Biomedical subjects

E Oribe

Publications and source records attributed to E Oribe.

6 recordsLinked to original sources

PubMed1997

Syncope: the diagnostic value of head-up tilt testing.

To determine the usefulness of prolonged head-up tilt in the diagnosis of neurally mediated syncope, 201 patients with history of syncope of unknown cause and 102 age and gender matched control subjects underwent a 40 minute 60 degrees head-up tilt test. Head-up tilt elicited syncope (i.e., was positive) in 74 of the 201 patients (37%) with a history of unexplained syncope and in only 6 of the 102 controls (6%). The specificity of the test was 100% in patients 60 years of age and older. Symptoms during tilt-induced syncope were identified by the patients as similar to those they had suffered during their spontaneous episodes. All 80 subjects who had tilt-induced syncope recovered without sequelae. The positive predictive value of a positive responses to head-up tilt was 93% and the negative predictive value was 43%. The results indicate that the prolonged head-up tilt test is a very specific procedure of high diagnostic value in patients with a history of unexplained syncope. It is particularly useful in the elderly age groups who have a high incidence of syncope.

Female↗

PubMed1996

Serum prolactin concentrations are elevated after syncope.

The distinction between syncope and epileptic seizures is a common clinical diagnostic problem. Elevated serum prolactin (PRL) concentrations are used to help differentiate epileptic from nonepileptic attacks such as pseudoseizures. Reports of PRL concentrations following syncope have been variable. To determine whether PRL rises after syncope, we measured serum PRL concentrations during a 45-minute passive 60-degree head-up tilt in 21 patients with a history of near-fainting or syncope. Head-up tilt triggered hypotension (mean arterial pressure 51 mm Hg, 95% CI = 45-57) with syncope in 11 patients. PRL concentrations were elevated ( > 19 ng/mL) and reached a maximum within the first 30 minutes after tilt-induced syncope in nine patients (PRL supine: 11 ng/mL, 95% CI = 7-15, vs. PRL after syncope: 52 ng/mL, 95% CI = 36-67; a greater than fourfold rise), while they remained unchanged in 10 patients who had a normal response to head-up tilt (PRL supine: 6 ng/mL, 95% CI = 5-8, vs. maximum PRL while upright: 8 ng/mL, 95% CI = 6-10). The findings indicate that elevated PRL concentrations are present after hypotensive syncope and are of little use in differentiating such syncope from epileptic seizures.

Aged↗

PubMed1992

Hypotension-induced vasopressin release distinguishes between pure autonomic failure and multiple system atrophy with autonomic failure.

To investigate whether activation of afferent and central baroreceptor pathways could differentiate between pure autonomic failure (PAF) and multiple system atrophy with autonomic failure (MSA), we determined the effect of upright tilt on circulating levels of vasopressin in patients with PAF and patients with MSA. We also studied 14 normal subjects, nine of whom developed acute hypotension due to vasovagal syncope. In patients with PAF and in normal subjects with vasovagal syncope, upright tilt induced marked hypotension and a pronounced increase in the plasma concentration of vasopressin (1.1 +/- 0.3 to 38.0 +/- 8.0 pmol/l in PAF and 1.0 +/- 0.2 to 27.4 +/- 7.2 pmol/l in vasovagal syncope, p less than 0.005 for both). In patients with MSA, upright tilt also elicited profound hypotension but circulating levels of vasopressin increased little (0.5 +/- 0.1 to 1.5 +/- 0.3 pmol/l, p less than 0.05). During upright tilt, the plasma concentration of norepinephrine significantly increased in normal subjects but did not increase in patients with autonomic failure. Our results indicate that afferent and central baroreceptor pathways involved in vasopressin release are normal in patients with PAF but are impaired in patients with MSA. Thus, measurement of baroreceptor-mediated vasopressin release appears to provide a clear marker to differentiate between patients with PAF and patients with MSA.

Adult↗

PubMed1991

Differential effect of L-threo-3,4-dihydroxyphenylserine in pure autonomic failure and multiple system atrophy with autonomic failure.

Treatment with L-threo-3,4-dihydroxyphenylserine (L-threo-dops), a synthetic precursor of norepinephrine, significantly increased upright blood pressure in patients with multiple system atrophy but had no effect on the upright blood pressure of patients with pure autonomic failure. These results suggest that the site of action of L-threo-dops is central and that its pressor effect requires intact peripheral sympathetic neurons.

Adult↗

PubMed1990

Atrial natriuretic factor in human autonomic failure.

To investigate whether excessive circulating levels of atrial natriuretic factor (ANF) are responsible for orthostatic hypotension and nocturnal polyuria in patients with autonomic failure, we determined the circadian variation in the plasma concentration of ANF as well as the response of this peptide to changes in posture and extracellular fluid volume in patients with autonomic failure. We found that the plasma concentration of ANF was significantly lower in patients with autonomic failure than in controls. Patients with autonomic failure had a significantly higher urinary sodium excretion during the night (8 PM to 8 AM) than during the day (8 AM to 8 PM), and the plasma concentration of ANF significantly decreased during the night in these patients, indicating that high circulating levels of ANF were not the cause of the nocturnal natriuresis. Furthermore, circulating levels of ANF responded appropriately to reductions in right atrial pressure induced by head-up tilt and extracellular fluid volume changes induced by mineralocorticoid administration. These results indicate that exaggerated circulating levels of ANF are not responsible for the orthostatic hypotension or nocturnal natriuresis in patients with autonomic failure, and that appropriate regulation of ANF occurs in patients with autonomic failure.

Adult↗

PubMedDate not supplied

Plasma endothelin during upright tilt: relevance for orthostatic hypotension?

Since plasma endothelin concentration increases with upright posture and decreases with volume expansion, a study was conducted to test whether activation of the baroreceptor reflex releases endothelin into plasma. The effect of passive upright tilt on the plasma concentrations of endothelin and vasopressin was examined in: (1) normal subjects; (2) patients with impaired baroreceptor reflex due to primary autonomic failure; (3) patients with normal afferent baroreceptor function but acute inhibition of vasoconstrictor sympathetic outflow (ie, with vasovagal syncope); and (4) patients with hypophysial diabetes insipidus. In normal subjects, upright tilt did not change arterial pressure and significantly increased the plasma concentrations of endothelin and vasopressin. In patients with autonomic failure, upright tilt induced a considerable fall in arterial pressure, no rise in plasma endothelin, and a slight increase in plasma vasopressin. In subjects with vasovagal syncope, arterial pressure dropped and the plasma concentrations of endothelin and vasopressin rose. In the subjects with diabetes insipidus, arterial pressure fell slightly, without change in plasma concentration of endothelin. The results suggest that activation of the baroreceptor reflex induces the release of endothelin into plasma, probably from the neurohypophysis, and they raise the possibility that impaired endothelin release contributes to the orthostatic hypotension of patients with primary autonomic failure.

Adult↗