Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1999-2-25
pubmed:abstractText
We hypothesized that the ability of prior hyperglycemia to suppress the sympatho-adrenal response would depend on the type of stress. To test this hypothesis, hyperglycemia was induced in chronically catheterized rats, before submitting them to either hypoxia (7.5% O2) or handling stress. Central venous blood samples were drawn for the determination of plasma glucose, epinephrine (EPI), norepinephrine (NOR) and insulin concentrations. Hypoxia caused significant increases in plasma EPI and NOR concentrations (deltaEPI = + 2.95+/-0.68 nmol/l, deltaNOR = + 12.45+/-1.29 nmol/l). Hyperglycemia, antecedent to hypoxia, dose dependently reduced the sympatho-adrenal response. In contrast, the sympatho-adrenal response to handling stress was not affected by even marked antecedent hyperglycemia (deltaEPI = + 2.48+/-0.46 nmol/l, deltaNOR = + 3.12+/-0.69 nmol/l at glucose = 20.7+/-0.6 mmol/l; vs. deltaEPI = + 2.48 + 0.58 nmol/l, deltaNOR= +2.97+/-0.11 nmol/l at glucose = 6.77+/-0.17 mg/dl). Thus, antecedent hyperglycemia suppresses the hypoxia-induced activation of both the sympathetic nerves and the adrenal medulla, but not the activation induced by handling. We conclude that the ability of hyperglycemia to suppress sympathetic activation depends on the stress producing the activation. We therefore speculate that hypoxic stress has a metabolic component to its central activation that handling stress does not.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0165-1838
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
149-55
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Hyperglycemia suppresses the sympatho-adrenal response to hypoxia, but not to handling stress.
pubmed:affiliation
Division of Endocrinology and Metabolism, Veterans Affairs Medical Center, Seattle, WA 98108, USA. b.benthem@biol.rug.nl
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't