Document Detail

Influence of hypoxia/ischemia on cerebrovascular responses to oxytocin in piglets.
MedLine Citation:
PMID:  9256092     Owner:  NLM     Status:  MEDLINE    
We examined the effects of hypoxic/ischemic stress on cerebral arteriolar responses to oxytocin in anesthetized piglets. Pial arteriolar diameters were measured using a cranial window and intravital microscopy. First, we evaluated arteriolar responses to topical application of oxytocin during normoxic conditions. We then determined whether 5-10 min of arterial hypoxia, ischemia, or asphyxia alters oxytocin-induced responses. Arterial hypoxia was produced by inhalation of 7.5% O2-92.5% N2 for 10 min. Ischemia was achieved by increasing intracranial pressure for 10 min. Asphyxia was achieved by turning off the ventilator for 5 min. During normoxic conditions, oxytocin dilated pial arterioles by 9 +/- 1% at 10(-8) and by 16 +/- 1% at 10(-6) mol/l (n = 47, p < 0.05). Arteriolar responses to oxytocin did not change with repeated applications (n = 10). Following hypoxia, dilator effect of oxytocin was not changed at 10(-8) (8 +/- 2%) but it was reduced at 10(-6) mol/l (7 +/- 2%; p < 0.05, n = 8). After asphyxia or ischemia, oxytocin did not dilate arterioles at 10(-8) mol/l, whereas 10(-6) mol/l resulted in a mild vasoconstriction (-4 +/- 3 to -6 +/- 4%, n = 6 and 8). Topically applied superoxide dismutase did not preserve arteriolar responses to oxytocin after asphyxia although the arterioles did not constrict to 10(-6) mol/l oxytocin (n = 5). Dilatation of cerebral arterioles in response to oxytocin was reversed to constriction by N(omega)-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg, i.v.; n = 5) and by endothelial impairment by intra-arterial infusion of phorbol ester (10[-5] mol/l; n = 5). We conclude that the absence of pial arteriolar dilation to oxytocin after ischemia and asphyxia indicates endothelial dysfunction which may be involved in the pathology of perinatal brain injury.
F Bari; R A Errico; T M Louis; D W Busija
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of vascular research     Volume:  34     ISSN:  1018-1172     ISO Abbreviation:  J. Vasc. Res.     Publication Date:    1997 Jul-Aug
Date Detail:
Created Date:  1997-09-03     Completed Date:  1997-09-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9206092     Medline TA:  J Vasc Res     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  312-20     Citation Subset:  IM    
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, N.C. 27157-1083, USA.
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MeSH Terms
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Animals, Newborn
Anoxia / physiopathology*
Brain / blood supply*
Brain Ischemia / physiopathology*
Cerebrovascular Circulation / drug effects*
Nitric Oxide / physiology
Oxytocin / pharmacology*
Potassium Channels / physiology
Prostaglandin Endoperoxides, Synthetic / pharmacology
Superoxides / metabolism
Thromboxane A2 / analogs & derivatives,  pharmacology
Vasoconstrictor Agents / pharmacology
Grant Support
Reg. No./Substance:
0/Potassium Channels; 0/Prostaglandin Endoperoxides, Synthetic; 0/Vasoconstrictor Agents; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; 50-56-6/Oxytocin; 57576-52-0/Thromboxane A2; 76898-47-0/15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid

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