atrial-natriuretic-factor and Brain-Injuries

Topics: Atrial Natriuretic Factor; Brain Injuries; Child; Diagnosis, Differential; Female; Fluid Therapy; Hemodynamics; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Syndrome

Hemodynamic mechanism for brain edema forrmation in patients with hypertensive encephalopathy is unclear. Potential roles of natriuretic peptides in the pathogenesis of hypertensive encephalopathy are discussed. A 32-year-old man presented with slight left hemiparesis. He was slightly confused, and his blood pressure was extremely high. Cranial plain computerized tomography scans revealed diffuse brain edema mainly in the supratentorial white matter region. Blood examination revealed that plasma concentrations of atrial and brain natriuretic peptides were significantly high. His left hemiparesis disappeared within a day, but he tended to be agitated. His altered mental status, however, resolved with control of blood pressure. Serial magnetic resonance imagings demonstrated that the magnitude of brain edema was attenuated in proportion to decline in plasma concentrations of natriuretic peptides. This case suggests that significant elevation of plasma concentrations of natriuretic peptides may contribute to an acute rise in blood pressure, and that these peptides potentially play an important role in development of brain edema in hypertensive encephalopathy.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Brain; Brain Injuries; Humans; Hypertensive Encephalopathy; Magnetic Resonance Imaging; Male; Natriuretic Peptide, Brain; Obesity; Radiography; Renin-Angiotensin System; Time Factors

Fluid and electrolyte disturbances are frequent after acute brain damage. Atrial natriuretic peptide (ANP), which can also be found in brain tissue, could be a hormone implicated in such disorders (cerebral salt wasting syndrome).. Plasma ANP levels were analyzed in 50 children with acute neurological deterioration (secondary to traumatic, infectious, convulsive tumor or vascular disorders) evaluated according to the modified Glasgow Coma Scale (GCS). Hemodynamic stability was determined by standard monitoring. ANP, renin and aldosterone levels were determined by RIA and the results compared with a control group of healthy children.. There was an increase in ANP levels in children with brain injury in comparison to the control group (p < 0.001), but not in children under one year of age. Renin and aldosterone were also significantly increased in this group of patients, with no difference in ANP, renin or aldosterone level found in function of their GCS score. All patients were hemodynamically stable and no correlation between hemodynamic and hormone variables was seen. Mechanical ventilation did not influence the hormone levels.. There is an important increase in ANP levels in patients with acute neurological pathologies, but it was not related to the hemodynamic condition and its importance has yet to be established. One of its possible consequences is a secondary hypotonic/hypovolemic condition, a potentially dangerous event for the patient with intracranial hypertension that needs immediate treatment. Differentiation of this syndrome from inappropriate vasopressin secretion could be very important in children with acute brain injury.

Topics: Acute Disease; Atrial Natriuretic Factor; Brain Injuries; Child; Child, Preschool; Female; Glasgow Coma Scale; Humans; Infant; Infant, Newborn; Injury Severity Score; Male; Prospective Studies

Atrial natriuretic peptide (ANP) plays an important role in body fluid homeostasis. ANP has been established as a marker of cardiac dysfunction and may play a role in brain edema development after traumatic brain injury (TBI). In order to identify its specific assignment following TBI, we related clinical data and treatment variables in 63 patients to longitudinal midregional (MR) proatrail natriuretic peptide (ANP) measurements. ANP correlated significantly to age (p < 0.0001) and vasopressin release (p < 0.001). Following TBI, ANP was increased initially and on day 3 (cut-off 100 pg/L) in 22% of the patients, in 31% on day 7, and was normalized at follow-up examination. The group comparison revealed that ANP levels did not significantly differ with regard to injury severity, but that high ANP levels predicted a worse Glasgow Outcome Score at 6 months (p < 0.05). While the initially intact osmoregulation - a correlation of urine volume and high serum sodium (r = 0.536, p = 0.003) or low urine osmolality (r = -0.556, p = 0.009) - got lost post-injury, the ANP release was triggered by volume load (p < 0.005). High ANP levels correlated with the neuroendocrine stress response, i.e., high cortisol (p = 0.05) and prolactin (p < 0.001) levels. We conclude that MR-proANP measurements reveal a significant predictive function for the prognosis of TBI.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Brain Injuries; Endocrine System; Female; Glasgow Outcome Scale; Homeostasis; Humans; Longitudinal Studies; Magnetic Resonance Imaging; Male; Middle Aged; Predictive Value of Tests; Time Factors; Water-Electrolyte Balance; Young Adult

