Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:[A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia]. 153 80

We studied retrospectively the relationship between hyponatremia and cerebral infarction in 134 consecutive patients with aneurysmal subarachnoid hemorrhage. In 44 patients sodium levels fell below 135 mmol/L on at least two consecutive days between the second and the tenth day after the hemorrhage. Twenty-five of these patients fulfilled the criteria for the syndrome of inappropriate secretion of antidiuretic hormone. Cerebral infarction developed in 27 of the 44 patients with hyponatremia and in 19 of the 90 patients with normal serum sodium levels (p less than 0.001). Cerebral infarctions were more often fatal in patients with hyponatremia (p less than 0.01). Twenty-six of the 44 patients had been treated with fluid restriction to correct the serum sodium levels, and infarctions developed in 21. Fluid restriction to correct hyponatremia appears to be potentially dangerous in patients with aneurysmal subarachnoid hemorrhage.
 ...
PMID:Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? 397 97

In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.
 ...
PMID:Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 713 49

Serum osmolality and antidiuretic hormone (ADH) levels were determined for 17 patients with cerebral infarction, 4 with subarachnoid hemorrhage, and 12 controls. The ADH levels were elevated significantly in the stroke patients. Hyponatremia was not observed. Stroke patients are at risk for developing electrolyte disturbances; thus, fluid intake and electrolyte levels should be closely observed.
 ...
PMID:Antidiuretic hormone levels in stroke patients. 723 33

We reported a case of neuroleptic malignant syndrome (NMS) associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 71-year-old woman, who had been diagnosed as hypertension and multiple cerebral infarction, was given sulpiride 150 mg daily for depressive state. Three days after started sulpiride, she developed fever, sweating, difficulty of movement and was admitted to the hospital. The white blood cell count rose to 16,300/mm3 and serum creatine kinase (CK) to 3,063 IU/L. Two days later CK rose to 20,050 IU/L regardless of stopping the drug, so she was transferred to our hospital for further investigation. On admission, it was the 6th day from the onset, she was mute and akinetic accompanied by muscle pain and rigidity in extremities. Serum CK was 1,831 IU/L, Na 122 mEq/L, osmolality 244 mOsm/kg, plasma antidiuretic hormone (ADH) level 6.5 pg/ml and urine Na was 101 mEq/L, osmolality 467 mOsm/kg. Renal and adrenal functions, plasma renin activity were normal. From the history, course and these data, diagnosis of NMS associated with SIADH was made. Intravenous sodium (130-200 mEq/day) and fluids (1,000-1,200 ml/day) were carefully infused. She became active, muscle pain disappeared and rigidity, akinesia decreased. CK, serum Na and osmolality gradually improved to normal. About the transient increase in ADH secretion, we considered that hypothalamic disturbance in NMS might induce leakage of stored ADH from neuroendocrine neurons in it.
 ...
PMID:[Neuroleptic malignant syndrome associated with the syndrome of inappropriate secretion of antidiuretic hormone]. 778 Dec 36

One-hundred-and-thirty-six children below 12 years of age hospitalized with a diagnosis of tuberculous meningitis (TBM) have been investigated to identify the underlying cause of convulsions. One-hundred-and-one children (74 per cent) presented with seizures before and/or during hospitalization. Generalized tonic and clonic seizures (GTCS) were the commonest (58 per cent) type of seizures followed by focal seizures (FS) (38 per cent) and tonic spasms (TS) (4 per cent). EEG changes were more frequently observed in cases with FS and in those children with GTCS who presented after first week of hospitalization. EEG findings included generalized dysrythmia with paroxysmal slow activity (38 per cent), interhemispheric asymmetry (23 per cent), multiple spike and wave pattern (10 per cent), and focal spike and wave pattern (15 per cent). CT scan findings were more common in those children with GTCS and TS who presented with recurrent seizures and/or seizures manifesting after first week of hospitalization. FS presenting at any stage of the disease were associated with CT scan abnormalities. Abnormalities detected in CT scan of brain included meningeal enhancement (55 per cent), hydrocephalus (32 per cent), tuberculomas (27 per cent), and cerebral infarctions (13 per cent). Clinical presentation and investigations indicate that the probable cause of convulsions could be attributed to cerebral edema (57 per cent), syndrome of inappropriate secretion of antidiuretic hormone (35 per cent), hydrocephalus (32 per cent), tuberculoma (27 per cent), abnormal electric focus (25 per cent), and cerebral infarction (13 per cent).
 ...
PMID:Convulsions in tuberculous meningitis. 898 21

