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At least 631 records · Page 35Linked to original sources
PubMed1998

Idiopathic hypovolemia: a self-perpetuating autonomic dysfunction?

Unexplained episodic hypertension, hypotension, or orthostatic intolerance, tachycardia, anxiety, and flushing in 21 patients were investigated for the possibility of hypovolemia by blood volume and individual plasma catecholamines (including autocrine paracrine-born dopamine), determinations baseline, in response to upright posture and catecholamines only during the episodic blood pressure swings. Blood volume was determined by Cr51 fixed to patients' hemoglobin, free norepinephrine, epinephrine, and dopamine with dopamine sulfate following sulfatase hydrolysis, radioenzymatically. The recumbent mean 27.4+/-3% (SE) blood volume decrease from predicted values accentuating to 33.5+/-4% upright was associated with normal baseline plasma free norepinephrine, epinephrine, dopamine, dopamine sulfate, plasma renin activity, and aldosterone with normal mean postural responses from all patients except a hyperresponsive compared to controls (p < 0.04), plasma renin activity increase from 0.657+/-0.1 to 4.47+/-1.8 ng/mL/hr. During the hypertensive, hypotensive, or tachycardic episodes the moderate increase of free norepinephrine and epinephrine (p < 0.04) (but not free dopamine) contrasted with an increase of dopamine sulfate from 2.5+/-0.9 to clearly pathological values of 16.8+/-8.3 ng/mL (p < 0.0003 on % increase of individual values). We conclude that the normal (but to the degree of hypovolemia inappropriately low orthostatism- and episodes-associated sympathetic arousal) is outpaced by considerable episodic dopamine sulfate surges, reflecting extraneuronal dopamine discharge. Whether this increase contributes to the increased natriuresis directly or by inhibiting aldosterone response to renin-angiotensin, perpetuating hypovolemia, remains to be established.

Adolescent↗
PubMed2004

Use of lower abdominal compression to combat orthostatic hypotension in patients with autonomic dysfunction.

The aim of this study was to investigate in patients with neurogenic orthostatic hypotension the mechanism and usefulness of abdominal compression to increase standing blood pressure. In three protocols, 23 patients underwent abdominal compression. Protocol 1 evaluated in a 40-60 degrees head-up-tilt position, the effect of abdominal compression on caval vein and femoral diameter, arterial blood pressure and hemodynamics. Protocol 2 documented the relationship between the level of compression and the arterial pressure response. Protocol 3 investigated the ability to maintain standing blood pressure by an elastic binder. During head-up-tilt, compression (40 mm Hg) resulted in a reduction in diameter of the caval vein (mean -2.6mm, range -1.4 to 0.6), without a change in femoral vein diameter. Stroke volume increased by 14 % (range -1 to 23) and blood pressure (systolic/diastolic) by 30/14 mmHg (range 7/2 to 69/36), both p < 0.05; 40 mmHg compression was associated with a higher pressure response than 20 mmHg (mean 18/8 mmHg, range 6/2 to 43/20 vs. mean 9/4 mmHg, range -1/0 to 18/8, p < 0.05). Elastic abdominal binding increased standing blood pressure with 15/6 mmHg (range -3/3 to 36/14, p < 0.05). We conclude that in patients with neurogenic orthostatic hypotension, abdominal compression increases standing blood pressure to a varying degree by increasing stroke volume.

Abdomen↗
PubMed1994

Motor neuron disease with multi-system involvement presenting as tetraparesis, ophthalmoplegia and sensori-autonomic dysfunction.

