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

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.
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PMID:Cytotoxic brain edema: assessment with diffusion-weighted MR imaging. 143 45

UNICEF promotes the use of a very effective, inexpensive treatment of dehydration in developing countries: oral rehydration therapy (ORT), which is oral administration of a solution with equimolar concentrations of sodium and glucose (osmolality of about 300 mosmol). The solution is isotonic with respect to total body water when it reaches the small intestine. It expands the extracellular fluid without changing serum osmolality, thus, brain edema does not occur. Further, metabolic degradation of glucose eventually releases free water. On the other hand, intravenous rehydration with saline solution can be lethal, causing excess free water to expand shrunken cells and, thereby, causing brain swelling, rupture of blood vessels and hemorrhage. Yet, physicians and other health workers in developed countries have been quite sow to accept ORT. Leading conditions of dehydration include insensible loss of water and heat through evaporation from the respiratory tract and skin (common in dry air, hot environment, and fever), sensible loss of water and heat through perspiration (common in hot, humid environment and with warm and absorbent clothing), and irritation of the intestinal mucosa by allergies, infections, toxins, and intolerance to some nutrients, resulting in diarrhea. Diarrhea is indeed the main cause of dehydration. Other causes of dehydration are: failure of the hypothalamus to secrete antidiuretic hormone (ADH), kidney unresponsiveness to ADH, diabetes mellitus, protein-rich nutrition, catabolic states, and brush-border lactase after weaning. Physiological changes in dehydration consist of rigidity of the connective tissue (vascular system and lungs) and intracellular fluid loss to the extracellular spaces, resulting in dry mucous membranes, shrunken muscle cells in the lips and the tongue, soft eyes, and adverse effects to the central nervous system. Children become dehydrated more readily than adults, but they tolerate it better.
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PMID:Water: mechanism of oral rehydration, water deficiency = deficiency in salt. 150 31

Blood glucose, plasma sodium, bicarbonate (HCO3-), vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3- (r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P less than 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.
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PMID:Correlates of brain edema in uncontrolled IDDM. 156 33

Brain edema formation was investigated in the vasopressin-deficient Brattleboro rat using a middle cerebral artery occlusion model of early ischemic injury. Water and sodium accumulation after 4 h of ischemia were attenuated 36 and 20%, respectively, in the Brattleboro strain as compared to the control Long-Evans strain. This effect was independent of differences in animal size and state of hydration. In addition, measurements of cerebral blood flow indicated that Brattleboro and Long-Evans rats had equal levels of ischemia following middle cerebral artery occlusion. Systemic treatment of Brattleboro rats with vasopressin normalized their serum electrolyte concentrations and osmolarity but did not alter sodium or water accumulation in the ischemic brain. In contrast, intraventricular administration of vasopressin in Brattleboro rats increased edema formation to that seen in control rats. The reduced water and sodium accumulation in Brattleboro rats subjected to middle cerebral artery occlusion may be related to alterations in blood-brain barrier permeability since the blood-to-brain sodium flux was 36% less in the ischemic tissue of the Brattleboro as compared to the Long-Evans strain. These results support the hypothesis that central vasopressin is a regulator of brain volume and electrolyte homeostasis. Furthermore, our findings suggest a role for central vasopressin in the development of ischemic brain edema.
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PMID:Attenuated development of ischemic brain edema in vasopressin-deficient rats. 161 46

Experiments on albino rats with experimental traumatic brain edema were made to study humoral factors of water-salt metabolism regulation: neuropeptides (vasopressin, angiotensin-II as well as aldosterone in the brain and body tissues using radioimmune analysis. Besides, the effect of natriuretic hormone on brain edema was assessed. It was established in preliminary investigations that the highest water content in the brain was recorded on the third day after the suffering of a craniocerebral injury. During the same time, the injured hemisphere showed an increase of sodium ions. The level of vasopressin in cerebral hemispheres rose whereas in the pituitary and blood plasma, it decreased. The injured hemisphere manifested a dramatic increase of angiotensin content. The craniocerebral injury gave rise to aldosterone secretion enhancement and to its elevation in the plasma and brain. The marked and non-uniform alterations in factors of water-salt metabolism and of the vascular tone regulation are important components in the pathogenesis of brain edema, which determines goal-oriented approaches to the search of agents for the treatment of the pathology under consideration.
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PMID:[Humoral factors of regulation of water-salt metabolism in experimental traumatic brain edema]. 196 60

