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Biomedical subjects

O Enulescu

Publications and source records attributed to O Enulescu.

At least 19 recordsLinked to original sources
PubMed1992

Deficiency of sympathetic nervous system function in myasthenia.

The norepinephrine (NE) and epinephrine (E) responses to forearm ischemia were studied in 24 myasthenic patients and 22 subjects with lumbar disc disease (control group). In some of these myasthenic (11 cases) and control (11 cases) subjects the NE and E responses to orthostasis were also investigated. In controls both stimuli induced a rise in NE urinary excretion without significantly changing the E excretion. On the other hand, in myasthenic patients forearm ischemia and orthostasis were followed by an augmentation in E excretion, the NE excretion remaining unchanged or even undergoing a depression. In other myasthenic patients (10 cases) and subjects with lumbar disc disease (10 cases) NE and E responses to exercise were tested. The results were similar to those presented above: controls reacted to exercise by a rise in NE excretion, while myasthenic patients, by an augmentation in E excretion; the NE excretion underwent no change or even decreased after exercise in myasthenia. The obliteration of NE response to all three testing stimuli found in myasthenic patients may be considered as a sign of their sympathetic deficiency. In such patients the normal E discharge produced by forearm ischemia, orthostasis or exercise may be interpreted as a compensatory reaction, being probably the consequence of sympathetic deficiency. The noradrenergic deficit of myasthenic patients is ascribable to their cholinergic hyperactivity.

Adult↗
PubMed1991

Norepinephrine and epinephrine responses to postural stimulus in orthostatic hypotension due to brainstem ischemic lesions.

Norepinephrine (NE) and epinephrine (E) responses to upright posture were investigated in 25 patients with orthostatic hypotension due to brainstem ischemic lesions and in 25 control subjects. In controls the postural stimulus induced constantly a rise in NE urinary excretion and a reduction in E excretion, while in patients with orthostatic hypotension it caused a depression in NE urinary excretion and a rise in E urinary excretion; the last alteration was noticed in all but one patient. The E discharge induced by posture in patients with orthostatic hypotension may be involved in the reduction of vascular peripheral resistance and then in postural fall of blood pressure displayed by such patients.

Adult↗
PubMed1990

Propranolol corrects the abnormal catecholamine response to light during migraine.

The catecholamine (CA) response to light before and after propranolol therapy was studied in 25 migrainous subjects. Before therapy an abnormal CA response to light consisting of a rise in epinephrine excretion and a depression in norepinephrine (NE) excretion was noticed in migrainous patients. After propranolol administration (60 mg daily for 10 days) the post-photic augmentation in epinephrine excretion and the post-photic depression in NE excretion no longer occurred. As epinephrine discharge may be pathogenetic for migraine attack, the favorable effect of propranolol in migraine therapy could be due to its ability to prevent the epinephrine release induced by light or other stimuli.

Adult↗
PubMed1988

Catecholamine response to light in migraine.

The effect of the shift from a low to a high luminosity of the environment on the urinary excretion of norepinephrine (NE) and epinephrine (E) was studied in migraineurs (26 cases) and controls (25 cases). In the latter the shift from a low to high light exposure increased NE excretion; in contrast, in migraineurs exposure to high luminosity resulted in a depression of NE excretion and an augmentation of E excretion. The possible participation of E discharge produced by photostimulation or by other stimuli in the pathogenesis of migraine attack is discussed.

Adult↗
PubMed1983

Inability to deactivate sympathetic nervous system in brainstem infarct patients.

Catecholamine urinary excretion under basal conditions and after head down tilting (4 degrees) was studied in normo- and hypertensive controls and in patients with hemisphere and brainstem infarction, respectively. Both the normo- and hypertensive controls and patients with hemisphere infarction displayed a conspicuous decrease (about 40%) in noradrenaline (NA) urinary excretion after head down tilting. In contrast the patients with brainstem infarction increased NA urinary excretion after the manoeuvre, suggesting activation instead of deactivation of the sympathetic nervous system (SNS). In normo- and hypertensive controls the values of night NA excretion were lower than those of day NA excretion, whereas in brainstem infarct patients the night NA excretion was close to the day NA excretion. This finding also supports the view that the brainstem infarct patients are not able to deactivate their SNS during night recumbency. The SNS reactivity disorder of such patients if associated with impairment of autoregulation of cerebral circulation might generate an abnormal increase in cerebral circulation during night recumbency.

Blood Pressure↗
PubMed1979

Unresponsiveness to hypoglycemia of centers controlling epinephrine release in cerebral infarct patients.

Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson's disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.

