pituitrin and Brain-Edema

Vasopressin is a peptide hormone produced in the hypothalamus and released from the posterior pituitary. Secretion of vasopressin is followed by activation of its receptors V1a, V1b, and V2 throughout the body. Each receptor type is responsible for a specific function of vasopressin. For example, V1a receptor activation triggers vasoconstriction, V1b receptor is responsible for modulation of mood and behavior, and V2 receptor induces water reabsorption in the kidney. Vasopressin is known to regulate blood pressure, blood osmolality, and blood volume. The effects of V1a and V2 receptors can be amplified when vasopressin is secreted in excessive amounts, and this condition may be experienced by patients undergoing a disease or stress. In pathological conditions such as stroke, traumatic brain injury, subarachnoid hemorrhage, liver disease, and other diseases, vasopressin can exacerbate brain edema. Oversecretion of vasopressin unleashes deleterious pathways leading to hyponatremia and brain edema. This book chapter describes important mechanisms and pathways linking vasopressin and brain edema triggered by various conditions.

Topics: Brain Edema; Humans; Receptors, Vasopressin; Signal Transduction; Vasopressins

Brain edema formation is a major cause of brain damages and the high mortality of ischemic stroke. The aim of this review is to explore the relationship between ischemic brain edema formation and vasopressin (VP) hypersecretion in addition to the oxygen and glucose deprivation and the ensuing reperfusion injury.. Pertinent studies involving ischemic stroke, brain edema formation, astrocytes, and VP were identified by a search of the PubMed and the Web of Science databases in January 2016. Based on clinical findings and reports of animal experiments using ischemic stroke models, this systematic review reanalyzes the implication of individual reports in the edema formation and then establishes the inherent links among them.. This systematic review reveals that cytotoxic edema and vasogenic brain edema in classical view are mainly under the influence of a continuous malfunction of astrocytic plasticity. Adaptive VP secretion can modulate membrane ion transport, water permeability, and blood-brain barrier integrity, which are largely via changing astrocytic plasticity. Maladaptive VP hypersecretion leads to disruptions of ion and water balance across cell membranes as well as the integrity of the blood-brain barrier. This review highlights our current understandings of the cellular mechanisms underlying ischemic brain edema formation and its association with VP hypersecretion.. VP hypersecretion promotes brain edema formation in ischemic stroke by disrupting hydromineral balance in the neurovascular unit; suppressing VP hypersecretion has the potential to alleviate ischemic brain edema.

Topics: Animals; Astrocytes; Brain; Brain Edema; Brain Ischemia; Humans; Phenotype; Prognosis; Risk Factors; Signal Transduction; Stroke; Up-Regulation; Vasopressins

Although many approaches have been tried in the attempt to reduce the devastating impact of stroke, tissue plasminogen activator for thromboembolic stroke is the only proved, effective acute stroke treatment to date. Vasopressin, an acute-phase reactant, is released after brain injury and is partially responsible for the subsequent inflammatory response via activation of divergent pathways. Recently there has been increasing interest in vasopressin because it is implicated in inflammation, cerebral edema, increased intracerebral pressure, and cerebral ion and neurotransmitter dysfunctions after cerebral ischemia. Additionally, copeptin, a byproduct of vasopressin production, may serve as a promising independent marker of tissue damage and prognosis after stroke, thereby corroborating the role of vasopressin in acute brain injury. Thus, vasopressin antagonists have a potential role in early stroke intervention, an effect thought to be mediated via interactions with aquaporin receptors, specifically aquaporin-4. Despite some ambiguity, vasopressin V1a receptor antagonism has been consistently associated with attenuated secondary brain injury and edema in experimental stroke models. The role of the vasopressin V2 receptor remains unclear, but perhaps it is involved in a positive feedback loop for vasopressin expression. Despite the encouraging initial findings we report here, future research is required to characterize further the utility of vasopressin antagonists in treatment of stroke.

Topics: Brain Edema; Hemostatics; Humans; Stroke; Vasopressins

Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors--discrepancy between skull size and brain size--are important in the genesis of brain damage. In adults, certain hormones--estrogen and vasopressin (usually elevated in cases of hyponatremia)--have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na(+)-K(+)-ATPase system to extrude cellular Na(+). In menstruant women, estrogen + vasopressin inhibits the Na(+)-K(+)-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po(2) and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones.

Topics: Adaptation, Physiological; Age Factors; Blood-Brain Barrier; Brain; Brain Edema; Cell Size; Estrogens; Humans; Hyponatremia; Hypoxia; Organ Size; Sex Factors; Vasopressins

The study gives an overview on the regulation of cerebral water content and of brain volume. The molecular mechanisms of the development and resolution of various oedema forms are discussed in detail. The physiological and pathophysiological role of the recently discovered molecular water channel proteins aquaporin-1 (AQP1) and aquaporin-4 (AQP4) as well as the importance of central neuroendocrine regulation by vasopressin and atriopeptin are reviewed based on the relevant literature and personal studies. Quantitative water maps based on the combination of multicompartment-T2, diffusion weighted MRI and T1 studies have proven to be powerful tools for studying new drugs against brain oedema brought about by various neuropathological conditions and for testing their efficacy both in animal experimental and clinical conditions. Non-peptide vasopressin antagonists, atriopeptin agonists and drugs targeting AQP4 are potential new families of oedema-decreasing drugs.

