atrial-natriuretic-factor and Brain-Diseases

There is significant evidence to show that many patients with hyponatremia and intracranial disease who were previously diagnosed with SIADH actually have CSW. The critical difference between SIADH and CSW is that CSW involves renal salt loss leading to hyponatremia and volume loss, whereas SIADH is a euvolemic or hypervolemic condition. Attention to volume status in patients with hyponatremia is essential. The primary treatment for CSW is water and salt replacement. The mechanisms underlying CSW are not understood but may involve ANP or other natriuretic factors and direct neural influence on renal function. Future investigation is needed to better define the incidence of CSW in patients with intracranial disease, identify other disorders that can lead to CSW, and elucidate the mechanisms underlying this syndrome.

Topics: Animals; Atrial Natriuretic Factor; Brain Diseases; Diagnosis, Differential; Disease Models, Animal; Fluid Therapy; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Diseases

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the pathogenetic mechanism of the hyponatremia was assessed based on the therapeutic effect obtained. The subjects were 14 patients (6 with subarachnoid hemorrhage, 3 with hypertensive intracerebral hemorrhage, 2 with cerebral infarct and 3 with head injury) who developed hyponatremia, as a complication during their hospital stay for their intracranial lesions from April to December 1992. Patients with serum Na levels below 135 mEq/l for more than 2 days with no other discernible etiology were defined as having hyponatremia of central origin. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. When improvements occurred within 3 days, in 3 to 7 days, or 8 days or more efficacy was rated "excellent", "good" or "poor", respectively. The mean interval until the onset of hyponatremia was 10.4 days, its mean duration was 5.7 days, and the mean minimum serum sodium level was 129.5 mEq/l. The dose of fludrocortisone administration was 0.1 mg/day except for one patient who was treated with 0.3 mg/day. The mean period of administration was 3.7 days (range: 3 to 6 days), and the route was via a stomach tube in 5 cases and oral in 9 cases. The therapeutic effect was excellent in 9 cases, good in 3 cases and poor in 2 cases, the efficacy rate being 86%. None of the patients manifested side effects. Plasma atrial natriuretic peptide levels were above 100 pg/ml in 2 patients and 50-100 pg/ml in 8 patients and neither of the former 2 patients exhibited "excellent" efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Brain Diseases; Cerebral Hemorrhage; Cerebral Infarction; Female; Fludrocortisone; Humans; Hyponatremia; Male; Middle Aged; Sodium; Subarachnoid Hemorrhage

Topics: Atrial Natriuretic Factor; Brain Diseases; Humans; Inappropriate ADH Syndrome; Postoperative Complications; Water-Electrolyte Balance

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.

Topics: Adult; Animals; Atrial Natriuretic Factor; Brain Diseases; Contraindications; Humans; Hyponatremia; Hypovolemia; Male; Natriuresis; Rats; Subarachnoid Hemorrhage; Syndrome; Urination Disorders; Vasopressins

The aim of this study is to report our experience with diagnosis and management of cerebral salt wasting (CSW) in children and to evaluate the role of atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP) in pediatric patients.. We present nine children suffering from prevalent cerebral disease--seven of whom underwent anesthesia and surgical procedures--with features of CSW, seen within a 22-month period. The symptoms, patient characteristics (including hormone status), monitoring, treatment protocol, and outcome are described.. Natriuresis (urine Na+ concentrations 131 to >250 mmol/l) and polyuria (5.5+/-1.5 ml/kg/h) with increased Na+ turnover (maximum Na+ loss: median 1.50 mmol Na+/kg/h, range 0.47 to >3.50) vanished within 2 weeks in 6/9 patients (increase in serum Na+ from 127+/-2 mmol/l to 136+/-1). K+ excretion was also high (maximum K+ loss: median 0.18 mmol K+/kg/h, range 0.09-0.53). ANP/BNP as suspected causes of salt wasting were elevated only in 1/6 and 2/7 patients, respectively. Plasma renin activities and aldosterone levels were either suppressed or in the low normal range.. Natriuresis and polyuria are the main diagnostic criteria for CSW. The fluid balance in CSW is negative, in contrast to a positive fluid balance in SIADH. The length of the disease is self-limited and generally ceases within 2 weeks, while Na+, K+, and fluid turnover should be monitored carefully. Only a minority of our children showed elevated ANP/BNP levels. A dose/effect relationship for natriuretic peptide levels and increased Na+ turnover could not be established.

