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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The transcatheter method appropriate for use in the control of arteriocapillary gastrointestinal bleeding is a point of controversy. Intraarterial
vasopressin
infusion, which has been performed in more than 500 patients at the Massachusetts General Hospital, has achieved control in 90% of patients actively bleeding from the stomach and colon. In view of the severity of hemorrhage and associated illnesses in these patients, the complication rate associated with this method was low. Intraarterial
vasopressin
infusions were ineffective in pyloroduodenal and postoperative bleeding sites and hemorrhage from abscesses. While embolization can control bleeding in these areas, complications have been shown despite precise selective catheter placement. Because of catheterization difficulties and the permanency of the vascular occlusion, embolization is
reserved
for patients in whom surgical intervention would be associated with extreme risks.
...
PMID:Transcatheter embolization versus vasopressin infusion for the control of arteriocapillary gastrointestinal bleeding. 697 77
Vasopressin produced analgesia in mice as estimated by using abdominal constriction tests (ED50 8.5 micrograms/kg i.v.) or hot plate method (ED50 63 micrograms/kg i.v.). However,
vasopressin
(10 micrograms/kg i.v.) produced no depression of locomotor activity in mice. Vasotocin had slight analgesic action; oxytocin or norepinephrine had none and there was no direct correlation between pressor response and analgesia. The analgesic action was nonopiate in nature as it was uninfluenced by the narcotic antagonist naltrexone at 5 to 15 mg/kg, but it was
reserved
by a
vasopressin
antagonist. Intraventricular administration of
vasopressin
(1-10 micrograms/kg) to mice produced no significant analgesia, suggesting a primarily peripheral locus of analgesic action. Vasopressin may play a role as an endogeneous pain regulating substance.
...
PMID:Characterization of vasopressin analgesia. 705 94
The term heart failure is a complex of clinical syndromes caused by "neuroendocrine" compensatory responses that are renal, neural, hormonal and hemodynamic in nature. Activation of these multiple systems--as a result of renin, angiotensin II and the action of circulatory catecholamines--causes the release of norepinephrine
vasopressin
and aldosterone. These responses contribute to the arteriolar constriction and salt and water retention that promote central pooling with an increase in pre- and afterload of the already failing heart, causing deterioration of the congestive heart failure (CHF). Therapy for this clinical syndrome is aimed at reducing both pre- and afterload with vasodilators, which produce a profoundly favorable effect on left ventricular performances. Beta blocking agents, which inhibit the increased sympathetic mediated vasoconstriction, up-regulate beta receptors and thus restore responsiveness to the failing heart. Inotropic agents, such as digitalis and amrinone/milrinone are
reserved
for patients with dilated failing heart and impaired systolic function; recently a synthetic atrial natriuretic factor has been developed for potential use in CHF. Ultrafiltration is also used in refractory preoperative CHF with cardiac abnormalities. Neuroendocrine responses to CHF are treated today directly by improving central hemodynamic imbalance in these patients.
...
PMID:Management of congestive heart failure: neuroendocrine approach. 845 56
A systematic review of available treatments for controlling active variceal bleeding provides important guidelines for choosing an overall strategy. The initial prerequisite of a diagnostic endoscopy provides the opportunity for early intervention with local endoscopic techniques, such as injection sclerotherapy, direct intravariceal injection of tissue adhesives and banding ligation of varices. This approach currently represents the optimal strategy. If the endoscopic expertise is not available, the use of vasoactive drugs may provide temporary control of bleeding while allowing time for more definitive treatment. Vasopressin and its analogues are the most widely used vasoactive drugs, but somatostatin holds promise. In view of the systemic haemodynamic complications associated with
vasopressin
(and probably glypressin), these drugs should be given in combination with nitrates. Balloon tamponade remains an important alternative for patients in whom massive, life-threatening haemorrhage has occurred. Surgical techniques, such as shunting and devascularisation, are increasingly
reserved
for the management of variceal bleeding that endoscopic therapy has failed to control.
...
PMID:The management of active variceal bleeding. 849 68
Decreases in blood pressure are well known to increase the release of
vasopressin
. Studies were carried out to investigate whether
vasopressin
responses to postural changes in blood pressure are maintained in diabetic patients with orthostatic hypotension [DM-OH(+)] as well as non-diabetic patients with orthostatic hypotension [nonDM-OH(+)] and these responses were compared with those observed in normal subjects and diabetic patients without orthostatic hypotension [DM-OH(-)]. After 30 min in the supine position, the upright posture for 40 min was maintained and then the supine for 10 min. Blood pressure and heart rate (HR) were measured every 5 min and plasma
vasopressin
levels (plasma AVP) were determined every 10 min. In normal subjects and DM-OH(-), mean arterial blood pressure (MABP) did not change, but HR increased significantly by the upright position. Plasma AVP did not change in these groups. On the other hand, in DM-OH(+) MABP fell abruptly and remained to decrease during the upright posture. The HR responses in this group, however, were similar to those in normal control and DM-OH(-). Plasma AVP in DM-OH(+) significantly increased only at 30 min during upright. These increases were significantly greater than those in normal and DM-OH(-). There were significant correlation in changes in MABP (delta MAP) and plasma AVP (delta AVP) in DM-OH(+) (delta AVP = -0.13 MABP + 1.5, r = -0.32, p < 0.01). Relationship between delta MABP and delta AVP in nonDM-OH(+) was similar to that in DM-OH(+). It is concluded that AVP responses to orthostatic hypotension in diabetic and non-diabetic neuropathies were attenuated, but heart rate responses in these patients ware well
reserved
.
