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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred fourteen patients with ruptured cerebral aneurysms were reviewed in regard to the incidence and etiological factors of preoperative disturbances of water and electrolyte metabolism. Patients with inadequate salt intake, evidence of renal disease, cardiac failure or excessive diuretic therapy were excluded. Twenty-five (21.9%) patients developed water and electrolyte disturbances. Hyponatremia (less than 130 mEq/l) occurred in 18 (15.8%) of 114 patients. The majority of those patients with hyponatremia showed laboratory findings and/or clinical features suggesting the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The mean interval between the last subarachnoid hemorrhage (SAH) and the development of hyponatremia was 13.5 days (range 6 to 26 days). No patients developed hypernatremia (more than 155 mEq/l). Preoperative diabetes insipidus (DI) occurred in 7 (6.1%) of 114 patients. The mean interval between the last SAH and the onset of DI was 26.5 days (range 15 to 35 days). When compared with the onset of hyponatremia following SAH, the development of DI was significantly delayed. The present study showed that the following five types of patients significantly related to the development of preoperative water and electrolyte disturbances after SAH due to cerebral aneurysms. The patients with ruptured aneurysms of anterior communicating, anterior cerebral artery or internal carotid artery. The patients in grade III, IV according to Hunt & Hess. The patients with high density in the basal subarachnoid space on the CT scan. The patients with a small hematoma in the region of the basal frontal interhemispheric fissure in cases with aneurysms of the anterior communicating or anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Etiology of water and electrolyte metabolism imbalance following the rupture of cerebral aneurysms--with special reference to preoperative condition]. 646 63

A monkey model of subarachnoid hemorrhage (SAH) was used to study both the incidence of hyponatremia and natriuresis and the associated changes in antidiuretic hormone (ADH) secretion and salt and water balance. Following SAH, seven of nine monkeys became natriuretic and hyponatremic. The natriuretic period lasted an average of 4.4 +/- 0.4 days. The mean nadir of serum sodium content was 125.7 +/- 1.6 mEq/liter, and occurred on the average on the 5th day following SAH. The sodium balance after SAH was negative as compared to the preoperative positive sodium balance (p less than 0.001). The plasma vasopressin level was usually elevated for a day following surgery, but there was no significant difference in the levels during the preoperative period and during the period of natriuresis following SAH. The daily urine output and aldosterone levels were not significantly different, and the plasma volume was slightly, but not significantly, decreased after SAH. Four of the animals that had a hyponatremic and natriuretic response following SAH showed a normal regulation of vasopressin in response to both a water challenge and hypertonic saline challenge. The three monkeys that underwent sham procedures did not become hyponatremic and natriuretic postoperatively. The sham-operated monkeys did not show significant differences in their plasma vasopressin levels, urine volume, plasma volume, and aldosterone levels following surgery. These observations are more consistent with primary natriuresis as the cause of hyponatremia rather than the syndrome of inappropriate secretion of ADH. The cause of the renal loss of sodium is not known, but the possibility of a brain natriuretic factor or an alteration in the neural control of the kidney should be considered.
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PMID:Hyponatremia and natriuresis following subarachnoid hemorrhage in a monkey model. 669 49

Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.
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PMID:Involvement of vasopressin in brain edema formation: further evidence obtained from the Brattleboro diabetes insipidus rat with experimental subarachnoid hemorrhage. 672 46

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.
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PMID:Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 713 49

The intraventricular administration of vasopressin or DDAVP (desmopressin acetate) increased the brain water content from 78.2% to 79.2-79.5%. This was achieved without an accompanying water load. The applied water load alone did not increase the water content of the brain. There was no significant difference in the water content of the brain between animals treated with intraventricular vasopressin and intravenous water load and animals receiving only intraventricular vasopressin. The water content of the olfactory bulbs of the control animals was 3.8% higher than that of the hemispheres. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% subsequent to the intraventricular administration of DDAVP. Measurement of the brain electrolyte content was not conclusive as to the mechanism of water permeability changes. The possible mechanism is discussed. Although no tissue or cerebrospinal fluid concentrations of vasopressin enabling comparison with clinical pathological conditions have been measured, it is suggested that increased secretion of vasopressin into the cerebrospinal fluid in conditions such as subarachnoid hemorrhage or intracranial hypertension of various origins might play a role in edema formation.
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PMID:Brain water accumulation after the central administration of vasopressin. 713 57

