Document Detail


Beneficial effect induced by a beta-adrenoceptor blocker on fetal growth in streptozotocin-diabetic rats.
MedLine Citation:
PMID:  9096896     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Treatment by a beta 1-beta 2-adrenoceptor antagonist has been much used during pathological pregnancies. These agents can reduce the oxygen consumption of the myocardium, increase the coronary blood flow towards ischemic heart areas and improve return of venous blood flow towards the heart. The aim of this study was to determine the mechanism of action of this agent and to investigate whether a total beta-adrenoceptor antagonist could reduce the fetoplacental disorders elicited in streptozotocin-diabetic pregnant rats. Diabetes was engendered on day 7.5 of pregnancy, and the animals were studied on day 21. Untreated nondiabetic rats or nondiabetic rats treated with propranolol, a total beta-adrenoceptor blocker (2 mg kg-1/ day, i.p.), had a healthy placenta without vascular disturbances, with normal arterial blood velocity in the uterine artery, placenta, umbilical cord and fetal aorta, and showed eutrophic fetuses (3.9 +/- 0.0 g, mean +/- SEM). Untreated diabetic rats had severe placental lesions, with a reduction of arterial blood velocity in the uterine artery (p < 0.01), placenta (p < 0.01) and umbilical artery (p < 0.05), and exhibited fetal hypotrophy (2.3 +/- 0.1 g, mean +/- SEM, p < 0.001) compared with nondiabetic untreated rats. Treatment of diabetic rats with propranolol (2 mg kg-1/day, i.p.) enhanced fetal weight (3.66 +/- 0.2 g) and slightly increased fetal insulin secretion, restored arterial blood velocity to control values in the uterine artery and fetal aorta and reduced placental lesions. In conclusion, our results suggest that the beneficial effects of propranolol were at least in part related to an improvement of uteroplacental hemodynamics; it induced a better redistribution of the blood towards the placenta and the fetal systemic circulation. Propranolol treatment could protect cell membranes against free oxygen radicals and lipid peroxidation, involved in the pathogenesis of ischemic injury in diabetes.
Authors:
M Clabaut; B Stirnemann; B Bouftila; I Robert
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Biology of the neonate     Volume:  71     ISSN:  0006-3126     ISO Abbreviation:  Biol. Neonate     Publication Date:  1997  
Date Detail:
Created Date:  1997-06-09     Completed Date:  1997-06-09     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0247551     Medline TA:  Biol Neonate     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  171-80     Citation Subset:  IM    
Affiliation:
Laboratory of Feto-Maternal Physiology, Faculty of Sciences, University of Rouen, Mont-Saint-Aignan, France.
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MeSH Terms
Descriptor/Qualifier:
Abortion, Veterinary / prevention & control
Adrenergic beta-Antagonists / pharmacology*
Animals
Blood Flow Velocity / drug effects
Blood Glucose / metabolism
Diabetes Mellitus, Experimental / physiopathology*
Embryonic and Fetal Development / drug effects*
Female
Heart Rate / drug effects
Insulin / blood
Organ Size / drug effects
Placenta / drug effects,  pathology,  physiopathology
Pregnancy
Pregnancy in Diabetics / physiopathology*
Propranolol / pharmacology*
Pulse / drug effects
Rats
Rats, Wistar
Receptors, Adrenergic, beta-1 / physiology
Receptors, Adrenergic, beta-2 / physiology
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Blood Glucose; 0/Receptors, Adrenergic, beta-1; 0/Receptors, Adrenergic, beta-2; 11061-68-0/Insulin; 525-66-6/Propranolol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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