...
PMID:Changes in plasma vasopressin levels and cardiovascular function due to postural changes in diabetic neuropathy. 869 86
Diabetes insipidus is a heterogeneous condition characterized by polyuria and polydipsia caused by a lack of secretion of
vasopressin
, its physiological suppression following excessive water intake, or kidney resistance to its action. In many patients, it is caused by the destruction or degeneration of the neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus. Known causes of these lesions include: germinoma or craniopharyngioma; Langerhans cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma following surgery or accident; and, rarely, genetic defects in
vasopressin
biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Magnetic resonance imaging (MRI) allows identification of the posterior pituitary hyperintensity and of hypothalamic-pituitary abnormalities. Thickening of the pituitary stalk is the second most common finding on MRI scans in several local inflammatory pathologies and autoimmune diseases or germinoma, but it is not specific to any single subtype. A progressive increase in the size of the anterior pituitary gland should alert physicians to the possibility that a germinoma is present, whereas a decrease can suggest the presence of an inflammatory or autoimmune process. Most children with acquired central diabetes insipidus and a thickened pituitary stalk have anterior pituitary hormone deficiencies during follow-up. Biopsy of enlarged pituitary stalk should be
reserved
for patients with a hypothalamic-pituitary mass and progressive thickening of the pituitary stalk, since spontaneous recovery may occur.
...
PMID:Diabetes insipidus. 1256 20
Ascites accumulation is the product of a complex process involving hepatic, renal, systemic, hemodynamic, and neurohormonal factors. The main pathophysiologic theories of ascites formation include the "underfill," "overflow," and peripheral arterial vasodilation hypotheses. These theories are not necessarily mutually exclusive and are linked at some level by a common pathophysiologic thread: The body senses a decreased effective arterial blood volume, leading to stimulation of the sympathetic nervous system,
arginine-vasopressin
feedback loops, and the renin-angiotensin-aldosterone system. Cornerstones of ascites management include dietary sodium restriction and diuretics. Spironolactone is generally tried initially, with furosemide added if clinical response is suboptimal. More refractory patients require large-volume paracentesis (LVP) accompanied by volume expansion with albumin. Placement of a transjugular intrahepatic portosystemic shunt is
reserved
for individuals with compensated liver function who require very frequent sessions of LVP. Peritoneovenous shunts are not used in contemporary ascites management. Liver transplantation remains the definitive therapy for refractory ascites. Although treatment of ascites fails to improve survival, it benefits quality of life and limits the development of such complications as spontaneous bacterial peritonitis.
...
PMID:Pathophysiology and management of pediatric ascites. 1273 47
Traditionally, embolization has been
reserved
for treatment of upper gastrointestinal bleeding whereas lower gastrointestinal (LGI) bleeding has been controlled with
vasopressin
infusion. This is based on findings in older literature in which infarction frequently complicated LGI embolization. With modern embolization techniques, clinically significant bowel ischemia has become an uncommon complication. Although the efficacies of
vasopressin
and embolization are fairly comparable, embolotherapy has advantages in terms of quicker completion of therapy and decreased likelihood of systemic complications. Although
vasopressin
is still probably preferable for diffuse lesions and cases in which superselective catheterization is not technically possible, embolization should be considered a primary option for treating LGI bleeding.
...
PMID:Treatment of lower gastrointestinal bleeding: vasopressin infusion versus embolization. 1276 6
Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate
antidiuretic hormone
(SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy
reserved
for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.
...
PMID:Management of hyponatremia. 1516 58
Diabetes insipidus is a heterogeneous condition characterised by polyuria and polydipsia caused by a lack of secretion of
vasopressin
, its physiological suppression following excessive water intake, or kidney resistance to its action. The clinical and laboratory diagnosis is confirmed by standard tests, but recent advances in molecular biology and imaging techniques have shed new light on the pathophysiology of this disease. In many patients, central diabetes insipidus is caused by a germinoma or craniopharyngioma; Langerhans' cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma from surgery or accident; and, rarely, genetic defects in
vasopressin
biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Tumour-associated central diabetes insipidus is uncommon in children younger than 5 years old. Biopsy of enlarged pituitary stalk should be
reserved
for patients with hypothalamic-pituitary mass and progressive thickening of the pituitary stalk since spontaneous recovery may occur. Molecular biology in selected patients may identify those with apparently idiopathic diabetes insipidus carrying the
vasopressin-neurophysin II
gene mutation.
...
PMID:Current perspective on the pathogenesis of central diabetes insipidus. 1612 39
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