Document Detail


Intact nitric oxide production is obligatory for the sustained flow response during hypercapnic acidosis in guinea pig heart.
MedLine Citation:
PMID:  15769448     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: The mechanisms underlying hypercapnic coronary dilation remain unsettled. This study tests the hypothesis that flow dependent NO production is obligatory for the hypercapnic flow response. METHODS/RESULTS: In isolated, constant pressure (CP) perfused guinea pig hearts a step change of arterial pCO(2) from 38.6 to 61.4 mm Hg induced a bi-phasic flow response with an early transient (maximum 60 s) and a consecutive persisting flow rise (121.6+/-6.6 (S.D.) % after 10 min). In contrast, when perfused with constant flow (CF), perfusion pressure only transiently (2 min) fell by 7.4+/-4.8 % following the step change of arterial pCO(2). In CP perfused hearts L-NAME (100 micromol/l) specifically abolished the delayed flow rise during hypercapnic acidosis (102.37+/-2.9% after 10 min), whereas the inhibitor had no effect on perfusion pressure response in CF perfused hearts. Under CP perfusion arterial hypercapnia resulted in a transient rise of coronary cGMP release (from 0.69+/-0.35 to 1.12+/-0.68 pmol/ml), which was abolished after L-NAME. Surprisingly, the K(+)ATP channel blocker glibenclamide did not have any significant effect on the hypercapnic flow response but largely blunted reactive hyperemia after a 20 s flow stop. CONCLUSIONS: The delayed steady state hypercapnic flow response in guinea pig heart requires intact NO production. The absence of a persisting decrease in coronary resistance under CF perfusion points to an important role of shear stress dependent NO production.
Authors:
Anke Heintz; Thea Koch; Andreas Deussen
Related Documents :
492348 - Rat jejunum perfused in situ: effect of perfusion rate and intraluminal radius on absor...
21311298 - Favorable outcome in traumatic brain injury patients with impaired cerebral pressure au...
1535028 - Effect of hypertension and hypertrophy on coronary microvascular pressure.
23149558 - Critical closing pressure determined with a model of cerebrovascular impedance.
8033508 - Sympathetic restraint of baroreflex control of heart period in normotensive and hyperte...
2197008 - Intraoperative anaphylaxis to latex.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-12-19
Journal Detail:
Title:  Cardiovascular research     Volume:  66     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-03-16     Completed Date:  2005-08-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  55-63     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Intensive Care Medicine, Medical Faculty Carl Gustav Carus, University Hospital Dresden, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Anke.Heintz@mailbox.tu-dresden.de
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acidosis / metabolism,  physiopathology*
Animals
Coronary Circulation* / drug effects
Endothelium, Vascular / metabolism*
Female
Glyburide / pharmacology
Guinea Pigs
Hypercapnia / metabolism,  physiopathology*
Male
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / metabolism*
Nitric Oxide Synthase / antagonists & inhibitors
Oxygen Consumption
Perfusion
Potassium Channel Blockers / pharmacology
Potassium Channels / metabolism
Time Factors
Vasodilation / drug effects,  physiology
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 10102-43-9/Nitric Oxide; 10238-21-8/Glyburide; 17035-90-4/omega-N-Methylarginine; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase
Comments/Corrections
Comment In:
Cardiovasc Res. 2005 Apr 1;66(1):7-8   [PMID:  15769442 ]

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


Previous Document:  Human cord blood cells induce angiogenesis following myocardial infarction in NOD/scid-mice.
Next Document:  Gap junctional remodeling by hypoxia in cultured neonatal rat ventricular myocytes.