To study the influence of the vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid (CSF), plasma and CSF were sampled simultaneously in 27 patients with central nervous system lesions. A significant elevation of arginine vasopressin (AVP) levels in plasma and CSF and a significant increase in the osmotic pressure gradients of plasma and CSF were observed in hyponatremic patients. The significant increases in the osmotic pressure gradients may be attributable to hemodilution and CSF concentration resulting from the elevated AVP level, because the sodium concentration gradients of plasma and CSF did not significantly increase. The elevated AVP levels in plasma and CSF and the increased osmotic pressure gradients of plasma and CSF normalized in parallel with improvement of consciousness. These findings suggest that the increased osmotic pressure gradients of plasma and CSF, derived from increased AVP secretion into blood and CSF, exacerbates brain edema induced by the primary lesion and may contribute to the clinical deterioration of some patients with intracranial lesions.
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PMID:Influence of vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid in patients with intracranial lesions. 248 May 37

Considerable evidence indicates that regulation of the ionic environment of the brain is coordinated by a central neuroendocrine system capable of affecting the capillary endothelium, the choroid plexus, and the astroglia. All three cell groups are responsible for precise control of brain volume through adjustment of cell water and electrolyte content. With these considerations in mind, we have attempted to elucidate the possible involvement of the central vasopressin (AVP) and atrial natriuretic factor (ANF) systems in the regulation of the water and ion homeostasis of the brain tissue of rats: Vasopressin-positive vascular connections, investigated by immuno-electronhistochemistry, were found in close or direct contact with brain microvessels. Central administration of AVP (125 ng) or DDAVP (0.5 micrograms), with or without an accompanying water load, brought about a 1-1.3% water accumulation. Brain oedema caused by experimental subarachnoid haemorrhage had a different course in Wistar and Brattleboro DI rats, the latter being unable to synthetize AVP. These findings suggest that the centrally released AVP leads to brain water accumulation by increasing the water permeability of capillaries, and may facilitate the production of brain oedema in various pathological conditions. On the other hand, central administration of synthetic rat ANF (2 micrograms) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. The better understanding of these hormone receptors and their manipulations have exciting clinical implications.
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PMID:Regulation of brain water and electrolyte contents: the opposite actions of central vasopressin and atrial natriuretic factor (ANF). 297 42

To determine factors contributing to life-threatening brain herniation in patients treated for severe diabetic ketoacidosis, we analyzed history, laboratory data, rate and composition of fluid and insulin administration, and time to onset of brain herniation in nine new cases and 33 prior reports. The overall rate of fluid administration was inversely correlated with the time of onset of herniation (r = -0.32, p = 0.04). Only 4 of 40 cases occurred at fluid intakes less than or equal to 4.0 L/m2/day. During treatment, "calculated" serum sodium concentrations fell significantly and were less than 130 mEq/L in 33% of cases at the time of herniation. These data indicate that excessive secretion of vasopressin may exacerbate the brain edema, and that limitation of the rate of fluid administration may be prudent.
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PMID:Factors associated with brain herniation in the treatment of diabetic ketoacidosis. 313 55

Vasogenic brain edema occurs as a result of a diverse spectrum of central nervous system pathology. The fundamental physiologic abnormality of vasogenic brain edema is an increase in cerebral capillary permeability. It is hypothesized that the recent development of new, potent, synthetic vasopressin antagonists will make it possible to impede the formation of vasogenic brain edema by the intraventricular administration of such agents with the subsequent inhibition of the neural control of brain capillary permeability by the locus ceruleus. The action of the vasopressin antagonists should be synergistic with the anti-edema effects of central alpha-adrenergic blockade produced by phentolamine. The combination of these two modes of therapy is expected to produce an increase in intracranial pressure which will require additional forms of medical therapy to control, in spite of the overall decrease of brain parenchymal water content.
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PMID:Neuropharmacologic control of cerebral capillary permeability: current implications for therapy of vasogenic brain edema. 339 90

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


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