Topics: Animals; Aquaporin 1; Aquaporin 4; Aquaporins; Atrial Natriuretic Factor; Biological Transport; Blood Group Antigens; Brain Edema; Humans; Vasopressins; Water

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Topics: Adrenal Insufficiency; Adult; Brain Edema; Edema; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Models, Biological; Osmolar Concentration; Potassium; Pregnancy; Syndrome; Vasopressins

Competitive antagonists of the antidiuretic (ADH) activity of vasopressin were first described some six years ago. When studied in vitro, ADH antagonists displace vasopressin from specific renal binding sites and antagonize, in a competitive fashion, vasopressin stimulation of adenylate cyclase and transepithelial water, salt, and urea fluxes. When studied in vivo, the ADH antagonists increase renal water excretion and antagonize, in a competitive fashion, the ADH activity of vasopressin. Marked species heterogeneity is apparent with ADH antagonists in vivo, and inconsistencies between in vitro and in vivo findings within the same species are reported. Other renal responses associated with administration of ADH antagonists include changes in renal hemodynamics and renal salt and urea excretion. The effects on salt excretion appear to be limited to those species in which vasopressin stimulation of epithelial salt reabsorption has been demonstrated. In summary, the role of vasopressin as the principal factor regulating renal water handling is supported by experience with ADH receptor antagonists. However, that experience also indicates the emerging significance of autocoids, and other synergistic factors, to affect ADH receptor/effector mechanisms and to modulate renal ADH responses.

Topics: Animals; Brain Edema; Diuresis; Electrolytes; Hemodynamics; Humans; Kidney; Receptors, Angiotensin; Receptors, Vasopressin; Structure-Activity Relationship; Urea; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine Vasopressin; Brain Edema; Cerebrovascular Disorders; Cortisone; Drug Therapy; Humans; Hydrocortisone; Stroke; Vasopressins

Arginine vasopressin (AVP) is often used as an alternative pressor to catecholamines (CATs). However, unlike CATs, AVP is a powerful antidiuretic that could promote edema. We tested the hypothesis that AVP promoted cerebral edema and/or increased requirements for osmotherapy, relative to those who received CATs, for cerebral perfusion pressure (CPP) management after traumatic brain injury (TBI). This is a retrospective review of 286 consecutive TBI patients with intracranial pressure monitoring at a single institution from September 2008 to January 2015. Cerebral edema was quantitated using CT attenuation in prespecified areas of gray and white matter.. To maintain CPP >60 mm Hg, 205 patients required no vasopressors, 41 received a single CAT, 12 received AVP, and 28 required both. Those who required no pressors were generally less injured; required less hyperosmolar therapy and less total fluid; and had lower plasma Na, lower intracranial pressure, less edema, and lower mortality (all P < 0.05). Edema; daily mean, minimum, and maximum Na levels; and mortality were similar with AVP versus CATs, but the daily requirement of mannitol and 3 per cent NaCl were reduced by 45 and 35 per cent (both P < 0.05). In patients with TBI who required CPP therapy, AVP reduced the requirements for hyperosmolar therapy and did not delay resolution or increase cerebral edema compared with CATs.

Topics: Adult; Brain Edema; Brain Injuries, Traumatic; Catecholamines; Cerebrovascular Circulation; Female; Humans; Male; Middle Aged; Retrospective Studies; Trauma Severity Indices; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Head injury frequently results in increased intracranial pressure and brain edema. Investigators have demonstrated that ischemic injury causes an increase in cerebrospinal fluid (CSF) levels of antidiuretic hormone (ADH); increased CSF ADH levels exacerbate cerebral edema, and inhibition of the ADH system with specific ADH antagonists reduces cerebral edema. The current study was designed to test the hypothesis that elevated levels of ADH are present in the CSF of subjects with head injury.. Ventricular CSF and blood samples were taken from 11 subjects with head injury and 12 subjects with no known head trauma or injury. ADH levels were analyzed using radioimmunoassay. Severity of increased intracranial pressure (ICP) was rated in head-injured subjects using a four-point ordinal scale, based on which treatments were necessary to reduce ICP.. Subjects with head injury had higher CSF (3.2 versus 1.2 pg/ml; P<0.02) and plasma (4.1 versus 1.4 pg/ml; P<0.02) levels of ADH than did control subjects. In head-injured subjects, CSF ADH levels positively correlated with severity of ICP.. The results of this study suggest that ADH plays a role in brain edema associated with closed head injury.

