pituitrin and Brain-Injuries

Causes of hyponatremia in children include the syndrome of appropriate antidiuretic hormone secretion, the syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The purpose of this review is to distinguish these possibilities, focusing on cerebral salt wasting.. Most cases of hyponatremia in children are due to the syndrome of appropriate antidiuretic hormone secretion. The syndrome of inappropriate antidiuretic hormone secretion can be seen with neurological injury, pain and medication use. Recent studies suggest that cerebral salt wasting is a rare cause of hyponatremia. When cerebral salt wasting is diagnosed, it is often difficult to make a direct link with the central nervous system insult.. The clinical condition, assessment of extracellular fluid space volume status, measurement of urinary electrolytes and responses to infusion of saline solutions can distinguish between syndrome of appropriate antidiuretic hormone secretion, syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The word 'cerebral' in 'cerebral salt wasting syndrome' can thus be inappropriate, conveying inaccurate causation.

Topics: Brain Injuries; Child; Diagnosis, Differential; Humans; Hyponatremia; Hypovolemia; Inappropriate ADH Syndrome; Sodium; Vasopressins

The authors present a brief review of the problem of diabetes insipidus in neurosurgical patients, with particular emphasis on the differential diagnosis of postoperative and posttraumatic polyuria and the management of diabetes insipidus in these periods. A listing of drugs currently used in its treatment is given.

Topics: Administration, Intranasal; Benzothiadiazines; Brain Injuries; Carbamazepine; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuretics; Humans; Hypothalamo-Hypophyseal System; Lypressin; Methods; Polyuria; Postoperative Complications; Sodium Chloride Symporter Inhibitors; Vasopressins; Water-Electrolyte Balance

After traumatic brain injury (TBI), catecholamines (CAs) may be needed to maintain adequate cerebral perfusion pressure (CPP), but there are no recommended alternative vasopressor therapies. This is an interim report of the first study to test the hypothesis that arginine vasopressin (AVP) is a safe and effective alternative to CAs for the management of CPP in patients with severe TBI.. Since 2008, all TBI patients requiring intracranial pressure monitoring at this Level 1 trauma center have been eligible for a randomized trial to receive either CA or AVP if vasopressors were required to maintain CPP greater than 60 mm Hg.. To date, 96 patients have been consented and randomized. Demographics, vital signs, and laboratory values were similar. As treated, 60 required no vasopressors and were the least severely injured group with the best outcomes. Twenty-three patients received CA (70% levophed, 22% dopamine, 9% phenylephrine) and 12 patients received AVP. The two vasopressor groups had similar demographics, but Injury Severity Score (ISS) and fluid requirements on intensive care unit Day 1 were worse in the AVP versus the CA groups (all p < 0.05) before treatment. These differences indicate more severe injury with accompanying hemodynamic instability. Nevertheless, adverse events were not increased with AVP versus CA. Trends favored AVP versus CA, but no apparent differences were statistically significant at this interim point. There was no difference in mortality rates between CA and AVP.. These preliminary results suggest that AVP is a safe and effective alternative to CA for the management of CPP after TBI and support the continued investigation and use of AVP when vasopressors are required for CPP management in TBI patients.. Therapeutic study, level II.

Topics: Adult; Blood Pressure; Brain Injuries; Female; Follow-Up Studies; Humans; Injury Severity Score; Intracranial Pressure; Male; Prospective Studies; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Topics: Alzheimer Disease; Amino Acid Sequence; Brain Injuries; Clinical Trials as Topic; Dementia; Humans; Memory; Memory Disorders; Middle Aged; Structure-Activity Relationship; Vasopressins

To understand mechanisms underlying vasopressin hypersecretion in stroke and its association with brain injury, we investigated effects of blocking aquaporin 4 (AQP4) in the supraoptic nucleus (SON) on vasopressin neuronal activity and cerebral injuries in male rats of unilateral middle cerebral artery occlusion (MCAO).. Establishing MCAO model without or with microinjection of TGN-020 into the SON, performing Western blots and immunohistochemistry and analyzing the expression levels and spatial distribution of functional proteins in the SON and/or the cerebral cortex.. MCAO increased plasma vasopressin levels, caused neurological damage and increased glycogen synthase kinase 3β (GSK-3β) in the SON and the cortex of MCAO side. In the SON, MCAO significantly increased c-Fos in vasopressin neurons and astrocytic somata in the ventral glial lamina. MCAO significantly reduced glial fibrillary acidic protein (GFAP) and AQP4 around vasopressin neurons, which accompanied separation of GFAP from AQP4. By contrast, blocking AQP4 by microinjection of TGN-020 into the SON blocked MCAO-evoked GSK-3β increase as well as the reduction of AQP4 relative to GFAP around vasopressin neurons in the SON. In the cortex, TGN-020 in the SON also blocked MCAO-evoked increase in GSK-3β while reduced neurological damages.. These findings indicate that MCAO disrupts interactions of GFAP with AQP4 in astrocytic processes in the SON, which increases vasopressin neuronal activity. Blocking AQP4 in the SON can block abnormal activation of vasopressin neurons and alleviate ischemic brain injury, which provides novel targets for alleviating ischemic brain injury.