We carried out a postmortem examination on two Japanese patients, 64- and 80-year-old men whose survival was prolonged with an artificial respirator. They had no family history of neuropsychiatric disorders and were suspected, clinically, as having a motor neuron disease that differed from amyotrophic lateral sclerosis (ALS). As well as upper and lower motor neuron impairment, they showed a variety of symptoms, such as sensory disturbances, hypohidrosis, impotence, ophthalmoparesis and/or atonic neurogenic bladder, and their protein content in cerebrospinal fluid was elevated markedly. Pathological examination revealed the following extensive nervous system involvement: (1) the upper and lower voluntary motor systems, including the IIIrd, IVth and VIth cranial nerve nuclei: (2) the reticular formation and its major afferent pathways; (3) the vestibulospinal and tectospinal systems; (4) the spinocerebellar system and the exteroceptive somatic afferent pathways; (5) the dentatorubral and pallidoluysian systems; and (6) the substantia nigra, locus ceruleus and intermediolateral and Onufrowicz's nuclei. Neither Bunina bodies, Lewy body-like hyaline inclusions nor ubiquitin immunoreactive skein-like structures were observed. The distribution of the lesions was quite different from that in patients with ALS and the other known related diseases. Recently, seven autopsied cases with clinical and histopathological similarities to our patients have been reported in Japan. Our conclusion is that our two and these seven patients should be classified as having a new motor neuron disease entity, which can be is differentiated from ALS.

Aged↗
PubMed2000

Reduced baroreflex sensitivity in elderly humans is not due to efferent autonomic dysfunction.

A progressive decline in baroreflex sensitivity (BRS) is a characteristic feature of human aging, the basis of which is poorly understood. The purpose of the present study was to determine whether alterations in efferent baroreflex function might contribute to the age-related decrease in BRS. We studied 10 healthy young (mean age 30.5 years; age range 22-40 years; six male) and 10 healthy elderly (mean age 70.7 years; age range 67-75 years; five male) volunteers. We tested efferent cardiac vagal function using the bradycardiac response to the cold face test, and efferent sympathetic function using heart rate and blood pressure responses to four stress tests: (i) low-level cognitive stress, (ii) high-level cognitive stress, (iii) hand immersion in ice water (cold pressor test) and (iv) isometric sustained hand-grip. Haemodynamic responses to these stresses are mediated via efferent baroreflex pathways, whereas the afferent components of each reflex response are independent of afferent baroreflex pathways. BRS was measured from simultaneous Finapres-derived continuous blood pressure and digital ECG R-R interval data using the sequence analysis paradigm. As expected, BRS was significantly reduced in the elderly group (7. 29+/-0.74 ms/mmHg; mean+/-S.E.M.) compared with the young group (13. 84+/-1.13 ms/mmHg; P<0.001). However, neither the bradycardiac responses to the cold face test nor the efferent sympathetically mediated heart rate/blood pressure responses to the stress test battery were significantly different between the young and elderly groups. We conclude that the age-related decrease in BRS is not attributable to impairments in the efferent sympathetic or parasympathetic system components of the baroreceptor reflex pathway.

Adult↗
PubMed1993

Autonomic dysfunction and the development of hypertension in patients treated with recombinant human erythropoietin (r-HuEPO).

Hypertension is the most common complication of r-HuEPO therapy in dialysis patients. The aim of this study was to test the hypothesis that hypertension develops in patients who fail to autoregulate adequately their hemodynamic response to correction of anemia. Twenty-five dialysis patients (17-71 yrs, 13 male, 13 CAPD) initially received r-HuEPO 50 U/kg 3 times/week intravenously or subcutaneously. Hypertension, defined as a rise in mean blood pressure (BP) of greater than 15 mmHg during therapy developed in 44% (Group 1: stable BP; Group 2: rise in BP). There was no difference in sex, age, mode of dialysis or route of administration of r-HuEPO between the groups. Before commencement and after 6-12 months of r-HuEPO therapy, assessment of the baroreflex arc was performed using the Valsalva ratio and orthostatic BP testing, sympathetic efferent nerve function was assessed by the cold pressor test and afferent parasympathetic function by the 30:15 ratio and heart rate variation (HRV). No difference was detected prior to r-HuEPO therapy between the two groups in Valsalva ratio (Group 1: 1.26 +/- 0.06 vs Group 2: 1.23 +/- 0.06, mean +/- SEM); 30:15 ratio (1.06 +/- 0.02 vs 1.03 +/- 0.01), or systolic, diastolic, mean BP or pulse rate after standing for 3 minutes or following hand immersion in ice slush. Both groups had a fall in systolic and diastolic BP (p < 0.05) and a rise in pulse rate (p < 0.05) on standing. HRV during deep respiration between the 2 groups was not different (9.6 +/- 2.3 vs 7.1 +/- 1.4 beats/minute).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Increased pulse-wave velocity in patients with anxiety: implications for autonomic dysfunction.