Topics: Adult; Aged; Brain Edema; Brain Injuries; Child; Head Injuries, Closed; Humans; Intracranial Hypertension; Male; Middle Aged; Neurophysins; Protein Precursors; Vasopressins

Increased transport of Na across an intact blood-brain barrier (BBB) contributes to cerebral edema formation in ischemic stroke. Our previous studies have shown that ischemic factors stimulate activity of a luminal BBB Na-K-Cl cotransporter, and we have hypothesized that during ischemia, the cotransporter together with the abluminal Na/K pump mediates increased transport of Na from blood into the brain. However, it is possible that elevated Na-K-Cl cotransporter activity could also cause cell swelling if it outpaces ion efflux pathways. The present study was conducted to evaluate the effects of hypoxia on intracellular volume of BBB cells. Cerebral microvascular endothelial cell (CMEC) monolayers were exposed to varying levels of hypoxia for 1 to 5 h in an O(2)-controlled glove box, and cell volume was assessed using 3-O-methyl-D-[(3)H]glucose and [(14)C]sucrose as markers of total and extracellular water space, respectively. Cells exposed to either 7.5%, 3%, or 1% O(2) showed gradual increases in volume (compared with 19% O(2) normoxic controls) that became significant after 3 or more hours. By ion chromatography methods, we also found that a 30-min exposure to 7.5% O(2) caused an increase in bumetanide-sensitive net Na uptake by the cells without increasing cell Na content. CMEC Na content was significantly increased, however, following 3 or more hours of exposure to 7.5% O(2). These findings are consistent with the hypothesis that during cerebral ischemia, the BBB Na-K-Cl cotransporter is stimulated to mediate transendothelial uptake of Na into the brain and that increased cotransporter activity also contributes to gradual swelling of the cells.

Topics: Animals; Blood-Brain Barrier; Brain; Brain Edema; Bumetanide; Cattle; Cell Hypoxia; Cell Size; Cells, Cultured; Disease Models, Animal; Endothelial Cells; Extracellular Fluid; Glucose; Guanidines; Infarction, Middle Cerebral Artery; Intracellular Fluid; Microcirculation; Potassium; Rats; Sodium; Sodium Potassium Chloride Symporter Inhibitors; Sodium-Hydrogen Exchangers; Sodium-Potassium-Chloride Symporters; Sulfones; Time Factors; Vasopressins

Topics: Aquaporins; Brain Edema; Burns; Diarrhea; Fluid Therapy; Humans; Hypotonic Solutions; Inappropriate ADH Syndrome; Isotonic Solutions; Kidney; Neurons; Transcription Factors; Vasopressins; Vomiting; Water-Electrolyte Balance

The effects of the non-peptide vasopressin V(2) receptor antagonist 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine hydrochloride (OPC-31260) on the cerebral oedema induced by general cerebral hypoxia were studied in rats. The general cerebral hypoxia was produced by bilateral common carotid ligation in Sprague-Dawley rats of the CFY strain. By 6 h after the ligation, half of the rats had died, but the survival rate was significantly higher following OPC-31260 administration. Electron microscopic examinations revealed typical ischaemic changes after the carotid ligation. The carotid ligation increased the brain contents of water and Na(+) and enhanced the plasma vasopressin level. The increased brain water and Na(+) accumulation was prevented by OPC-31260 administration, but the plasma vasopressin level was further enhanced by OPC-31260. These results demonstrate the important role of vasopressin in the development of the disturbances in brain water and electrolyte balance in response to general cerebral hypoxia. The carotid ligation-induced cerebral oedema was significantly reduced following oral OPC-31260 administration. The protective mechanism exerted by OPC-31260 stems from its influence on the renal vasopressin V(2) receptors. These observations might suggest an effective approach to the treatment of global hypoxia-induced cerebral oedema in humans.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Body Water; Brain; Brain Edema; Brain Ischemia; Disease Models, Animal; Kidney; Male; Microscopy, Electron, Transmission; Rats; Receptors, Vasopressin; Sodium; Survival Rate; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

Topics: Accidents, Traffic; Adult; Brain Edema; Brain Injuries; Catecholamines; Fatal Outcome; Glasgow Coma Scale; Hematoma, Subdural; Humans; Hyperglycemia; Hyperkalemia; Hypokalemia; Hypothermia; Insulin; Intracranial Hypertension; Male; Mannitol; Norepinephrine; Potassium; Vasopressins

Topics: Body Water; Brain Edema; Child; Humans; Hypernatremia; Male; Osmolar Concentration; Thirst; Vasopressins; Water-Electrolyte Balance