Topics: Animals; Brain Injuries; Ischemic Stroke; Male; Microinjections; Neurons; Niacinamide; Rats; Rats, Wistar; Supraoptic Nucleus; Thiadiazoles; Vasopressins

We describe institutional vasopressor usage, and examine the effect of vasopressors on hemodynamics: heart rate (HR), mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygenation (PbtO(2)), and jugular venous oximetry (SjVO(2)) in adults with severe traumatic brain injury (TBI).. We performed a retrospective analysis of 114 severely head injured patients who were admitted to the neurocritical care unit of Level 1 trauma center and who received vasopressors (phenylephrine, norepinephrine, dopamine, vasopressin or epinephrine) to increase blood pressure. Phenylephrine was the most commonly used vasopressor (43%), followed by norepinephrine (30%), dopamine (22%), and vasopressin (5%). Adjusted for age, gender, injury severity score, vasopressor dose, baseline blood pressure, fluid administration, propofol sedation, and hypertonic saline infusion, phenylephrine use was associated with 8 mmHg higher mean arterial pressure (MAP) than dopamine (P = 0.03), and 12 mmHg higher cerebral perfusion pressure (CPP) than norepinephrine (P = 0.02) during the 3 h after vasopressor start. There was no difference in ICP between the drug groups, either at baseline or after vasopressor treatment.. Most severe TBI patients received phenylephrine. Patients who received phenylephrine had higher MAP and CPP than patients who received dopamine and norepinephrine, respectively.

Topics: Adult; Blood Pressure; Brain Injuries; Dopamine; Female; Heart Rate; Humans; Intracranial Pressure; Male; Norepinephrine; Phenylephrine; Retrospective Studies; Vasoconstrictor Agents; Vasopressins; Young Adult

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

Topics: Animals; Arginine Vasopressin; Brain Chemistry; Brain Injuries; Cerebral Cortex; Endothelium, Vascular; Hypernatremia; Hypothalamus; Immunohistochemistry; Macrophages; Male; Microglia; Microscopy, Confocal; Rats; Rats, Long-Evans; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Vasopressins

Arginine vasopressin (AVP) has previously been shown to promote disruption of the blood-brain barrier, exacerbate edema, and augment the loss of neural tissue in various forms and models of brain injury. However, the mechanisms underlying these AVP actions are not well understood. These mechanisms were studied in AVP-deficient Brattleboro rats (Avp(di/di)), and their parental Long-Evans strain, using a controlled cortical impact model of traumatic brain injury (TBI). The increased influx of inflammatory cells into the injured cortex in wild-type versus Avp(di/di) rats was associated with higher levels of cortical synthesis of the CXC and CC chemokines found in wild-type versus Avp(di/di) rats. These chemokines were predominantly produced by the cerebrovascular endothelium and astrocytes. In astrocyte and brain endothelial cell cultures, AVP acted synergistically with tumor necrosis factor-alpha (TNF-alpha) to increase the TNF-alpha-dependent production of CXC and CC chemokines. These AVP actions were mediated by c-Jun N-terminal kinase (JNK), as shown by Western blotting and pharmacological inhibition of JNK activity. The activity of JNK was increased in response to injury, and the differences in the magnitude of its post-traumatic activation between Avp(di/di) and wild-type rats were observed. These data demonstrate that AVP plays an important role in exacerbating the brain inflammatory response to injury.

Topics: Animals; Blotting, Western; Brain; Brain Injuries; Cells, Cultured; Chemokine CCL2; Chemokine CXCL1; Chemokine CXCL2; Immunohistochemistry; Immunoprecipitation; Inflammation Mediators; JNK Mitogen-Activated Protein Kinases; Male; Rats; Rats, Brattleboro; Rats, Long-Evans; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha; Vasopressins

The San Antonio Vasopressin Symposium reviewed substantial accumulated data concerning vasopressin in haemorrhagic, septic, and cardiac arrest shock conditions and found that there is considerable evidence to support the use of vasopressin in overcoming vasopressin deficiency or insufficiency. The value of vasopressin in the setting of trauma requires further investigation. It was concluded that a large, multicenter controlled trial of vasopressin is needed to assess the therapeutic benefit of vasopressin replacement in the setting of trauma with haemorrhagic shock that is prolonged and profound.

Topics: Brain Injuries; Evidence-Based Medicine; Heart Arrest; Humans; Shock; Texas; 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

To study any possible relation between hyponatremia following brain injury and the presence of cerebral salt-wasting syndrome (CSWS) or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and if vasopressin, brain natriuretic peptide (BNP) and aldosterone have a role in its mechanism.. Patients with brain injury admitted to the intensive care unit were included and had their BNP, aldosterone and vasopressin levels dosed on day 7.. Twenty six adult patients were included in the study. Nine (34.6%) had hyponatremia and presented with a negative water balance and higher values of urinary sodium, serum potassium and diuresis than patients with normonatremia. The serum levels of BNP, aldosterone, and vasopressin were normal and no relation was observed between plasma sodium and BNP, aldosterone or vasopressin.. The most likely cause of hyponatremia was CSWS and there was no correlation between BNP, aldosterone and vasopressin with serum sodium level.