Blood Glucose↗
PubMed1978

Abnormal epinephrine urinary excretion in Parkinsonians: correction of the disorder by levodopa administration.

Epinephrine (E) and norepinephrine (NE) as well as vanilmandelic acid (VMA) urinary excretion was investigated in 54 patient with Parkinsonism and 29 controls. In Parkinsonians the mean value of NE excretion was normal, while that of E was significantly higher than in controls (P less than 0.001). Analysis of results in terms of age showed that only the patients in the 5th and 6th decades displayed significant increases in E excretion when compared to age-matched controls. No age-group differences were found for NE excretion. VMA was significantly higher in Parkinsonians than in controls. Both in Parkinsonians and in controls VMA excretion correlated significantly with that of NE but not with the E excretion. Ten-day treatment with levodopa (1.5 g/day) of Parkinsonians below the age of 60 was followed by a constant decrease in the excretion of E and a less consistent, nonsignificant increase in the excretion of NE. The abnormality of E excretion noticed in younger Parkinsonians suggests involvement in the pathologic process, of adrenal medulla, the main site of E synthesis.

Adult↗
PubMed1975

Facilitation through hyperventilation of therapeutic effect of pyrithioxin in cerebral infarct patients.

A method of treatment consisting in administration of a neurodynamic drug, pyrithioxin, combined with a short period of hyperventilation (HV) was applied in cerebral infarct patients with hemiplegia. The combination was superior to pyrithioxin alone for the motor recovery of these patients. In some cases, it induced immediately a partial restoration of motility. The combination constantly brought about an increase in urinary excretion of norepinephrine and vanilmandelic acid, which failed to occur after pyrithioxin or HV alone. HV appears to facilitate the neural effects of the drug by promoting its transfer into the CNS.

Aged↗
PubMedDate not supplied

Abnormal catecholamine urinary excretion after emotional stimulus in patients with cerebral hemorrhage.

The epinephrine (E) and norepinephrine (NE) urinary excretion before and after a mild "emotional stimulus" (ES) was determined in 22 patients with cerebral infarction and 30 patients with cerebral hemorrhage, as well as in 18 normotensive and 18 hypertensive controls. In patients with cerebral infarction, the majority normotensive, the "emotional stimulus" induced a significant increase in NE excretion, but non-significant alterations in E excretion. Similar changes were noted in normotensive controls. In patients with cerebral hemorrhage, almost all hypertensive, and in hypertensive controls, ES brought about a consistent rise in E excretion without influencing significantly the NE excretion. The presence of a constant increase in E excretion after a mild emotion not only in patients with cerebral hemorrhage but also in subjects with uncomplicated essential hypertension, suggests that the E release found in patients with cerebral hemorrhage is related to the hypertensive state pre-existing the stroke rather than to hemorrhagic stroke itself. The pattern of catecholamine discharge in hypertensive patients might play a part in the occurrence of cerebral hemorrhagic accidents. The epinephrine discharges induce sudden increases in systolic blood pressure which could lead to the rupture of cerebral vessels with hyalinotic or atherosclerotic alterations.

Brain Ischemia↗
PubMedDate not supplied

Correction by centrophenoxine of abnormal catecholamine response to postural stimulus in patients with orthostatic hypotension due to brainstem ischemia.

The effects of centrophenoxine on catecholamine (CA) response to orthostasis and on postural blood pressure fall of 25 patients with orthostatic hypotension due to brainstem ischemia were studied. Before therapy, the patients responded to posture by a depression in norepinephrine (NE) excretion and a rise in epinephrine (E) excretion. After a 10-day treatment with centrophenoxine, 800 mg daily, the patients responded to posture like normals, i.e. by a rise in NE excretion and a reduction in E excretion. Although the orthostatic blood pressure fall was less marked after treatment, the favourable clinical effect of the drug could not be correlated significantly with the restoration of CA response to posture after treatment.

Blood Pressure↗
PubMedDate not supplied

Influence of continuous photostimulation on catecholamine urinary excretion in patients with cerebral hemorrhage.

Hypertensives with (25 cases) or without (27 cases) cerebral hemorrhage (CH) and normotensives (25 cases) were exposed from 7 to 8.30 a.m. to a low light input and from 8.30 to 10 to a high light input (HLI), and urinary epinephrine (E) and norepinephrine (NE) were measured at the end of these periods. In normotensives HLI had no effect on E and NE excretion; in hypertensives with and without CH it increased E excretion and depressed NE excretion. Light activation of E release may be responsible for the daytime occurrence of CH in hypertensives.

Cerebral Hemorrhage↗