Topics: Adolescent; Atrial Natriuretic Factor; Brain Diseases; Child; Child, Preschool; Female; Humans; Infant; Male; Natriuretic Peptide, Brain; Radioimmunoassay; Salts; Time Factors; Vasopressins

Central nervous system feedback loops centered on hypothalamic neurons control atrial natriuretic peptide (ANP). We evaluated the ANP response to arterial hypotension, isotonic blood volume expansion, and increase in plasma osmolality in 14 patients with multiple system atrophy (MSA). Seven of the patients were characterized by a lack of vasopressin response to hypotension (MSA type B), suggesting chronic sinoaortic denervation, and seven by a preserved response (MSA type A). Orthostatic hypotension decreased ANP in controls and type A patients, whereas ANP in type B was not affected. Isotonic saline infusion increased ANP and diuresis in controls and type A patients, whereas it did not affect ANP in type B. Osmotic load increased plasma osmolality and vasopressin in controls and MSA patients and ANP in controls and type A but not in type B patients. In MSA patients with altered afferent control of vasopressin, ANP secretion is not stimulated by blood volume expansion, osmotic load, or blood pressure, suggesting that afferent excitatory control plays a role in the release of ANP.

Topics: Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Brain Diseases; Diuresis; Female; Humans; Hypertension; Isotonic Solutions; Male; Middle Aged; Nerve Degeneration; Osmolar Concentration; Posture; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.

Topics: Adult; Aged; Aged, 80 and over; Aldosterone; Atrial Natriuretic Factor; Brain Diseases; Female; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19 +/- 2, 13 +/- 3, and 8 +/- 2 pg/ml, respectively); atrial natriuretic factor concentration was less than 4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16 +/- 3, 8 +/- 2, 10 +/- 1 pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 +/- 38 and 92 +/- 20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Brain Diseases; Fluid Therapy; Glucose; Hematoma; Hemodynamics; Humans; Hydrocephalus; Intracranial Pressure; Osmolar Concentration; Proteins; Spinal Puncture; Subarachnoid Hemorrhage

Patients with intracranial disease are at risk of developing clinical deterioration due to a hyponatremic syndrome associated with an inappropriate degree of natriuresis, the "syndrome of inappropriate secretion of anti-diuretic hormone (ADH)" or SIADH. To investigate the hypothesis that atrial natriuretic peptide (ANP) is related to the natriuresis in SIADH, serum samples were obtained from 8 neurosurgical patients with intracranial disease seen consecutively who fulfilled the traditional clinical and laboratory criteria for SIADH. In one patient with a hemorrhagic cerebral infarction an elevation of serum ADH (5.7 pg/ml; normal = 1 to 5 pg/ml) in association with a normal level of serum ANP (49.8 pg/ml; normal = 10 to 60 pg/ml) was seen. Six patients (2 with intracerebral hemorrhage and 1 with hemorrhagic cerebral infarction, 1 with aneurysmal subarachnoid hemorrhage, 1 with glioblastoma multiforme, and 1 with Creutz-feldt-Jakob disease) had elevated serum ANP levels (197.0, 112.0, 92.0, 432.0, 97.5, and 138.0 pg/ml, respectively) associated with either normal or low ADH levels (1.3, 2.5, 1.2, 0.7, 2.3, and 0.5 pg/ml, respectively). Another patient with an intracerebral hemorrhage had a normal serum ANP level (37.0 pg/ml) and undetectable ADH level (less than 0.5 pg/ml). In the 7 patients in whom either ADH or ANP alone was elevated, a reciprocal relationship was observed between serum ADH and ANP levels, which could be expressed in logarithmic form (correlation coefficient, r = 0.727). In the 6 patients in whom serum ANP level alone was elevated, a near linear relationship was observed between serum ANP levels and urine sodium excretion (r = 0.851).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Brain Diseases; Humans; Hyponatremia; Sodium; Vasopressins

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

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Atrial Natriuretic Factor; Brain; Brain Diseases; Female; Humans; Hyponatremia; Male; Natriuresis; Vasopressins