Topics: Adolescent; Adult; Aldosterone; Brain Diseases, Metabolic; Brain Injuries; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuretic Peptide, Brain; Vasopressins; Young Adult

Transplantation of vital human organs is a lifesaving therapy for patients with end-stage organ failure who are medically fit to undergo the surgical procedure. However, deceased donor management remains one of the most neglected areas in transplantation medicine. Brainstem death leads to hemodynamic, metabolic, and immune consequences. Failure to recognize them and provide adequate physiological support accounts for loss of the scarce source of valuable donor organs. Donor optimization leads to increased organ procurement and contributes to improved organ function in the recipient. This article reviews the management advances and controversies of the brainstem-dead donor in an intensive care unit.

Topics: Brain Death; Brain Injuries; Humans; Kidney; Liver; Living Donors; Lung; Reperfusion Injury; Resuscitation; Thyroid Hormones; Tissue and Organ Procurement; Tissue Donors; Vasopressins

To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early post-traumatic hormone alterations.. A 12-month prospective study.. Forty-six consecutive patients with TBI (mild: N = 22; moderate: N = 9; severe: N = 15).. Baseline and stimulated hormone concentrations were assessed in the early phase (0-12 days post-traumatically), and at 3, 6 and 12 months postinjury. Pituitary tests included the Synacthen-test (acute +6 months) and the insulin tolerance test (ITT) or the GHRH + arginine test if the ITT was contraindicated (3 + 12 months). Insufficiencies were confirmed by retesting.. Early post-traumatic hormone alterations mimicking central hypogonadism or hypothyroidism were present in 35 of the 46 (76%) patients. Three months post-traumatically, 6 of the 46 patients failed anterior pituitary testing. At 12 months, one patient had recovered, whereas none developed new insufficiencies. All insufficient patients had GH deficiency (5 out of 46), followed by ACTH- (3 out of 46), TSH- (1 out of 46), LH/FSH- (1 out of 46) and ADH deficiency (1 out of 46). Hypopituitary patients had more frequently been exposed to severe TBI (4 out of 15) than to mild or moderate TBI (1 out of 31) (P = 0.02). Early endocrine alterations including lowered thyroid and gonadal hormones, and increased total cortisol, free cortisol and copeptin were positively associated to TBI severity (P < 0.05), but not to long-term development of hypopituitarism (P > 0.1), although it was indicative in some.. Long-term hypopituitarism was frequent only in severe TBI. During the 3-12 months follow-up, recovery but no new insufficiencies were recorded, indicating manifest hypothalamic or pituitary damage already a few months postinjury. Very early hormone alterations were not associated to long-term post-traumatic hypopituitarism. Clinicians should, nonetheless, be aware of potential ACTH deficiency in the early post-traumatic period.

Topics: Acute Disease; Adolescent; Adrenocorticotropic Hormone; Adult; Brain Injuries; Case-Control Studies; Female; Gonadotropins, Pituitary; Growth Hormone; Humans; Hypopituitarism; Logistic Models; Male; Middle Aged; Odds Ratio; Pituitary Function Tests; Prospective Studies; Thyrotropin; Time; Vasopressins

Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis.. To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI.. Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < or= 8) and an estimated time of injury

Topics: Acute Disease; Adult; Biomarkers; Brain Injuries; Case-Control Studies; Female; Glasgow Coma Scale; Humans; Male; Osmolar Concentration; Prospective Studies; Sodium; Vasopressins; Water-Electrolyte Imbalance

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

Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension.. Prospective randomized, blinded animal study.. University laboratory.. Thirty-three swine.. In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation.. In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin).. Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Topics: Animals; Blood Pressure; Brain Injuries; Fluid Therapy; Intracranial Pressure; Resuscitation; Shock, Hemorrhagic; Swine; Vasopressins

Topics: Brain Injuries; Cerebrovascular Circulation; Humans; Hypotension; Oximetry; Ultrasonography, Doppler, Transcranial; Vasoconstrictor Agents; Vasopressins

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

To investigate the changes and clinical significance of arginine vasopressin (AVP) in elderly patients with acute traumatic cerebral injury.. With radioimmunoassay, the plasma levels of AVP were measured in 32 elderly patients with acute traumatic cerebral injury, 30 traumatic patients without cerebral injury and 30 healthy elderly volunteers, respectively.. The plasma level of AVP in patients with acute traumatic cerebral injury in the early stage (48.30 ng/L +/- 8.28 ng/L) was much higher than that of the traumatic patients without cerebral injury (25.56 ng/L +/- 4.64 ng/L, P<0.01), which was much higher than that of the healthy volunteers (5.06 ng/L +/- 4.12 ng/L, P<0.01). The level of AVP in the patients with acute traumatic cerebral injury was negatively related with GCS scores.. AVP may play an important role in the pathophysiological process in patients with acute traumatic cerebral injury in the early stage. The severer the cerebral injury is, the higher the level of AVP is, which indicates that the level of AVP may be one of the severity indices of traumatic cerebral injury in elderly patients.

Topics: Acute Disease; Aged; Aged, 80 and over; Brain Injuries; Female; Glasgow Coma Scale; Humans; Injury Severity Score; Male; Middle Aged; Neurophysins; Protein Precursors; Vasopressins

Small-dose IV vasopressin infusion may be beneficial in acute brain injury patients with unstable hemodynamics who are refractory to fluid resuscitation and catecholamine vasopressors.