Atrial natriuretic peptide (ANP) plays an important role in the regulation of water and sodium in the body via cyclic GMP (cGMP) pathway. Although ANP has been shown to be protective in cerebral ischemia or intracerebral hemorrhage, its role in traumatic brain injury (TBI) has yet to be elucidated. We herein assessed ANP effects on brain water and sodium in TBI. Controlled cortical impact (3 mm depth, 6 m/sec) was used to induce an experimental cortical contusion in rats. Continuous administration of ANP 0.2 (n = 6) or 0.7 microg/kg/24 h (n = 6), cGMP analogue (8-Bromo-cGMP) 0.1 (n = 5) or 0.3 mg/kg/24 h (n = 5), or vehicle (n = 6) was begun 15 minutes after injury, using a mini-osmotic pump implanted into the peritoneal cavity. At 24 hours after injury, ANP significantly exacerbated brain edema in the injured hemisphere in a dose-dependent manner while it reduced brain sodium concentrations in both hemispheres. These ANP effects could be mimicked by a cGMP analogue. In the second series (n = 20), BBB integrity was assessed by evaluating the extravasation of Evans blue dye. ANP or cGMP analogue significantly worsened BBB disruption in the injured hemisphere at 24 hours after injury. These findings suggest that ANP administration exacerbates brain edema after the experimental cortical contusion in rats, possibly because of an increase in the BBB permeability via cGMP pathway, whereas it reduces brain sodium levels.

Topics: Animals; Atrial Natriuretic Factor; Blood-Brain Barrier; Body Weight; Brain Injuries; Coloring Agents; Cyclic GMP; Electrolytes; Evans Blue; Injections, Intraperitoneal; Male; Potassium; Rats; Rats, Sprague-Dawley; Sodium; Water; Water-Electrolyte Balance

To investigate whether dexamethasone (DXM) regulate the expression of Calcitonin gene-related peptide (CGRP), Endothelin (ET), Atrial natriuretic peptide (ANP), Angiotensin II (AII) in brain injury induced by endotoxin in rabbit.. Sixty-five New Zealand white rabbits were randomly divided into 3 subgroups: endotoxin group (A group), endotoxin + DXM group (B group) and normal saline group (C group). 100 microg/kg endotoxin was intracerebroventricularly injected in A group, endotoxin 100 microg/kg + DXM 1 mg/kg in B group and same volume of normal saline in C group as control. Neuropeptide level were detected by radioimmunoassay in variable periods (3 h, 6 h, 12 h, 24 h, 48 h, 72 h after injection) in the plasma, cerebrospinal fluid (CSF) and brain tissue (hippocampus area), and brain water content was measured by dry method.. CGRP, ET, ANP, AII concentrations in plasma, CSF and brain tissue changed in variable periods after injection. The higher or the lower neuropeptide levels were emerged on 12 - 24 hours after injection (P < 0.05 or P < 0.01), and changed remarkably in A group (P < 0.05 or P < 0.01). Brain water content were significantly higher and reached to peak level on 24 hours after injection. But there was a significantly increasing in A group compared to that of B group (P < 0.05 or P < 0.01).. The timely changes of CGRP, ET, ANP, AII were related to brain injury and brain edema induced by endotoxin, and DXM regulated the expression of neuropeptides and lighten brain edema.

Topics: Angiotensin II; Animals; Anti-Inflammatory Agents; Atrial Natriuretic Factor; Brain Edema; Brain Injuries; Calcitonin Gene-Related Peptide; Dexamethasone; Disease Models, Animal; Endothelins; Endotoxins; Female; Male; Neuropeptides; Rabbits

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.

Topics: Acute Disease; Adrenocorticotropic Hormone; Aldosterone; Atrial Natriuretic Factor; Brain; Brain Injuries; Child, Preschool; Humans; Hydrocortisone; Hyponatremia; Male; Sodium; Vasopressins

We used the method of RIA determined the contents of atrial natriuretic peptide (ANP), angiotensin II (ANG II) in plasma and brain tissues after brain injury in 70 rats. The results showed that the ANP was significantly decreased in brain tissues on 6, 72 hours after brain injury. At the same time, the plasma and brain tissues ANG II, brain water contents were significantly increased. The results suggested that the unbalance of ANP and ANG II may be related to the pathophysiological process of brain edema.

Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Brain; Brain Edema; Brain Injuries; Male; Rats; Rats, Sprague-Dawley

Topics: Atrial Natriuretic Factor; Brain Injuries; Child; Female; Humans; Hyponatremia; Natriuresis; Vasopressins

Topics: Atrial Natriuretic Factor; Brain Injuries; Central Nervous System Stimulants; Coma; Consciousness; Contusions; Humans; Skull Fractures

Topics: Acute Disease; Atrial Natriuretic Factor; Brain; Brain Injuries; Central Nervous System Stimulants