Linked Life Data

11551850

Source:http://linkedlifedata.com/resource/pubmed/id/11551850

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-9-11
pubmed:abstractText
This study was aimed at assessing the role of carotid body function in neuroendocrine and glucoregulatory responses to exercise. The carotid bodies and associated nerves were removed (CBR, n = 6) or left intact (Sham, n = 6) in anesthetized dogs >16 days before experiments, and infusion and sampling catheters were implanted. Conscious dogs were studied at rest and during 150 min of exercise. Isotopic dilution was used to assess glucose production (R(a)) and disappearance (R(d)). Arterial glucagon was reduced in CBR compared with Sham at rest (29 +/- 3 vs. 47 +/- 3 pg/ml). During exercise, glucagon increased more in Sham than in CBR (47 +/- 9 vs. 15 +/- 2 pg/ml). Cortisol and epinephrine levels were similar in the two groups at rest and during exercise. Basal norepinephrine was similar in CBR and Sham. During exercise, norepinephrine increased by 432 +/- 124 pg/ml in Sham, but by only 201 +/- 28 pg/ml in CBR. Basal arterial plasma glucose was 108 +/- 2 and 105 +/- 2 mg/dl in CBR and Sham, respectively. Arterial glucose dropped by 10 +/- 3 mg/dl at onset of exercise in CBR (P < 0.01) but was unchanged in Sham (decrease of 3 +/- 2 mg/dl, not significant). Basal glucose kinetics were equal in Sham and CBR. At onset of exercise, R(a) and R(d) were transiently uncoupled in CBR (i.e., R(d) > R(a)) but were closely matched in Sham. In steady-state exercise, R(a) and R(d) were closely matched in both groups. Insulin was equal in the basal period and decreased similarly during exercise. These studies suggest that input from the carotid bodies, or receptors anatomically close to them, 1) is important in control of basal glucagon and the exercise-induced increment in glucagon, 2) is involved in the sympathetic response to exercise, and 3) participates in the non-steady-state coupling of R(a) to R(d), but 4) is not essential to glucoregulation during sustained exercise.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E742-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11551850-Animals, pubmed-meshheading:11551850-Blood Glucose, pubmed-meshheading:11551850-Carotid Body, pubmed-meshheading:11551850-Dogs, pubmed-meshheading:11551850-Epinephrine, pubmed-meshheading:11551850-Fatty Acids, Nonesterified, pubmed-meshheading:11551850-Female, pubmed-meshheading:11551850-Glucagon, pubmed-meshheading:11551850-Glycerol, pubmed-meshheading:11551850-Homeostasis, pubmed-meshheading:11551850-Hormones, pubmed-meshheading:11551850-Hydrocortisone, pubmed-meshheading:11551850-Insulin, pubmed-meshheading:11551850-Lactates, pubmed-meshheading:11551850-Liver, pubmed-meshheading:11551850-Male, pubmed-meshheading:11551850-Neurosecretory Systems, pubmed-meshheading:11551850-Norepinephrine, pubmed-meshheading:11551850-Physical Conditioning, Animal, pubmed-meshheading:11551850-Physical Exertion, pubmed-meshheading:11551850-Rest, pubmed-meshheading:11551850-Time Factors
pubmed:year
2001
pubmed:articleTitle
Role of carotid bodies in control of the neuroendocrine response to exercise.
pubmed:affiliation
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't