Topics: Brain Injuries; Catecholamines; Humans; Hypotension; Male; Middle Aged; Myocardial Ischemia; Pulmonary Edema; Resuscitation; Vasoconstrictor Agents; Vasopressins

Pial artery dilation in response to activators of the ATP-sensitive K(+) (K(ATP)) and calcium-sensitive K(+) (K(Ca)) channels is impaired after fluid percussion brain injury (FPI). Vasopressin, when coadministered with the K(ATP) and K(Ca) channel agonists cromakalim and NS1619 in a concentration approximating that observed in cerebrospinal fluid (CSF) after FPI, blunted K(ATP) and K(Ca) channel-mediated vasodilation. Vasopressin also contributes to impaired K(ATP) and K(Ca) channel vasodilation after FPI. In addition, protein kinase C (PKC) activation generates superoxide anion (O(2)(-)), which in turn contributes to K(ATP) channel impairment after FPI. We tested whether vasopressin generates O(2)(-) in a protein kinase C (PKC)-dependent manner, which could link vasopressin release to impaired K(ATP) and K(Ca) channel-induced pial artery dilation after FPI.. Injury of moderate severity (1.9 to 2.1 atm) was produced with the lateral FPI technique in anesthetized newborn pigs equipped with a closed cranial window. Superoxide dismutase-inhibitable nitroblue tetrazolium (NBT) reduction was determined as an index of O(2)(-) generation.. Under sham injury conditions, topical vasopressin (40 pg/mL, the concentration present in CSF after FPI) increased superoxide dismutase-inhibitable NBT reduction from 1+/-1 to 23+/-4 pmol/mm(2). Chelerythrine (10(-7) mol/L, a PKC inhibitor) blunted such NBT reduction (1+/-1 to 9+/-2 pmol/mm(2)), whereas the vasopressin antagonist l-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid)2-(o-methyl)-Tyr-arginine vasopressin (MEAVP) blocked NBT reduction. Chelerythrine and MEAVP also blunted the NBT reduction observed after FPI (1+/-1 to 15+/-1, 1+/-1 to 4+/-1, and 1+/-1 to 5+/-1 pmol/mm(2) for sham-, chelerythrine-, and MEAVP-treated animals, respectively). Under sham injury conditions, vasopressin (40 pg/mL) coadministered with cromakalim or NS1619 blunted dilation in response to these K(+) channel agonists, whereas chelerythrine partially restored such impaired vasodilation for cromakalim but not NS1619. Cromakalim- and NS1619-induced pial artery dilation also was blunted after FPI. MEAVP partially protected dilation to both K(+) channel agonists after FPI, whereas chelerythrine did so for only cromakalim responses (for cromakalim at 10(-8) and 10(-6) mol/L, 13+/-1% and 23+/-1%, 2+/-1% and 5+/-1%, 9+/-1% and 15+/-2%, and 9+/-1% and 16+/-2% for sham-, FPI-, FPI-MEAVP-, and FPI-chelerythrine-pretreated animals, respectively).. These data show that vasopressin, in concentrations present in CSF after FPI, increased O(2)(-) production in a PKC-dependent manner and contributes to such production after FPI. These data show that vasopressin contributes to K(ATP) but not K(Ca) channel function impairment in a PKC-dependent manner after FPI and suggest that vasopressin contributes to K(Ca) channel function impairment after FPI via a mechanism independent of PKC activation.

Topics: Adenosine Triphosphate; Animals; Animals, Newborn; Arteries; Benzimidazoles; Brain Injuries; Brain Ischemia; Calcitonin Gene-Related Peptide; Cromakalim; Disease Models, Animal; Enzyme Activation; Enzyme Activators; Enzyme Inhibitors; Female; Male; Pia Mater; Potassium Channels; Protein Kinase C; Superoxides; Swine; Vasodilation; Vasopressins; Wounds, Nonpenetrating; Xanthine Oxidase

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.

Topics: Acute Disease; Adrenocorticotropic Hormone; Aldosterone; Atrial Natriuretic Factor; Brain; Brain Injuries; Child, Preschool; Humans; Hydrocortisone; Hyponatremia; Male; Sodium; Vasopressins

This study was designed to characterize the role of vasopressin in nociceptin/orphanin FQ (NOC/oFQ)-induced impairment of NMDA cerebrovasodilation after fluid percussion brain injury (FPI) as a function of age in newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window. Previous studies have observed that NOC/oFQ is released into CSF and contributes to impaired NMDA induced pial artery dilation following FPI to a greater extent in newborn versus juvenile pigs. Topical vasopressin (40 pg/mL), a concentration approximating that observed in CSF following FPI in the newborn, increased CSF NOC/oFQ from 69 +/- 3 to 102 +/- 8 pg/mol under non-FPI conditions. CSF NOC/oFQ was elevated within 60 min of FPI (70 +/- 3 to 444 +/- 51 pg/mL), but release was attenuated by MEAVP, a vasopressin antagonist, in the newborn (71 +/- 3 to 146 +/- 11 pg/mL). CSF vasopressin and NOC/oFQ were not elevated as greatly in the juvenile following FPI and MEAVP correspondingly did not attenuate CSF NOC/oFQ release as much as in the newborn. Under noninjury conditions, vasopressin (40 pg/mL) coadministered with NMDA (10(-8), 10(-6) M) attenuated pial dilation to this excitatory amino acid (9 +/- 1% and 16 +/- 1% vs. 3 +/- 1% and 5 +/- 2%). Following FPI in the newborn, NMDA-induced pial artery dilation was reversed to vasoconstriction, and both NOC/oFQ and vasopressin receptor antagonists partially prevented these alterations (9 +/- 1%) and 16 +/- 1%, sham control; -7 +/- 1% and -12 +/- 1%, FPI; -2 +/- 1% and -3 +/- 1%, FPI-NOC/oFQ antagonist; and 1 +/- 1% and 4 +/- 1%, FPI-vasopressin antagonist). NMDA-induced pial dilation was only attenuated following FPI in the juvenile and modestly restored by NOC/oFQ and vasopressin receptor antagonists. These data show that vasopressin, in concentrations present in CSF following FPI, contributes to the release of CSF NOC/oFQ following such an insult. The greater release of vasopressin following FPI in the newborn contributes to the corresponding greater release of NOC/oFQ in the newborn versus the juvenile. Moreover, vasopressin also contributes to the impairment of NMDA cerebrovasodilation after brain injury to a greater extent in newborn versus juveniles. These data suggest that vasopressin modulates NOC/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury in an age-dependent manner.