Experimental evidence obtained in various animal models of brain injury indicates that vasopressin promotes the formation of cerebral edema. However, the molecular and cellular mechanisms underlying this vasopressin action are not fully understood. In the present study, we analyzed the temporal changes in expression of vasopressin V1a receptors after traumatic brain injury (TBI) in rats. In the intact brain, the V1a receptor was expressed in neurons located in all layers of the frontoparietal cortex. The V1a receptor-immunoreactive product was predominantly localized to neuronal nuclei and had both a diffused and punctate staining pattern. The V1a receptors were also expressed in astrocytes, especially in layer 1 of the frontoparietal cortex. In these cells, two distinctive patterns of immunopositive staining for V1a receptors were observed: a diffused cytosolic staining of cell bodies and processes and a clearly punctate staining pattern that was predominantly localized to the astrocytic cell bodies. The real-time reverse-transcriptase polymerase chain reaction analysis of changes in mRNA for the V1a receptor demonstrated that after TBI, there is an early (4 h post-TBI) increase in the number of transcripts in the ipsilateral frontoparietal cortex, when compared to the contralateral hemisphere or the sham-injured rats. This increase in the message was followed by the up-regulation of expression of the V1a receptors at the protein level. This was most evident in cortical astrocytes in the areas surrounding the lesion. The number of the V1a receptor-immunopositive astrocytes in the traumatized parenchyma gradually increased, starting at 8 h and peaking at 4-6 days after TBI. Furthermore, a redistribution of V1a receptors from the astrocytic cell bodies to the astrocytic processes was observed. In addition to astrocytes, an increased expression of V1a receptors was found in the endothelium of both blood microvessels and the large-diameter blood vessels in the frontoparietal cortex ipsilateral to injury. This increase in the V1a receptor expression was apparent between 2 and 4 days after TBI. As early as 1-2 h following the impact, there was also a striking increase in the number of the V1a receptor-immunopositive beaded axonal processes, with greatly enlarged varicosities, that were localized to various areas of the injured parenchyma. It is suggested that the increased expression of V1a receptors plays an important role in the vasopressin-mediated formatio

Topics: Animals; Astrocytes; Axons; Blood-Brain Barrier; Brain; Brain Edema; Brain Injuries; Cerebral Cortex; Disease Models, Animal; Disease Progression; Endothelium, Vascular; Male; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; RNA, Messenger; Up-Regulation; Vasopressins

Cerebral hyperemia is an important contributor to the development of brain edema in fulminant hepatic failure. Rats receiving an ammonia infusion after portacaval anastomosis (PCA) demonstrate a rise in cerebral blood flow (CBF) with brain edema at 180 min. Vasopressin (VP), a systemic vasoconstrictor which in the rat dilates cerebral vessels through V(2) receptors, was used to ascertain the effects of increasing CBF.. Changes in CBF were measured with Laser Doppler flowmetry (LDF). Absolute CBF was measured with radioactive microspheres to calculate oxygen and ammonia uptake.. Compared to the NH(3)+Vehicle group, VP+NH(3) infusion accelerated the rise in CBF (117+/-21 vs. -6+/-12%, P<0.01), and the development of brain edema (81.09+/-0.17 vs. 80.29+/-0.06%, P<0.01). Radioactive microspheres confirmed these results (254+/-44 vs. 106+/-9.5 ml/min/100 g, P<0.01). Oxygen uptake was similar. Ammonia uptake was more than twofold higher in the VP+NH(3) group. A V(1) antagonist negated the higher mean arterial pressure (MAP) that occurs with VP but cerebral hyperemia still occurred. A V(2) antagonist resulted in similar systemic pressures, CBF and brain water compared to the VP+NH(3) group.. In this model, an increase in CBF with VP hastens the development of brain edema while increasing ammonia delivery to the brain.

Topics: Ammonia; Animals; Antidiuretic Hormone Receptor Antagonists; Blood Pressure; Brain Edema; Cardiac Output; Cerebrovascular Circulation; Drug Synergism; Heart Rate; Intracranial Pressure; Laser-Doppler Flowmetry; Male; Oxygen; Portacaval Shunt, Surgical; Rats; Rats, Sprague-Dawley; Renal Circulation; Vasoconstrictor Agents; Vasopressins; Water

Central salt wasting syndrome may be caused by pathological increases in serum natriuretic peptides after subarachnoid hemorrhage (SAH). However, it is unclear as to why the serum concentration of atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) increases in the subacute phase of SAH. The present study was designed to assess the correlation between focal brain edema and serum concentration of ANP or BNP in patients with SAH. Focal brain edema was found in 8 SAH-patients and peaked between days 4 and 7 of SAH. The mean serum ANP and BNP levels in patients with focal brain edema were significantly higher than those in patients without focal brain edema between days 4 and 14 of SAH. These results suggest that focal brain edema might correlate with increased levels of ANP and BNP in the subacute phase of SAH.

