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

Cerebrospinal fluid (CSF) levels of vasopressin (AVP) are elevated in some disorders associated with raised intracranial pressure. We have previously demonstrated that intracerebroventricular infusion of AVP in the conscious goat leads to elevation of intracranial pressure by a mechanism independent of changes in arterial blood pressure or circulating neurohypophysial peptide concentrations. We have now examined the effect of increasing CSF AVP levels on CSF dynamics using the technique of ventriculo-cisternal perfusion in the conscious goat. Intracerebroventricular perfusion with 5 pmol/min AVP in artificial CSF did not alter CSF formation rate but significantly reduced CSF absorption rate (24% decrease; p less than 0.01), when compared with perfusion using artificial CSF alone. This AVP-mediated reduction in CSF absorption rate may represent increased resistance to resorption of CSF or may reflect the effect of raised intracranial pressure.
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PMID:Intracerebroventricular vasopressin reduces CSF absorption rate in the conscious goat. 185 57

A case of tuberculous meningitis in a 2-year-old boy is reported. The main critical care problems are irregular breathing, raised intracranial pressure and syndrome of inappropriate secretion of antidiuretic hormone. Cranial CT-Scan and ventricular shunting are shown to be of high importance for this disease.
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PMID:[Tuberculous meningitis in intensive care]. 666 Apr 47

This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture. Increased intracranial pressure, which releases vasopressin by altering normal hypothalamic anatomy, may represent a unique type of stress to neuroendocrine systems and may contribute to adrenal secretion by a mechanism that requires intact brainstem function. Endocrine function should be monitored in brain-injured patients with basilar skull fractures and protracted posttraumatic amnesia, and patients with SIADH or DI should be closely monitored for other endocrine abnormalities.
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PMID:Neuroendocrine abnormalities in patients with traumatic brain injury. 1153 74