Decreased vagal function is associated with vascular dysfunction. In this study, we compared vascular indices and correlated heart rate and QT variability measures with vascular indices in patients with anxiety disorders and normal controls. We compared age- and sex-matched controls (n=23) and patients with anxiety (n=25) using the Vascular Profiler (VP-1000; Colin Medical Instruments, Japan), approved by the US Food and Drug Administration. Using this machine, we obtained ankle and brachial blood pressure (BP) in both arms (brachial), both legs (ankle), and carotid artery, and lead I electrocardiogram (ECG) and phonocardiogram. Using these signals, pulse-wave velocity (PWV), and arterial stiffness index % and preejection period can be calculated. We also obtained ECG sampled at 1000 Hz in lead II configuration in supine posture to obtain beat-to-beat interbeat interval (R-R) and QT interval variability for 256 s. Patients with anxiety had significantly higher carotid mean arterial pressure (MAP) %, brachial-ankle PWV (BAPWV), arterial stiffness index %, MAP, and diastolic BP of the extremities compared to controls. We found significant negative correlations (r values from .4 to .65; P<.05 to .007) between R-R interval high-frequency (0.15-0.5 Hz) power (which is an indicator of cardiac vagal function), and increased BAPWV and systolic BP of the extremities only in patients. We were unable to find such correlations in controls. We also found significant positive correlations between QT variability index (a probable indicator of cardiac sympathetic function) and MAP of the extremities and BAPWV only in the patient group. These findings suggest an important association between decreased vagal and increased sympathetic function, and decreased arterial compliance and possible atherosclerotic changes and increased BP in patients with anxiety.

Adult↗
PubMed1983

Congenital autonomic dysfunction with universal pain loss.

Three patients who appear to have a previously undescribed congenital neuropathy are described. None is of Ashkenazi Jewish extraction, but each seems to fulfill the clinical diagnostic criteria for familial dysautonomia. All lack overflow tears, fungiform papillae, and deep-tendon reflexes; intradermal administration of histamine did not produce an axon flare. Intraocular instillation of dilute mecholyl produced miosis in the one patient tested. In contrast to patients with familial dysautonomia, the three patients had universal loss of pain sensation, profound hypotonia, and unusual facies. Pathologic examination of the sural nerve in one patient was not consistent with the usual findings in familial dysautonomia. These patients are believed to have a previously undescribed congenital neuropathy.

Child, Preschool↗
PubMed1997

The correction of autonomic dysfunction in cirrhosis by captopril.

BACKGROUND/AIMS: Vagal dysfunction is reported in about 70% of patients with cirrhosis, irrespective of aetiology, as detected by cardiovascular reflex tests. We have previously shown that RR-variability on 24-h ECG is a more sensitive marker of vagal dysfunction in cirrhosis. Angiotensin II inhibits vagal function in animals, and it is elevated in cirrhosis and may be the cause of the vagal dysfunction. Our aim was to observe the effect of captopril on vagal dysfunction in cirrhosis. METHODS: Eight patients with cirrhosis (biopsy proven, male two, female six, mean age 54.25) had 24-h ECG RR-variability performed. They then received captopril 25 mg t.d.s. for 48 h. The 24-h ECG was repeated on therapy. RESULTS: Mean blood pressure remained unchanged: baseline 89.8 +/- 4.8 mmHg (mean +/- sem) versus 91.8 +/- 5.9 mmHg, p = not significant. Median baseline RR-variability was 791 (range 18-5344) counts/24 h and increased in all but one patient, with captopril, to 1548 (56-4824) p = 0.008. Three increased into the normal range. CONCLUSION: The vagal dysfunction of cirrhosis is caused by neuromodulation by angiotensin II and is not due to a neuropathy.

Adult↗