Topics: Atrial Natriuretic Factor; Brain Edema; Humans; Natriuretic Peptide, Brain; Retrospective Studies; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Vasopressins

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; Water-Electrolyte Imbalance

The effects of the non-peptide vasopressin V2 receptor antagonist, 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrah ydro-1 H-benzazepine hydrochloride (OPC-31260) on the cerebral oedema induced by subarachnoid haemorrhage were studied in rats. Subarachnoid haemorrhage induced significant water retention after water loading, increased the brain content of water and Na+ and increased plasma vasopressin levels. The water retention and brain water and Na+ accumulation were prevented by OPC-31260 administration, but the plasma vasopressin levels were further enhanced by OPC-31260. These results demonstrate the important role of vasopressin in the development of antidiuresis and disturbances in brain water and electrolyte balance in response to subarachnoid haemorrhage. The subarachnoid haemorrhage-induced cerebral oedema was significantly reduced following oral OPC-31260 administration. The protective mechanism exerted by OPC-31260 stems from its influence on renal tubular function: it blocks the renal vasopressin V2 receptors. These observations might suggest a new, effective approach to the treatment of subarachnoid haemorrhage-induced cerebral oedema in humans.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Body Water; Brain; Brain Edema; Diuresis; Dose-Response Relationship, Drug; Drinking; Male; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Sodium; Subarachnoid Hemorrhage; Urination; Urine; Vasopressins

Vasopressin (VP) levels were evaluated by radioimmunoassay (RIA) in the arterial (A), peripheral (Vp) and jugular (Vj) vein blood and in CSF in 102 patients with brain tumors. In 60 cases the patients' state was complicated by brain edema (BE) and hemodynamic disturbances (HDD). The obtained data revealed significantly higher VP levels: 1) in A, Vp and CSF in patients with BE (Group A) in comparison with patients without BE (Group B), 2) in Vj in patients with HDD only (Group Bc) and 3) in Vp in patients with HDD and BE (Group Ac) in comparison with Group Bc (p < 0.05). There were marked extremely high VP levels in Vj in patients with severe haemorrhage, tachycardia and high blood pressure (BP) and in CSF in patients with tachycardia, high BP and cardiac arrest (p < 0.05 correspondingly in each of the cases). Our results on a clinical basis confirmed CSF VP influence on BE development. We also confirmed the neurohumoral (through blood) and neurotransmitter (possibly through CSF and/or vasopressinergic pathways) VP influences on cardiovascular regulation mechanisms. We content that this is a pathogenetic basis for application of VP direct or indirect antagonists for preventing and treating brain edema in neurosurgical patients.

Topics: Adolescent; Adult; Aged; Blood-Brain Barrier; Brain Edema; Brain Neoplasms; Cerebral Hemorrhage; Child; Child, Preschool; Female; Heart Arrest; Hemodynamics; Humans; Hypertension; Male; Middle Aged; Postoperative Complications; Radioimmunoassay; Synaptic Transmission; Tachycardia; Vasopressins

The study of renin-angiotensin-aldosterone (RAA) and vasopressin (VP) systems in neurosurgical patients with brain tumors and brain edema (BE) had revealed an excessive activity of these systems with secondary hyperaldosteronism especially with BE that proves the pathogenetic role of these systems. Measurement of Aldosterone (Ald) in CSF may serve as a diagnostic test to help manage the patient's clinical condition. Mechanisms of Ald penetration in CSF assumed to be the result of blood-brain-barrier (BBB) destruction (especially in astrocytomas) and/or the mediation by neuropeptides (for example increasing activity of VP V1-receptors). Results serve as a basis for application of the neuropeptide and hormone antagonists and inhibitors on all stages of cascade reactions taking part in the water and sodium retention.

Topics: Adolescent; Adult; Aged; Aldosterone; Astrocytoma; Blood-Brain Barrier; Brain Edema; Brain Neoplasms; Cerebral Hemorrhage; Child; Child, Preschool; Female; Heart Arrest; Hemodynamics; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Postoperative Complications; Prognosis; Radioimmunoassay; Renin-Angiotensin System; Tachycardia; Vasopressins

Topics: Animals; Arginine Vasopressin; Body Water; Brain; Brain Edema; Electrolytes; Inappropriate ADH Syndrome; Male; Rats; Rats, Wistar; Subarachnoid Hemorrhage; Vasopressins

Injection of arginine vasopressin into the cerebral ventricles in animals with brain injury increased brain water, whereas injection of atrial natriuretic peptide reduced water content. Therefore, to determine the role of endogenous arginine vasopressin in brain edema, we attempted to inhibit edema from a hemorrhagic lesion with an arginine vasopressin V1 receptor antagonist or atrial natriuretic peptide.. Adult Sprague-Dawley rats with hemorrhages induced by 0.4 IU bacterial collagenase were treated with 75 ng (n = 9) or 8 micrograms (n = 9) of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)Arg, 3.2 micrograms (n = 4) atrial natriuretic peptide injected intracerebrally, or 5 micrograms/kg per hour (n = 7) atrial natriuretic peptide intraperitoneally. They were compared with control groups injected with 0.4 IU collagenase only. Brain water and electrolytes were measured 24 hours later. Brain uptake of [14C]sucrose was measured 30 minutes after lesions were induced by 0.4 IU collagenase alone (n = 5) or after collagenase injection and 50 micrograms/kg per hour (n = 5) atrial natriuretic peptide injected intravenously.. The arginine vasopressin V1 receptor antagonist and atrial natriuretic peptide significantly (p < 0.05) reduced water and sodium contents in the posterior edematous regions. Brain uptake of [14C]sucrose was significantly reduced by intravenous atrial natriuretic peptide.. Antagonists to arginine vasopressin V1 receptors and atrial natriuretic peptide both significantly reduce hemorrhagic brain edema, and atrial natriuretic peptide appears to protect the blood-brain barrier.

