| Muscle microvascular oxygenation in chronic heart failure: role of nitric oxide availability. | |
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MedLine Citation:
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PMID: 16911248 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM: To test the hypothesis that diminished vascular nitric oxide availability might explain the inability of individuals with chronic heart failure (CHF) to maintain the microvascular PO(2)'s (PO(2mv) proportional, variant O(2) delivery-to-uptake ratio) seen in healthy animals. METHODS: We superfused sodium nitroprusside (SNP; 300 microm), Krebs-Henseleit (control, CON) and L-nitro arginine methyl ester (L-NAME; 1.5 mM) onto the spinotrapezius muscle and measured PO(2mv) by phosphorescence quenching in female Sprague-Dawley rats (n = 26) at rest and during twitch contractions (1 Hz). Seven rats served as controls (Sham) while CHF was induced by myocardial infarction. CHF rats were grouped as moderate (MOD; n = 15) and severe CHF (SEV; n = 4) according to morphological data and baseline PO(2mv). RESULTS: In contrast to Sham and MOD, L-NAME did not affect the PO(2mv) response (dynamics and steady-state) of SEV when compared with CON. SNP restored the PO(2mv) profile of SEV to that seen in Sham animals during CON. Specifically, the effect of L-NAME expressed as Delta(L-NAME - CON) were: Baseline PO(2mv) [in mmHg, DeltaSham = -7.0 +/- 1.6 (P < 0.05); DeltaSEV =-1.2 +/- 2.1], end-contractions PO(2mv) [in mmHg, DeltaSham = -5.0 +/- 1.0 (P < 0.05); DeltaSEV = -2.5 +/- 0.5] and time constant of PO(2mv) decrease [in s, DeltaSham = -6.5 +/- 3.0 (P < 0.05); DeltaSEV = -3.2 +/- 1.8]. CONCLUSION: These data provide the first direct evidence that the pathological profiles of PO(2mv) associated with severe CHF can be explained, in part, by a diminished vascular NO availability. |
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Authors:
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L F Ferreira; K S Hageman; S A Hahn; J Williams; D J Padilla; D C Poole; T I Musch |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Acta physiologica (Oxford, England) Volume: 188 ISSN: 1748-1708 ISO Abbreviation: Acta Physiol (Oxf) Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-08-16 Completed Date: 2007-05-29 Revised Date: 2009-02-03 |
Medline Journal Info:
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Nlm Unique ID: 101262545 Medline TA: Acta Physiol (Oxf) Country: England |
Other Details:
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Languages: eng Pagination: 3-13 Citation Subset: IM |
Affiliation:
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Clarenburg Research Laboratory, Department of Anatomy and Physiology, and Department of Kinesiology, Kansas State University, Manhattan, KS 66506-5802, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Vessels / metabolism* Exercise Tolerance Heart Failure / metabolism* Male Microcirculation Muscle, Skeletal / blood supply* Myocardial Infarction / metabolism NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / metabolism* Nitric Oxide Synthase / antagonists & inhibitors Nitroprusside / pharmacology Oxygen / metabolism* Rats Rats, Sprague-Dawley Vasodilator Agents / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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AG-19228/AG/NIA NIH HHS; HL-50306/HL/NHLBI NIH HHS; HL-69739/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 50903-99-6/NG-Nitroarginine Methyl Ester; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase |
| Comments/Corrections | |
Comment In:
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Acta Physiol (Oxf). 2006 Sep;188(1):1
[PMID:
16911247
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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