Topics: Aging; Animals; Animals, Newborn; Blood Gas Analysis; Blood Pressure; Brain Injuries; Cerebrovascular Circulation; Excitatory Amino Acid Agonists; Female; Male; N-Methylaspartate; Nociceptin; Opioid Peptides; Receptors, N-Methyl-D-Aspartate; Swine; Vasodilation; Vasodilator Agents; Vasopressins

This study determined if vasopressin generates superoxide anion (O2(-)) in a cyclooxygenase dependent manner and if such production contributes to impairment of dilation to activators of ATP sensitive K(+) (K(ATP)) and calcium sensitive K(+) (K(ca)) channels following fluid percussion brain injury (FPI) in newborn pigs equipped with closed cranial windows. Superoxide dismutase (SOD) inhibitable nitroblue tetrazolium (NBT) reduction was determined as an index of O2(-) generation. Under non-brain injury conditions, topical vasopressin (40 pg/ml, the concentration present in CSF following FPI) increased SOD inhibitable NBT reduction from 1+/-1 to 25+/-4 pmol/mm(2). Indomethacin, a cyclooxygenase inhibitor, blunted such NBT reduction (1+/-1 to 5+/-1 pmol/mm(2)), while the vasopressin antagonist, l-(beta-mercapto-beta beta-cyclopentamethylene propionic acid) 2-(o-methyl)-Tyr-AVP (MEAVP) blocked NBT reduction. MEAVP and indomethacin also blunted the NBT reduction observed after FPI. Under non-brain injury conditions, vasopressin (40 pg/ml) coadministered with the K(ATP) and K(ca) channel agonists, cromakalim and NS1619 (10(-8), 10(-6) M) diminished dilation to these K(+) channel agonists while indomethacin partially prevented such impairment (13+/-1 and 23+/-1 vs. 4+/-1 and 10+/-2 vs. 8+/-1 and 19+/-1% for cromakalim in untreated, vasopressin, and vasopressin plus indomethacin treated piglets, respectively). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI, while indomethacin or MEAVP preadministration partially prevented such impairment (13+/-1 and 23+/-1, sham control; 1+/-1 and 4+/-1, FPI; 8+/-1 and 16+/-3%, FPI-indomethacin pretreated for responses to cromakalim 10(-8), 10(-6) M, respectively). These data show that vasopressin increased O2(-) production in a cyclooxygenase dependent manner and contributed to this production after FPI. These data also show that vasopressin blunted K(ATP) and K(ca) channel mediated cerebrovasodilation in a cyclooxygenase dependent manner. These data suggest that vasopressin induced cyclooxygenase dependent O2(-) generation contributes to K(ATP) and K(ca) channel function impairment after FPI.

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal; Arginine Vasopressin; Benzimidazoles; Blood; Brain Injuries; Brain Ischemia; Calcitonin Gene-Related Peptide; Cerebral Arteries; Cerebrovascular Circulation; Cromakalim; Female; Indomethacin; Male; Potassium Channels; Prostaglandin-Endoperoxide Synthases; Superoxides; Swine; Vasodilation; Vasodilator Agents; Vasopressins

This study was designed to characterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (K(ATP)) and calcium sensitive K (K(ca)) channel following fluid percussion brain injury (FPI) in newborn pigs equipped with a closed cranial window. Topical vasopressin was coadministered with the K(ATP) and K(ca) channel agonists cromakalim and NS1619 in a concentration approximating that observed in CSF following FPI. Vasopressin so administered attenuated pial artery dilation to these K(+) channel activators under conditions of equivalent baseline diameter during non injury conditions (13+/-1 and 23+/-1 vs. 4+/-1 and 10+/-2% for cromakalim 10(-8), 10(-6) M before and after vasopressin, respectively). Attenuated responses were fully restored when these agonists were coadministered with vasopressin and the vasopressin antagonist [l-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid) 2-(o-methyl)-Tyr-AVP] (MEAVP). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and MEAVP preadministration partially prevented such impairment (13+/-1 and 23+/-1, sham control; 2+/-1 and 5+/-1, FPI; and 9+/-1 and 15+/-2%, FPI-MEAVP pretreated for responses to cromakalim 10(-8), 10(-6) M, respectively). These data show that vasopressin blunts K(ATP) and K(ca) channel mediated cerebrovasodilation. These data suggest that vasopressin contributes to impaired K(ATP) and K(ca) channel function after brain injury.

