Document Detail


Chronic prenatal exposure to cocaine alters cerebrovascular responses in newborn pigs.
MedLine Citation:
PMID:  15337837     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Maternal cocaine abuse may increase the incidence of perinatal asphyxia. In nonexposed asphyxiated neonates, decreased cerebrospinal fluid (CSF) cAMP concentrations are associated with poor neurological outcome. On the other hand, cocaine increases central nervous system (CNS) cAMP. Therefore, we hypothesized that in utero cocaine exposure may increase brain cAMP and thereby preserve cerebrovascular responses to cAMP-dependent stimuli following asphyxia. Pregnant pigs received either cocaine (1 mg/kg, i.v.) twice weekly during the last trimester or normal saline vehicle (sham-control) and were allowed to deliver vaginally at term. Cranial windows were implanted in the newborn pigs within the first week of life and used to collect CSF for cAMP determinations and to assess changes in pial arteriolar diameters (PAD). In the first part of the study, pial arteriolar responses to different vasodilator and vasoconstrictor stimuli were evaluated in piglets prior to asphyxia (n = 20). In newborn pigs exposed to cocaine, cerebrovascular responses to hypercapnia and norepinephrine were significantly exaggerated compared to controls. Then, piglets were randomly selected for the second part of the study that involved prolonged asphyxia (n = 12). In cocaine-exposed but not sham-control piglets, CSF cAMP increased markedly during asphyxia. In the sham piglets, but not the cocaine-exposed piglets, CSF cAMP fell progressively below the baseline during recovery. Cerebrovascular reactivity to cAMP-dependent stimuli (hypercapnia and isoproterenol) was preserved during recovery from asphyxia in the cocaine-exposed piglets but significantly attenuated in the sham controls. We conclude that piglets with chronic prenatal exposure to cocaine show exaggerated cerebrovascular responses to vasogenic stimuli and preserved cAMP-dependent cerebral vasoreactivity following asphyxia.
Authors:
Massroor Pourcyrous; Henrietta S Bada; Kari E Blaho; Mildred M Randolph; Helena Parfenova; Timothy D Mandrell; Kris Arheart; Sheldon B Korones; Charles W Leffler
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Experimental biology and medicine (Maywood, N.J.)     Volume:  229     ISSN:  1535-3702     ISO Abbreviation:  Exp. Biol. Med. (Maywood)     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-08-31     Completed Date:  2004-10-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100973463     Medline TA:  Exp Biol Med (Maywood)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  819-25     Citation Subset:  IM    
Affiliation:
Laboratory for Research in Neonatal Physiology, Department of Pediatrics, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA. mpourcyrous@utmem.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Arterioles / drug effects,  physiopathology
Blood Pressure / drug effects
Carbon Dioxide / blood
Cerebrovascular Circulation / drug effects*
Cocaine / toxicity*
Cyclic AMP / cerebrospinal fluid,  metabolism
Female
Hydrogen-Ion Concentration
Muscle, Smooth, Vascular / drug effects,  physiopathology
Oxygen / blood
Partial Pressure
Pregnancy
Prenatal Exposure Delayed Effects*
Swine
Chemical
Reg. No./Substance:
124-38-9/Carbon Dioxide; 50-36-2/Cocaine; 60-92-4/Cyclic AMP; 7782-44-7/Oxygen

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


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