To clarify the characteristics of vasopressin (AVP) secretion in patients with the syndrome of inappropriate antidiuresis (SIAD) related to central nervous system disorders, we examined the response of AVP secretion to osmotic stimulus by hypertonic saline infusion and analyzed the possible causative factors in six patients with SIAD associated with head trauma or cerebral infarction. Hyponatremia developed after head trauma in four patients and cerebral infarction in two patients. In all patients the clinical state and laboratory findings fulfilled the criteria for SIAD, which was supported by either nonsuppressible plasma AVP levels or effectiveness of treatments with water restriction, demeclocycline, nonpeptide V2 AVP antagonist or diphenylhydantoin. Although patterns of plasma AVP response to the osmotic stimulus varied, plasma AVP concentrations neither increased nor decreased to undetectable levels with a rise in plasma osmolality. In one patient, plasma AVP levels responded to increasing plasma osmolality when plasma osmolality normalized; in which the threshold and the sensitivity of osmostat were normal. In two other patients, AVP secretion responded to plasma osmolality after the treatment. The changes in AVP secretion were not due to nonosmotic stimuli for AVP release. In conclusion, this study shows that patients with SIAD and central nervous system disorders may have persistent AVP secretion with a loss of hypotonic suppression such as found in patients with adrenal insufficiency or depletional hyponatremia in central nervous system disorders, indicating that careful evaluation is necessary to determine the relationship between persistent AVP secretion and the pathogenesis of hyponatremic disorders.
 ...
PMID:Osmoregulation of vasopressin secretion in patients with the syndrome of inappropriate antidiuresis associated with central nervous system disorders. 1046 11

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls.
 ...
PMID:[Cerebral salt wasting. Half a century of a largely undefined syndrome]. 1180 34

Aquaporin-2, a water-channel protein, is known to increase water permeability due to vasopressin binding to V2 receptors at the renal collecting duct and is excreted into the urine. It is still unclear whether a hyponatremic state is caused by vasopressin-dependent aquaporin-2 in patients clinically diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone. To determine this, we measured urinary aquaporin-2 and vasopressin by radioimmunoassay in normonatremic or hyponatremic patients after cerebral infarction and in healthy controls. In the normonatremia group, urinary aquaporin-2 and plasma AVP levels were higher than in controls. In the hyponatremia group, plasma AVP was relatively high despite low plasma osmolality in each patient. However, urinary aquaporin-2 in hyponatremia was significantly increased when compared with the other two groups. In conclusion, AQP-2 increment does not directly reflect non-osmotic AVP secretion in a hyponatremic state. This result indicates that the urinary excretion of AQP-2 is not only AVP-dependent in hyponatremic states.
 ...
PMID:Urinary excretion of aquaporin-2 and inappropriate secretion of vasopressin in hyponatremic patients after cerebral infarction. 1266 73

For expansion of the extravascular space, secretion of antidiuretic hormone and increment of vascular permeability, a large quantity of non-functional extracellular fluid is accumulated in an extravascular space from all over the operation. Extracellular fluid returns from an extravascular space to blood vessels in refilling stage, and decrement of a pulmonary vascular bed after pneumoresection make it easy to cause pulmonary edema and tachyarrhythmia. Therefore volume of postoperative infusion is apt to be limited after pneumoresection. However, the fluid management that extremely imbalanced in dry side increases the risk of arrhythmia, myocardial infarction and cerebral infarction. It is important to perform reasonable fluid therapy without excess and deficiency postoperatively while observing amount of urine, specific gravity of urine, heart rate, blood pressure, volume of chest drainage and central venous pressure. We have few opportunity to consider about nutritional management after pneumoresection so that ingestion is started for an early postoperative period. But, the grave case that ingestion cannot start for an early postoperative period should start total parenteral nutrition or enteral feeding. In that case, the enteral feeding which is more physiological than intravenous nutrition is recommended.
 ...
PMID:[Fluid and nutritional management after pneumoresection]. 2071 9


1 2 Next >>