Circulatory reflexes in cerebral ischaemia involving different vascular territories. Clin Sci (Colch). 1970;38:491–502.[Medline] [Order article via Infotrieve]
14.
Robinson TG, James M, Youde J, Panerai R, Potter
J. Cardiac baroreceptor sensitivity is impaired after acute stroke
as assessed by power spectral analysis. Stroke. 1997;28:1671–1676.
15. Robinson T, Ward-Close S, Potter J. A comparison of beat-to-beat blood pressure variability in acute and subacute stroke patients with cerebral infarction. Cerebrovasc Dis. 1997;7:214–219.
16. Mancia G, Ferrari A, Gregorini L, Parati G, Pomidossi G, Bertinieri G, Grassi G, Zanchetti A. Blood pressure variability in man: its relation to high blood pressure, age and baroreceptor sensitivity: Clin Sci (Colch). 1980;59:401S–404S.
17.
Mancia G, Parati G, Pomidossi G, Casadei R, Di Rienzo
M, Zanchetti A. Arterial baroreflex and blood pressure and
heart rate variabilities in humans. Hypertension. 1986;8:147–153.
18.
Floras J, Hassan M, Vann Jones J, Osikowska B, Sever P,
Sleight P. Factors influencing blood pressure and heart rate
variability in hypertensive humans. Hypertension. 1988;11:273–281.
19.
Parati G, Frattola A, Di Rienzo M, Castiglioni P,
Pedotti A, Mancia G. Effects of aging on 24-h dynamic baroreceptor
control of heart rate in ambulant subjects. Am J
Physiol. 1995;268:H1606–H1612.
20.
Robinson T, Potter J. Postprandial and
orthostatic cardiovascular changes
following acute stroke. Stroke. 1995;26:1811–1816.
21. Shepherd R, Shepherd R. Control of blood pressure and the circulation in man. In: Bannister R, ed. Autonomic Failure. A Textbook of Clinical Disorders of the Autonomic Nervous System. NY, New York: Oxford University Press; 1988:80–96.
22.
Wolthius R, Bergman S, Nicogossian A.
Physiological effects of locally applied reduced
pressure in man. Physiol Rev. 1974;54:566–595.
23. Penaz J. Photoelectric measurement of blood pressure, volume and flow in the finger. In: Digest of the International Conference on Medicine and Biological Engineering, Conference Committee of the 10th International Conference on Medicine and Biological Engineering; Dresden, Germany; 1973:104.
24. Imholz B, van Montfrans G, Settels J, van der Hoeven G, Karemaker J, Wieling W. Continuous non-invasive blood pressure monitoring: reliability of Finapres device during Valsalva manoeuvre. Cardiovasc Res. 1988;22:390–397.[Medline] [Order article via Infotrieve]
25.
Parati G, Casadei R, Groppello A, di Rienzo M, Mancia
G. Comparison of finger and intra-arterial blood pressure
monitoring at rest and during laboratory testing.
Hypertension. 1989;13:647–655.
26.
Imholz B, Settels J, van der Meiracker A, Wesseling K,
Wieling W. Non-invasive continuous finger blood pressure measurement
during orthostatic stress compared to
intra-arterial pressure. Cardiovasc Res. 1990;24:214–221.
27.
Bland J, Altman D. Multiple significance tests: the
Bonferroni method. Br Med J. 1995;310:170.
28. Johnson J, Rowell L, Niederberg M, Eismen M. Influence of right atrial versus aortic pressure changes on human splanchnic and forearm blood flows. Circulation. 1973;48(suppl IV):27. Abstract.
29.
Grassi G, Giannattasio C, Cleroux J, Cuspidi C,
Sampieri L, Bolla G, Mancia G. Cardiopulmonary reflex before
and after regression of left ventricular
hypertrophy in essential hypertension.
Hypertension. 1988;12:227–237.
30.
Taylor J, Hand G, Johnson D, Seals D.
Sympathoadrenal-circulatory regulation of arterial pressure
during orthostatic stress in young and older men.
Am J Physiol. 1992;263:R1147–R1155.
31.
Victor R, Leimbach W. Effects of lower body negative
pressure on sympathetic discharge to leg muscles in humans.
J Appl Physiol. 1987;63:2558–2562.
32. Zanchetti A, Mancia G. Cardiovascular reflexes and hypertension. Hypertension. 1991;18(suppl III):III-13-III-21.
33.
Hakumaki M, Wang B, Sundet W, Goetz K. Aortic
baroreceptor discharge during non-hypotensive hemorrhage in
anesthetized dogs. Am J Physiol. 1985;249:H393–H403.
34.
Cornish K, Gilmore J, McCulloch T. Central blood
volumes and blood pressure in conscious primates. Am J
Physiol. 1988;254:H693–H701.
35.
Fortney S, Tankersley C, Lightfoot J, Drinkwater D,
Clulow J, Gerstenblith G, O'Conner F, Becker L, Lakatta E, Fleg
J. Cardiovascular responses to lower body negative
pressure in trained and untrained older men. J Appl
Physiol. 1992;73:2693–2700.
36.
Baily R, Prophet S, Shenberger J, Zelis R, Sinoway L.
Direct neurohumoral evidence for isolated sympathetic nervous system
activation to skeletal muscle in response to cardiopulmonary
baroreceptor unloading. Circ Res. 1990;66:1720–1728.
37.
Abboud F, Eckberg D, Johansen U, Mark A. Carotid
and cardiopulmonary baroreceptor control of splanchnic and
forearm vascular resistance during venous pooling in man. J
Physiol. 1979;286:173–184.
38.
Herbault A-G, Cole J, Sedgewick E. A cerebral
hemisphere influence on cutaneous vasomotor reflexes in humans.
J Neurol Neurosurg Psychiatry. 1990;53:118–120.
39. Wanklyn P, Ilsley D, Greenstein D, Hampton I, Roger T, Kester R, Mulley G. The cold hemiplegic arm. Stroke. 1994;25:1765–1770.[Abstract]
40.
Wanklyn P, Forster A, Young J, Mulley G. Prevalence and
associated features of the cold hemiplegic arm. Stroke. 1995;26:1867–1870.
41. Cole J, Mani R, Sedgewick E. Cutaneous vasomotor reflexes following spinal cord injury in man. J Physiol. 1985;369:134. Abstract.
42. Mark A, Mancia G. Cardiopulmonary baroreflexes in humans. In: Shepherd J, Abboud F, eds. Handbook of Physiology, Section 2: The Cardiovascular System. Bethesda, Md: American Physiology Society; 1983;3:795–813.
This article has been cited by other articles:
 |
|
 |
|
  Q. Fu, S. Shibata, J. L. Hastings, A. Prasad, M. D. Palmer, and B. D. Levine Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H480 - H488. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. G. Stead, R. M. Gilmore, K. C. Vedula, A. L. Weaver, W. W. Decker, and R. D. Brown Jr Impact of acute blood pressure variability on ischemic stroke outcome Neurology, June 27, 2006; 66(12): 1878 - 1881. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P J Eames, M J Blake, S L Dawson, R B Panerai, and J F Potter Dynamic cerebral autoregulation and beat to beat blood pressure control are impaired in acute ischaemic stroke J. Neurol. Neurosurg. Psychiatry, April 1, 2002; 72(4): 467 - 472. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. L. Dawson, B. N. Manktelow, T. G. Robinson, R. B. Panerai, and J. F. Potter Which Parameters of Beat-to-Beat Blood Pressure and Variability Best Predict Early Outcome After Acute Ischemic Stroke? Stroke, February 1, 2000; 31(2): 463 - 468. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||