atrial-natriuretic-factor has been researched along with Craniocerebral-Trauma* in 4 studies
4 other study(ies) available for atrial-natriuretic-factor and Craniocerebral-Trauma
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Clinical analysis of hyponatremia in acute craniocerebral injury.
To explore pathological mechanisms of central hyponatremia and its treatment.. Synchronous assay was made for changes of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endogenous digitalis-like substance (EDLS), antidiuretic hormone (ADH) in blood, and Na(+) concentrations in blood and urine, and plasma- and urine-osmolality in 68 patients with acute craniocerebral injury (ACI).. Of the 68 patients with ACI, 27 were found to have hyponatremia, and such illness was mostly concentrated on severe cases.. The central hyponatremia in patients with ACI may be related to the increase in the secretion of EDLS and ADH as the result of damaged functions of the hypothalamic-hypophysial system, and it seems that the decrease in blood ANP and BNP has no direct effect on Na(+) concentrations in blood. Inappropriate secretion of antidiuretic hormone syndrome and cerebral salt-wasting syndrome are the two main reasons for hyponatremia in patients with craniocerebral injury. The pathological mechanism, diagnostic standards, as well as treatment methods for the two, however, are not just the same. Intravenous injection of extrinsic thyrotropin-releasing hormone might inhibit dilutional hyponatremia arising from the increase in ADH secretion by patients with ACI. Topics: Adolescent; Adult; Atrial Natriuretic Factor; Cardenolides; Case-Control Studies; Child; Child, Preschool; Craniocerebral Trauma; Female; Glasgow Coma Scale; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Male; Middle Aged; Natriuretic Peptide, Brain; Neurophysins; Protein Precursors; Saponins; Vasopressins; Young Adult | 2010 |
Secretion of natriuretic peptides caused by an epileptic attack.
To describe clinical features of a patient with secretions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) during an epileptic attack.. A 65-year-old woman experienced frequent bouts of polyuria, pyrexia and general fatigue after several years of a cerebral contusion involving the left fronto-temporal lobe caused by a traffic accident. Her urine output and urinary sodium excretion increased, and plasma ANP and BNP concentrations were markedly high during each attack. Electroencephalography (EEG) showed serial seizure discharge in the left anterior temporal region during the attacks, indicative of epileptic focus.. ANP and BNP secretions probably were triggered by epileptic stimulation on the diencephalon beyond the focus. Topics: Aged; Atrial Natriuretic Factor; Craniocerebral Trauma; Diuresis; Electroencephalography; Epilepsy, Post-Traumatic; Female; Humans; Magnetic Resonance Imaging; Natriuretic Peptide, Brain; Sodium; Temporal Lobe | 2002 |
Atrial natriuretic factor release during hypovolemia and after volume replacement.
To examine plasma atrial natriuretic factor activity during hypovolemia and after vascular volume replacement.. Prospective, descriptive study.. Scene of emergency, Emergency Department, and the ICU of a university hospital.. A total of 47 trauma patients with evidence of hypovolemia were grouped according to their major injury into a thoracic injury group (15 patients; mean Injury Severity Score = 38.5 +/- 3.1 [SEM], Hospital Trauma Index = 14.1 +/- 0.7), an abdominal injury group (14 patients; Injury Severity Score = 36 +/- 3.3, Hospital Trauma Index = 14 +/- 0.9), and a severe head injury group (18 patients; Injury Severity Score = 23 +/- 1.5, Hospital Trauma Index = 10 +/- 0.6).. Measurements were taken at the scene of emergency; after volume replacement in the Emergency Department; and after 3, 7, 12, 24, 36 hrs and on day 5 in the ICU. In all groups, the average plasma atrial natriuretic factor levels were increased at the scene of emergency and declined significantly to normal values with volume replacement. In the thoracic injury group, plasma atrial natriuretic factor activity decreased from 253 +/- 73 to 115 +/- 83 pg/mL (p less than .0017); in the abdominal injury group, plasma atrial natriuretic factor activity decreased from 194 +/- 42 to 91 +/- 24 pg/mL (p less than .006); in the severe head injury group, plasma atrial natriuretic factor activity decreased from 167 +/- 28 to 70 +/- 13 pg/mL (p less than .02) with volume replacement. Plasma atrial natriuretic factor levels at the scene of emergency were significantly (252 +/- 73 vs. 167 +/- 28 pg/mL; p less than .05) higher in the thoracic injury group and in the abdominal injury group (194 +/- 42 vs. 167 +/- 28 pg/mL; p less than .05), as compared with the severe head injury group.. In trauma patients, plasma atrial natriuretic factor concentrations were markedly increased in patients with untreated hypovolemia and were decreased to normal values with vascular volume replacement. Thus, atrial natriuretic factor seems to play an important physiologic role during hypovolemia. Topics: Abdominal Injuries; Atrial Natriuretic Factor; Craniocerebral Trauma; Female; Fluid Therapy; Hemodynamics; Humans; Injury Severity Score; Male; Prospective Studies; Shock, Traumatic; Spectrophotometry; Thoracic Injuries | 1992 |
[Plasma ANP levels and its relation to electrolyte and water regulation in neurosurgical intensive care patients].
We examined the relation between plasma atrial natriuretic peptide (ANP) and the changes of the regulating hormones ADH and renin aldosterone in 20 neurosurgical intensive care patients. All patients suffered from elevated intracranial pressure due to severe head trauma or severe subarachnoidal hemorrhage of the anterior circulation. Under controlled mechanical hyperventilation (CMV) with PEEP, 15 patients without evidence of central dysregulation showed no change in plasma ANP, ADH and aldosterone. In five patients with severe central dysregulation of either electrolytes or blood pressure, increases of plasma ANP of various degrees could be observed together with a decline in serum aldosterone. Topics: Aldosterone; Atrial Natriuretic Factor; Brain Diseases; Craniocerebral Trauma; Critical Care; Humans; Intracranial Pressure; Reference Values; Renin; Subarachnoid Hemorrhage; Vasopressins; Water-Electrolyte Balance | 1988 |