Topics: Angiotensin Receptor Antagonists; Animals; Arginine Vasopressin; Atrial Natriuretic Factor; Blood-Brain Barrier; Body Water; Brain Edema; Cerebral Hemorrhage; Collagenases; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Sodium; Sucrose; Vasopressins

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.

Topics: Adolescent; Arginine Vasopressin; Bicarbonates; Blood Glucose; Brain; Brain Edema; Child; Diabetes Mellitus, Type 1; Hematocrit; Humans; Osmolar Concentration; Regression Analysis; Sodium; Tomography, X-Ray Computed; Vasopressins

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.

Topics: Aminoisobutyric Acids; Animals; Blood-Brain Barrier; Brain Edema; Brain Ischemia; Cerebrovascular Circulation; Electrolytes; Osmolar Concentration; Permeability; Rats; Rats, Brattleboro; Rats, Inbred Strains; Sodium; Vasopressins

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.

Topics: Aldosterone; Angiotensin II; Animals; Brain; Brain Edema; Brain Injuries; Disease Models, Animal; Potassium; Rats; Sodium; Time Factors; Vasopressins; Water-Electrolyte Balance

Water diuresis was produced in rats after s.c. injections of d(CH2)5,D-Ile2,Ile4-AVP (compound 1) and d(CH2)5,Tyr(OEt)2Val4-AVP (compound 2). Compound 1 is known to be a more potent antagonist against the antidiuretic effect, while Compound 2 is a more potent antagonist against the vasopressor effect of vasopressin. Compound 1 (but not compound 2) also increased plasma osmolality significantly at the diuretic doses. In rats rendered ischemic of the forebrain by 4-hour occlusion of both common carotid arteries, the resulting increases in brain water were significantly reversed by the injection of compound 1. Compound 2 did not reduce the edema. The results suggests a novel approach to the treatment of cerebral edema.

Topics: Animals; Arginine Vasopressin; Blood; Brain Edema; Brain Ischemia; Diuresis; Male; Rats; Rats, Inbred F344; Vasopressins; Water-Electrolyte Balance

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.

Topics: Blood-Brain Barrier; Brain Edema; Capillary Permeability; Cerebrovascular Circulation; Humans; Injections, Intraventricular; Intracranial Pressure; Phentolamine; Vasopressins

U-50488 is a specific kappa opioid agonist which produces in rats water diuresis resulting in an elevation of plasma osmolarity. Pretreatment with U-50488H (the methanesulfonate salt) in Fisher rats prior to 4 h of bilateral carotid occlusion prevented the development of edema in the forebrain, and the effect was greater than that from pentobarbital anesthesia. An additional injection of an antidiuretic hormone which prevented the plasma hyperosmolarity also significantly reduced the anticerebral edemic effects of U-50488H. The plasma osmotic effect, however, may not completely account for the ischemic protection produced by U-50488H.

Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Animals; Body Water; Brain Chemistry; Brain Edema; Brain Ischemia; Diuresis; Male; Osmolar Concentration; Potassium; Pyrrolidines; Rats; Rats, Inbred F344; Receptors, Opioid; Sodium; Vasopressins

Centrally released arginine vasopressin (AVP) has been implicated in the regulation of intracranial pressure (ICP) and brain water, and is elevated in the cerebrospinal fluid (CSF) of some patients with pseudotumor cerebri or subarachnoid hemorrhage. The authors have examined the relationship of AVP levels in CSF to ICP and brain water content in three experimental groups of cats with and without cold-induced vasogenic edema. With the cats under general anesthesia, a cold lesion was made and cannulas were placed in the cisterna magna, lateral ventricle, and aorta. Subsequent central and systemic measurements were made while the animals were awake and free-roaming. In Experiment 1, endogenous AVP levels in CSF were measured every 12 hours over a 48-hour period by radioimmunoassay in cats with sham craniotomy, mild edema, or moderate edema; no significant difference was found between groups although a diurnal variation was seen (range 2 to 18 pg/ml). In Experiment 2, either carrier solution or AVP, in doses of 1.5 or 30 ng, was administered via a lateral ventricle every 2 hours over 24 hours in unlesioned cats. In Experiment 3, cats received 2 or 35 ng of carrier solution or AVP in a similar manner, but coupled with a cold lesion. The CSF AVP levels ranged from an average of 100 to 681 pg/ml and 1.4 to 11.9 ng/ml in the two dose groups in both experiments. Neither the low nor the high dose had an effect on brain water content in normal white matter (Experiment 2), but both doses increased brain water content in edematous white matter (p less than 0.05 in Experiment 3), as determined by wet and dry weight measurements of standardized pieces of white matter. The ICP was decreased by high-dose AVP in normal cats (p less than 0.01 at 24 hours), but in lesioned cats was unchanged by low-dose and increased by high-dose AVP (p less than 0.05 at 18 hours). The authors conclude that pharmacological doses of central AVP facilitate the production of vasogenic edema.

