| Pulse pressure-related changes in coronary flow in vivo are modulated by nitric oxide and adenosine. | |
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MedLine Citation:
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PMID: 8831510 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Acute increases in arterial pulsatile load imposed on the left ventricle can increase coronary flow without commensurate changes in myocardial oxygen consumption. One explanation is that augmenting pulsatile perfusion at the same mean pressure itself stimulates flow by releasing endothelium-mediated vasorelaxant factors such as NO. The present study tested this hypothesis and determined whether NO and adenosine modulate this response. In open-chest anesthetized dogs, the distal left anterior descending coronary artery (LAD) was whole-blood-perfused by a novel servopump system to control mean and pulsatile perfusion pressure within the isolated vascular bed. Central aortic pressure was measured, stored to computer memory, and then digitally modified (varying the pulse pressure [PP]) to generate a real-time servocommand that was still synchronous with ventricular contraction. Left heart workload was unchanged. LAD flow was measured before and after increasing the PP (to 60 to 100 mm Hg) from baselines of either 0 or 40 mm Hg. With normal basal coronary vascular tone, raising the PP increased flow (+9 +/- 2% at a PP of 100 mm Hg). This response was markedly amplified (+39 +/- 8%) when basal tone was first partially reduced by adenosine. Competitive inhibition of NO synthase by N omega-monomethyl-L-arginine reduced acetylcholine and PP-dependent flow responses by 50%. Thus, enhanced pulsatile perfusion increases in vivo coronary flow in part by triggering NO release. The marked augmentation of the PP response with reduced basal coronary tone from adenosine suggests that this mechanism may play a role in improving myocardial perfusion during exercise. |
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Authors:
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F A Recchia; H Senzaki; A Saeki; B J Byrne; D A Kass |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Circulation research Volume: 79 ISSN: 0009-7330 ISO Abbreviation: Circ. Res. Publication Date: 1996 Oct |
Date Detail:
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Created Date: 1996-11-27 Completed Date: 1996-11-27 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 849-56 Citation Subset: IM |
Affiliation:
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Division of Cardiology, Johns Hopkins University, Baltimore, Md, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine
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physiology* Animals Blood Pressure* Coronary Circulation / physiology* Dogs Enzyme Inhibitors / pharmacology Nitric Oxide / physiology* Nitric Oxide Synthase / antagonists & inhibitors, physiology omega-N-Methylarginine / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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HL-47511/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 58-61-7/Adenosine; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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