Linked Life Data

2183937

Source:http://linkedlifedata.com/resource/pubmed/id/2183937

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1990-5-29
pubmed:abstractText
STUDY OBJECTIVE - Catecholamine concentrations are raised during endotoxin shock and may be responsible for myocardial insulin resistance in such a condition. The purpose of the investigation was to examine the effect of insulin on myocardial contractility and glucose uptake in the presence of beta adrenergic blockade during endotoxin shock. DESIGN - Endotoxin shock was obtained in dogs by giving S Typhimurium endotoxin intravenously (1 mg.kg-1) and the cardiac responses to insulin were determined under hyperinsulinaemic (4 U.min-1) euglycaemic clamp conditions during continuous beta adrenergic blockade (propranolol 150 micrograms.kg-1 + 5 micrograms.kg-1.min-1). SUBJECTS - 19 mongrel dogs of either sex, weight 20-25 kg, were studied under pentobarbitone anaesthesia. Seven dogs received endotoxin plus propranolol, and seven others received propranolol alone (control group). Five dogs received endotoxin but no propranolol or insulin. All other procedures were the same in each group. MEASUREMENTS and RESULTS - The exposed heart was prepared for coronary sinus blood sampling and measurements of circumflex artery blood flow (Q), instantaneous left ventricular pressure, and left ventricular wall thickness. Glucose uptake was calculated from product of Q and aortic-coronary sinus concentration difference. End systolic pressure-dimension relationship was used to assess contractility. Myocardial performance was assessed from left ventricular dP/dtmax. Basal shock measurements were made 60 min post endotoxin. beta Adrenergic blockade did not interfere with insulin stimulated glucose uptake in controls, but was unable to restore the uptake response during endotoxin shock. Contractility was increased during endotoxin shock and this effect was abolished by beta adrenergic blockade. In controls the only variable affected by beta adrenergic blockade was left ventricular dP/dtmax (decreased). Insulin increased contractility during beta adrenergic blockade in controls but not in shock. Myocardial performance was depressed during shock. In controls, insulin increased myocardial performance; in shock this response was attenuated. CONCLUSIONS - The findings confirm that the myocardium becomes less responsive to the glucose uptake stimulating and positive inotropic effects of insulin during endotoxin shock. The data show that beta adrenergic activity is responsible for the increased contractile state of the heart during acute endotoxin shock, but is not the cause of the observed insulin resistant state.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
72-80
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Insulin and beta adrenergic effects during endotoxin shock: in vivo myocardial interactions.
pubmed:affiliation
Department of Surgery, Loyola University Medical Center, Maywood, IL 60153.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't