Topics: Animals; Animals, Newborn; Benzimidazoles; Brain Injuries; Cerebral Arteries; Cerebral Veins; Cromakalim; Female; Male; Potassium Channel Blockers; Potassium Channels; Swine; Vasodilation; Vasopressins

In this pilot study, 6 patients who complained of persisting coldness after brain injury were treated with intranasal vasopressin (DDAVP) twice daily for 1 month. Response was assessed after 1 month of treatment, DDAVP was discontinued, and response was reassessed 1 month later. Five of the 6 patients had a dramatic response to DDAVP, as soon as 1 week after initiating treatment, and no longer complained of feeling cold. Response persisted even after discontinuation of treatment. Patients denied any side effects from treatment with DDAVP. The experience of persisting coldness can respond dramatically to brief treatment with intranasal DDAVP. The authors discuss possible mechanisms of action to explain this phenomenon.

Topics: Adolescent; Adult; Body Temperature; Brain Injuries; Cold Temperature; Female; Humans; Middle Aged; Pilot Projects; Vasopressins

Topics: Brain Injuries; Female; Humans; Learning Disabilities; Male; Memory Disorders; Thermosensing; Vasopressins

Pial artery constriction following fluid-percussion injury to the brain is associated with elevated cerebrospinal fluid (CSF) vasopressin concentration in newborn pigs. It has also been observed that fluid-percussion injury reverses the function of vasopressin from that of a dilator to a constrictor. Endothelin-1 (ET-1), a purported mediator of cerebral vasospasm, can be released by several stimuli, including vasopressin. The present study was designed to investigate the role of ET-1 in pial artery constriction and in the reversal of vasopressin from a dilator to a constrictor, which is observed after fluid-percussion injury. Brain injury of moderate severity (1.9-2.3 atm) was produced in anesthetized newborn pigs that had been equipped with a closed cranial window. Endothelin-1 elicited pial dilation at low concentrations and vasoconstriction at higher concentrations. Fluid-percussion injury reversed the process of dilation to that of constriction at the low ET-1 concentration and potentiated this constriction at high ET-1 concentrations (10% +/- 1%, -8% +/- 1%, and -15% +/- 1% vs. -6% +/- 1%, -17% +/- 1%, and -26% +/- 2% for 10(-12), 10(10),10(-8) M ET-1 before and after fluid-percussion injury, respectively). Vasopressin modestly increased CSF ET-1 concentration before fluid-percussion injury. Fluid-percussion injury markedly increased CSF ET-1 concentration and the ability of vasopressin to release ET-1 (20 +/- 2, 26 +/- 3, and 40 +/- 4 pg/ml vs. 93 +/- 6, 141 +/- 9, and 247 +/- 31 pg/ml for control, 40 pg/ml vasopressin, and 400 pg/ml vasopressin before and after fluid-percussion injury, respectively). An ET-1 antagonist, BQ 123 (10(-6) M) blunted pial artery constriction following fluid-percussion injury (146 +/- 5 microns -127 +/- 6 microns vs.144 +/- 5 microns-136 +/- 4 microns). The BQ 123 also blocked the reversal of vasopressin's function from that of a dilator to a constrictor after fluid-percussion injury (8% +/- 1%, 21% +/- 3%, and -5% +/- 1%, -14% +/- 2% vs. 8% +/- 1%, 21% +/- 2% and 4% +/- 1%, 2% +/- 1% for 40 and 4000 pg/ml vasopressin before and after fluid-percussion injury in the absence and presence of BQ 123, respectively). The BQ 123 blocked the constrictor component to ET-1, whereas it had no effect on the dilator component. These data show that ET-1 contributes to pial constriction after fluid-percussion injury. These data also indicate that vasopressin-induced release of ET-1 contributes to the reversal of vasopressin from a dila

Topics: Animals; Animals, Newborn; Brain Injuries; Cerebral Arteries; Dose-Response Relationship, Drug; Endothelin-1; Female; Male; Swine; Vasoconstriction; Vasopressins

