Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1981-6-23
pubmed:abstractText
Arginine vasopressin, the antidiuretic hormone in man, in low concentrations increases reabsorption of water in the collecting ducts of the kidney, producing a concentrated urine. It is also a potent vasoconstrictor because of its direct effect on arteriolar smooth muscle, particularly the splanchnic, renal, and coronary vascular beds. This appears to be a dose-dependent response. In very high concentrations it is capable of producing a diuresis with increased urinary sodium excretion. The preponderance of evidence today has failed to show any significant increase in antidiuretic hormone levels with anesthesia alone, provided significant hemodynamic changes do not occur. It seems unlikely, then, that the inhalation anesthetics or high-dose narcotic anesthesia are a direct stimulus to ADH release. If a decrease in urine flow does occur, it is more likely caused by either the renal hemodynamic effects of the anesthetic or a secondary release of ADH. Surgical stimulation is capable of significantly increasing ADH levels. This apparently is a stress response that can be attenuated by the depth of anesthesia. Such a response to operation may produce ADH levels that can indeed decrease urinary flow, but more importantly may succeed in achieving levels that can exert a significant vasopressor effect. In unusual circumstances, vasopressin levels can occur that are capable of producing a diuresis and increased urine sodium excretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0191-247X
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
29-38
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
The effects of anesthesia on antidiuretic hormone.
pubmed:publicationType
Journal Article, Review