Arginine vasopressin was measured in the blood and cerebrospinal fluid (CSF) of 42 patients with subarachnoid haemorrhage. Increased concentrations of vasopressin were present in 10 patients, of whom eight had bled from an anterior communicating artery aneurysm. In three patients high blood vasopressin values were associated with gross hyponatraemia. Five patients were found to have increased CSF vasopressin concentrations in the presence of normal plasma values and in all of these the level of consciousness was severely disturbed. It is suggested that an increased secretion of vasopressin into the blood or CSF may be a contributory factor in the worsening condition of some patients with subarachnoid haemorrhage.
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PMID:Vasopressin in plasma and CSF of patients with subarachnoid haemorrhage. 722 44

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.
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PMID:Antidiuretic hormone levels in stroke patients. 723 33

The authors report a review of 290 patients admitted for the treatment of subarachnoid hemorrhage. Twenty-seven (9.3%) patients developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The diagnosis was established by means of daily laboratory investigations (serum electrolytes and osmolality; urine sodium and osmolality; and fluid balance). The patients were divided into two groups (severe and mild SIADH) on the basis of clinical symptoms and signs and laboratory findings. High values of urine osmolality and sodium concentration in patients with low values of serum osmolality and sodium concentration were demonstrated. Thirteen (4.5%) patients had severe and 14 (4.8%) patients had mild SIADH. The source of bleeding was not discovered in 14 patients (4.8%). Nearly 10% of the patients with an aneurysm on the anterior communicating artery developed SIADH. Fluid therapy for these patients is described, and the treatment of SIADH is discussed.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone after subarachnoid hemorrhage. 730 Oct 84

Arginine vasopressin was measured by RIA in samples of plasma and cerebrospinal fluid (CSF) taken synchronously from 62 patients with proven or suspected disorders of the central nervous system in order to determine the relationship between the secretion of vasopressin into the systemic circulation and that into the CSF. In 12 patients without endocrine or brain disease, mean plasma values (+/- SD) were 2.8 +/- 0.7 pg/ml and CSF values were 2.4 +/- 0.7 pg/ml. Thirty-six patients with various intracranial disorders had plasma and CSF values which were both within the range of 1-4 pg/ml. Eight patients had raised plasma concentrations, but their CSF levels were within the normal range. One patient with posttraumatic diabetes insipidus and 2 patients with subarachnoid hemorrhage had concentrations of CSF vasopressin which were greater than plasma levels. These results indicate that a blood CSF barrier to vasopressin exists in man and that under certain pathological conditions excessive amounts of the hormone can be secreted into the CSF independently of that which is released into the blood, a finding which could have clinical significance in disorders of brain function.
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PMID:Vasopressin in human cerebrospinal fluid. 735 20

Bradykinin, substance P and vasopressin induced a vasodilatation followed by a vasoconstriction in control perfused canine basilar arteries with endothelium. The dilatation was significantly reduced and the constriction was significantly enhanced by endothelial removal with saponin. The potentiated constriction was significantly blocked by sodium ozagrel, a thromboxane synthetase inhibitor. These results suggest that the dilatation due to these neuropeptides may depend on endothelium-derived relaxing factor, and that the augmented constriction after endothelial removal may be related to the thromboxane A2 production in cerebral arterial smooth muscles. This mechanism following the damage of endothelium might be implicated in cerebral vasospasm after subarachnoid haemorrhage.
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PMID:Origin of thromboxane-mediated constriction due to neuropeptides in canine basilar artery. 782 46


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