Pial artery constriction following fluid percussion brain injury (FPI) is associated with elevated CSF dynorphin and beta-endorphin concentration in newborn pigs. Additionally, dynorphin is a dilator under control conditions and a vasoconstrictor under decreased cerebrovascular tone conditions. Vasopressin contributes to beta-endorphin-induced pial constriction and the constrictor potential for dynorphin. Recently, it has been observed that FPI reverses vasopressin from a dilator to a constrictor. The present study was designed to characterize the effect of FPI on beta-endorphin-induced constriction and the role of vasopressin in that constriction as well as in the reversal of dynorphin's vascular response following FPI. Brain injury of moderate severity (1.9 - 2.3 atm) was produced in anesthetized newborn pigs equipped with a closed cranial window. Dynorphin in physiologic and pharmacologic concentrations (10(-10), 10(-8), 10(-6) M) was reversed from a dilator to a constrictor following FPI (7 +/- 1, 11 +/- 1, and 16 +/- 1 vs -4 +/- 1, -7 +/- 1, and -11 +/- 1% before and after FPI, respectively). Dynorphin-induced vascular changes were accompanied by increased cortical periarachnoid CSF vasopressin and these biochemical changes were potentiated following FPI (24 +/- 4 vs 134 +/- 7 and 53 +/- 7 vs 222 +/- 14 pg/mliter for control and dynorphin (10(-6) M) before and after FPI, respectively). In contrast, in animals pretreated with the vasopressin receptor antagonist [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid) 2-(O-methyl)-Tyr-AVP] (MEAVP, 5 micrograms/kg iv), dynorphin-induced constriction following FPI was attenuated (6 +/- 1, 12 +/- 1, and 16 +/- 1, vs -2 +/- 1, -4 +/- 1, and -7 +/- 1% before and after FPI, respectively). Additionally, beta-endorphin-induced pial constriction was potentiated following FPI (-7 +/- 1, -10 +/- 1, -15 +/- 1 vs -10 +/- 1 -15 +/- 2, and -21 +/- 2% for beta-endorphin (10(-10), 10(-8), 10(-6) M) before and after FPI, respectively). beta-endorphin-induced CSF vasopressin release was similarly potentiated following FPI. Further, MEAVP blunted the augmented constrictor responses to beta-endorphin observed following FPI (-5 +/- 1, -9 +/- 1, -14 +/- 1 vs -2 +/- 1, -5 +/- 1, and -8 +/- 1% before and after FPI, respectively). These data indicate that FPI potentiates beta-endorphin-induced pial construction and reverses dynorphin from a dilator to a constrictor. Additionally, these data show that vasopressin contribu

Topics: Animals; Arteries; beta-Endorphin; Brain Injuries; Cerebrovascular Circulation; Dose-Response Relationship, Drug; Dynorphins; Female; Male; Swine; Vasopressins

The present study was designed to investigate the effect of fluid percussion brain injury (FPI) on vasopressin-induced pial artery vasodilation and the role of superoxide anion generation in those observed effects. In the piglet, it was observed previously the FPI produces pial artery constriction associated with free radical generation. Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. FPI of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Vasopressin in physiological and pharmacological concentrations (10 and 1,000 microU/ml) produced vasodilation that was reversed to constriction after FPI (15 +/- 1 vs. -8 +/- 1 and 25 +/- 1 vs. 13 +/- 1% for 10 and 1,000 microU/ml before and after injury, respectively). Vasopressin-induced dilation was associated with increased cerebrospinal fluid guanosine 3', 5'-cyclic monophosphate, and these biochemical changes were blunted by FPI (407 +/- 12 and 720 +/- 28 vs. 4 and 272 +/- 5 fmol/ml for control and 10 microU/ml before and after injury, respectively). In contrast, polyethylene glycol superoxide dismutase (PEG-SOD) and catalase pretreatment 30 min before FPI partially restored vasopressin-induced pial artery dilation (14 +/- 1 vs. 3 +/- 1 and 22 +/- 1 vs. 2 +/- 4% for 10 and 1,000 microU/ml before and after FPI, respectively). Similarly, biochemical changes associated with vasopressin dilation were also partially restored by PEG-SOD and catalase after FPI. These data show that vasopressin is reversed from a dilator to a vasoconstrictor after FPI and suggests the superoxide anion generation contributes to the alteration of vasopressin cerebrovascular effects after injury and that such altered vasopressin cerebrovascular effects contribute to pial vasoconstriction after FPI.

Topics: Animals; Blood Pressure; Brain Injuries; Catalase; Cerebral Arteries; Cyclic GMP; Female; Male; Nitric Oxide Synthase; Nitroarginine; Pia Mater; Polyethylene Glycols; Superoxide Dismutase; Swine; Vasodilation; Vasopressins

Topics: Atrial Natriuretic Factor; Brain Injuries; Child; Female; Humans; Hyponatremia; Natriuresis; 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

Five children who developed diabetes insipidus as a manifestation of severe brain injury received continuous intravenous treatment with a solution containing both aqueous vasopressin and appropriate crystalloid replacement. Polyuria, hypernatraemia, and decreased urine osmolalities were safely corrected in all patients within eight to 28 hours.

Topics: Adolescent; Brain Injuries; Child; Diabetes Insipidus; Humans; Infant; Infusions, Intravenous; Osmolar Concentration; Sodium; Vasopressins

Nineteen children aged four months to 15 years with diabetes insipidus (DI) secondary to severe brain insults were studied. The main primary brain insult was severe head injury in 12, anoxic ischemic brain damage in four, encephalitis in two, Reye's syndrome in one. Sixteen children died, and three survived. The time from insult to onset of polyuria varied from several hours to one month, and was significantly shorter in head trauma patients, 1.8 +/- 0.9 vs. 9.3 +/- 1.9 days for patients with anoxic ischemic brain damage (p less than 0.03). Twelve of the 19 patients met the criteria for brain death at onset of DI. Treatment by appropriate fluids and vasopressin resulted in resolution of polyuria and increase in urine osmolality. Ten patients developed DI while being treated with dopamine for hemodynamic support. In two of these patients, the cessation of dopamine was time-related to the resolution of DI. Our results indicate that as many as 15% of children with DI (with 95% confidence) following severe brain injury may survive. Hence, despite the overall poor prognosis, its occurrence does not necessarily indicate brain death.