Topics: Animals; Brain Edema; Cats; Cerebrospinal Fluid; Cold Temperature; Intracranial Pressure; Subarachnoid Hemorrhage; Vasopressins

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.

Topics: Animals; Blood-Brain Barrier; Brain Edema; Capillary Permeability; Diabetes Insipidus; Female; Male; Rats; Rats, Brattleboro; Rats, Inbred Strains; Subarachnoid Hemorrhage; Vasopressins; Water-Electrolyte Balance

A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a long-acting vasopressin preparation (pitressin tannate ) together with a forced water intake. The treatment led to water retention, hypernatriuria , marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Body Water; Brain; Brain Edema; Diuresis; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Urination; Vasopressins

A young male presented within hours after closed head injury with hypotension, tachycardia, and polyuria. A diagnosis of post-traumatic diabetes insipidus was made. Although a rare entity, the rapid diagnosis of diabetes insipidus and early treatment with vasopressin may have been life-saving in this case. A detailed approach for treatment with continuous intravenous vasopressin may be the most accurate and efficient method of managing acute onset diabetes insipidus, especially in the hemodynamically compromised patient. This will allow for a controlled fluid management in order to achieve hemodynamic stability and prevent aggravation of cerebral edema.

Topics: Acute Disease; Adult; Brain Edema; Diabetes Insipidus; Facial Bones; Humans; Male; Skull Fractures; Subarachnoid Hemorrhage; Vasopressins

The effect of [1-(beta-mercapto-beta,beta- cyclopentamethylene -propionic acid)2-0- ethyltyrosine ,4-valine] arginine vasopressin on the water metabolism was studied in rat. The compound was found to be able to block the antidiuretic action of both exogenous and endogenous vasopressin. A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a posterior pituitary preparation (Pitressin tannate ) together with a forced water intake. The antagonist prevented water retention and averted the enhanced natriuresis and hyponatraemia, and cerebral oedema did not develop. The observations suggest that this vasopressin antagonist might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Brain; Brain Edema; Disease Models, Animal; Diuresis; Female; Inappropriate ADH Syndrome; Male; Natriuresis; Osmolar Concentration; Rats; Sodium; Vasopressins

Topics: Acute Kidney Injury; Adult; Blood Pressure; Blood Volume; Brain Edema; Chemoreceptor Cells; Edema; Female; Humans; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Male; Pressoreceptors; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Balance

Pontine myelinolysis can be suspected clinically on the basis of the following criteria: (1) Electrolyte disturbance manifested mainly by hyponatremia; (2) progressive neurologic deficits resulting in a "locked-in" syndrome; (3) usually, but not necessarily, alcohol abuse; and (4) frequent iatrogenic precipitation of the syndrome by inappropriate rehydration of patients at risk. A major pathophysiologic mechanism for this disorder seems to be the anatomic grid structure of the base of the pons, which is more vulnerable to edema than the cerebral hemispheres. Treatment should be focused on rapid reversal of electrolyte imbalance and judicious use of dehydrating agents. Early diagnosis and treatment might reverse an otherwise malignant syndrome.

Topics: Adolescent; Adult; Aged; Alcoholism; Brain Edema; Brain Stem; Child; Child, Preschool; Demyelinating Diseases; Female; Humans; Hyponatremia; Male; Middle Aged; Pons; Vasopressins; Water-Electrolyte Imbalance

Post-traumatic diabetes insipidus was observed in 14 among 702 patients with severe trauma. The cause of the abnormal vasopressin secretion may be cerebral oedema, cerebral contusion near the hypothalamus, pull on the hypophyseal stalk by displacement or gross destruction of the brainstem. The hormonal hypofunction disappears once the cerebral damage has regressed. Treatment consists of exact balancing of water and electrolyte loss, using salt-free solutions. Drug treatment with vasopressin and with ADH-secretion stimulators has given unsatisfactory results, but should be used. Seven of the 14 patients died of their injuries. The symptoms of the diabetes insipidus syndrome regressed in the survivors.

Topics: Adult; Brain Concussion; Brain Edema; Brain Injuries; Brain Stem; Child; Diabetes Insipidus; Female; Humans; Male; Middle Aged; Remission, Spontaneous; Vasopressins

Topics: Adolescent; Asphyxia Neonatorum; Brain; Brain Edema; Female; Humans; Hyponatremia; Hypoxia, Brain; Infant, Newborn; Ischemia; Male; Vasopressins

Topics: Adrenal Gland Diseases; Adrenal Glands; Age Factors; Aged; Brain Edema; Female; Humans; Hyponatremia; Iatrogenic Disease; Kidney; Liver Cirrhosis; Male; Sodium; Vasopressins; Water-Electrolyte Imbalance

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.