Topics: Adolescent; Brain Damage, Chronic; Brain Death; Brain Injuries; Child; Child, Preschool; Combined Modality Therapy; Diabetes Insipidus; Dopamine; Female; Fluid Therapy; Humans; Infant; Male; Prognosis; Vasopressins

This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.

Topics: Adult; Brain Injuries; Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Vasopressins

Topics: Adult; Brain Injuries; Diabetes Insipidus; Female; Humans; Kidney Concentrating Ability; Suicide, Attempted; Vasopressins

A case of delayed onset of diabetes insipidus (DI), which developed 27 days after a closed head injury, is reported. The patient sustained only a minor neurological deficit and, except for antidiuretic hormone (ADH) insufficiency, hypothalamic function was intact. This selective damage of posterior pituitary function was total and permanent. Ischemia due to vascular injury may be the most likely etiology. Once the diagnosis of delayed posttraumatic DI is confirmed, the treatment of choice is DDAVP (desmopressin acetate). In contradistinction to DI immediately following minor head injury, most patients with a delayed onset of DI after trauma have permanent ADH deficiency.

Topics: Adolescent; Brain Injuries; Diabetes Insipidus; Humans; Male; Vasopressins

Nine children with Schwartz-Bartter-syndrome are described. Seven suffered from severe diseases of the CNS, 2 developed the syndrome during treatment with vincristine, the damaging action of which on the CNS is known. The main symptoms of the syndrome are: hyponatremia with consecutive hypotonia of the extracellular space caused by excessive urinary sodium loss. The plasma volume is not diminished. Therapeutically administered NaCl appears in the urine which is hyperosmolar in spite of the hypoosmolarity of the plasma. The increased secretion of ADH which Schwartz et al. postulated to be the cause of the syndrome has been confirmed in recent years. The organism attempts to excrete the increased fluid volume which is retained by ADH, probably by means of a natriuretic hormone, so-called third factor. Enhanced activity of such a factor was assessed in one of our cases.

Topics: Brain Diseases; Brain Injuries; Cerebrospinal Fluid Shunts; Child; Cysts; Female; Humans; Inappropriate ADH Syndrome; Infant; Male; Tuberculosis, Meningeal; Vasopressins; Vincristine

Topics: Adolescent; Adult; Blood Pressure; Brain Injuries; Diabetes Insipidus; Female; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Vascular Resistance; Vasopressins

Diabetes insipidus (DI) developed in 14 of 16 children who satisfied criteria for brain death. The occurrence of DI after an hypoxic/ischemic insult may represent midbrain death and seems to be a clinically useful sign in the diagnosis of brain death in children. In two patients, DI resolved spontaneously; these patients and children without DI may have had small areas of residual cerebral blood flow and brain function. The onset or cessation of DI was temporally associated with the use of dopamine in three patients.

Topics: Adolescent; Brain Death; Brain Injuries; Child; Child, Preschool; Diabetes Insipidus; Humans; Infant; Vasopressins

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; Adult; Brain Injuries; Brain Neoplasms; Child; Child, Preschool; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Kidney Diseases; Male; Vasopressins

A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.

Topics: Adult; Blood; Blood Volume; Brain Injuries; Extracellular Space; Female; Humans; Hyponatremia; Hypothalamus; Kidney; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Brain Abscess; Brain Injuries; Enterococcus faecalis; Follow-Up Studies; Humans; Male; Meningitis; Military Medicine; Postoperative Complications; Prospective Studies; Pulmonary Embolism; Staphylococcal Infections; Streptococcal Infections; Surgical Wound Dehiscence; Surgical Wound Infection; Transportation of Patients; United States; Vasopressins; Vietnam; Warfare; Wounds, Gunshot

Topics: Adult; Body Water; Brain Injuries; Diabetes Insipidus; Facial Injuries; Female; Fractures, Bone; Humans; Hyponatremia; Hypothalamus; Male; Natriuresis; Osmolar Concentration; Pituitary Gland, Posterior; Prospective Studies; Skull Fractures; Sodium; Vasopressins

Topics: 17-Hydroxycorticosteroids; Blood Glucose; Brain Injuries; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Insulin; Metyrapone; Pituitary Hormone-Releasing Hormones; Pituitary-Adrenal Function Tests; Skull Fractures; Thyroid Function Tests; Thyroid Gland; Vasopressins

Topics: Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Brain Injuries; Circadian Rhythm; Humans; Vasopressins

Topics: Accidents, Traffic; Adolescent; Brain Injuries; Cerebrospinal Fluid Rhinorrhea; Diabetes Insipidus; Eye Injuries; Female; Humans; Lysine; Male; Orbit; Pneumocephalus; Radiography; Tomography; Vasopressins

Topics: Adrenal Insufficiency; Ascites; Brain Injuries; Diabetes Insipidus; Eclampsia; Endocrine System Diseases; Female; Humans; Liver Cirrhosis; Oxytocin; Pregnancy; Vasopressins; Water-Electrolyte Balance

Topics: Brain; Brain Injuries; Brain Neoplasms; Humans; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Topics: Brain; Brain Injuries; Craniocerebral Trauma; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Vasopressins

Topics: Brain; Brain Injuries; Diabetes Insipidus; Humans; Vasopressins; Wounds and Injuries