Topics: Blood; Brain Edema; Child; Child, Preschool; Diabetic Ketoacidosis; Female; Hormones, Ectopic; Humans; Hyponatremia; Infusions, Parenteral; Insulin; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Patients underlying the permanent endocrine substitution need a particular control and a competent conduction on account of their endangering by intercurrent events. Highly specialised knowledge of the physician and intensive collaboration of the patient from this reciprocity lead to essential aspects of the prophylaxis of the crisis-like exacerbations exhibited in detail. The optimum substitution is supplemented by issuing information and emergency cards. When the patient possesses such cards they will become of decisive importance in an urgent therapy necessary outside the controlling facility.

Topics: Arginine Vasopressin; Brain Edema; Diabetes Insipidus; Dihydrotachysterol; Humans; Hydrocortisone; Hypoparathyroidism; Hypothyroidism; Muscle Cramp; Pituitary Diseases; Thyroid Hormones; Vasopressins

Schwartz-Bartter-syndrome as a consequence of severe cerebral alterations like bacterial and tuberculous meningitis, encephalitis, hydrocephalus and brain haemorrhage has been observed in 7 cases. Massive natriuresis is followed by marked hyponatremia and hypochloremia which may lead to an intracellular brain edema. Sodium administered even in high dosage is lost rapidly through the kidney, and does not normalize the serum level of sodium. The Schwartz-Bartter-syndrome is caused by inadequatly elevated ADH-secretion with consecutive water retention and an increase in plasma volume. Consecutively an increased excretion of sodium takes place causing a substantial loss of bound water. An analogous situation was seen in a child with neurohormonal diabetes insipidus after an overdosage of ADH, which resulted in a hypervolemia, marked hyponatremia and massive natriuresis. The increased excretion of sodium may be the result of reduced reabsorption of sodium in the proximal tubuli of the kidney, caused by a humeral natriuretic factor (the socalled "third factor"). In the serum of one of our patients an increased natriuretic activity could be shown; this is the first time in a child with Schwartz-Bartter-syndrome.

Topics: Blood Volume; Brain Diseases; Brain Edema; Cerebral Hemorrhage; Child; Chlorides; Encephalitis; Female; Humans; Hydrocephalus; Hyponatremia; Infant; Infant, Newborn; Male; Meningitis; Natriuresis; Osmolar Concentration; Syndrome; Tuberculosis, Meningeal; Vasopressins

Topics: Brain Edema; Carotid Artery Diseases; Cerebral Arterial Diseases; Circle of Willis; Dexamethasone; Diabetes Insipidus; Humans; Intracranial Aneurysm; Postoperative Complications; Potassium; Sodium; Thirst; Trimethaphan; Vasopressins; Water-Electrolyte Balance

Topics: Brain; Brain Edema; Craniocerebral Trauma; Craniotomy; Humans; Hyponatremia; Natriuresis; Nutrition Disorders; Osmolar Concentration; Pituitary Gland; Postoperative Complications; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Anti-Bacterial Agents; Brain Edema; Child; Child, Preschool; Coma; Electroencephalography; Encephalitis; Female; Humans; Hyponatremia; Male; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Aged; Astrocytoma; Brain Edema; Brain Neoplasms; Cerebral Angiography; Echoencephalography; Electroencephalography; Female; Humans; Male; Middle Aged; Neoplasm Metastasis; Pituitary Gland; Radionuclide Imaging; Vasopressins

Topics: Animals; Brain; Brain Edema; Extracellular Space; Microscopy; Microscopy, Electron; Microscopy, Phase-Contrast; Neuroglia; Neurons; Rats; Vasopressins; Water; Water Intoxication

Topics: Animals; Body Weight; Brain Chemistry; Brain Edema; Liver; Muscles; Rats; Vasopressins; Water; Water Intoxication; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Adult; Aged; Angiography; Brain Edema; Cerebrovascular Disorders; Craniocerebral Trauma; Echoencephalography; Electroencephalography; Electrooculography; Female; Humans; Male; Middle Aged; Oxytocin; Perfusion; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Aged; Brain Edema; Cerebrovascular Disorders; Female; Humans; Male; Vasopressins

Topics: Adrenocorticotropic Hormone; Aged; Brain Edema; Cerebrovascular Disorders; Female; Humans; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Brain Edema; Drug Therapy; Humans; Neurosurgery; Neurosurgical Procedures; Oxytocin; Physiology; Syndrome; Vasopressins

Topics: Adenosine Triphosphatases; Brain Edema; Demyelinating Diseases; Glucosephosphate Dehydrogenase; Histocytochemistry; Myelin Sheath; Neurochemistry; Neuroglia; Oxidoreductases; Pathology; Rats; Research; Tin; Vasopressins