| Impedance in isolated mouse lungs for the determination of site of action of vasoactive agents and disease. | |
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MedLine Citation:
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PMID: 20162354 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypoxic pulmonary hypertension is a disease of the lung vasculature that is usually quantified by pulmonary vascular resistance (PVR). However, a more complete description of lung vascular function and right ventricular afterload is provided by pulmonary vascular impedance (PVZ) from spectral analysis of pulsatile pressure-flow relationships. We studied pulsatile pressure-flow relationships in isolated, perfused lungs of mice in normoxia, after induction of hypoxic pulmonary hypertension by 10 days of hypoxic exposure, and after the administration of the vasoactive agents sodium nitroprusside and serotonin in order to gain insight into the effects of disease and vasoactive agents on afterload. Chronic hypoxia exposure increased 0 Hz impedance (Z(0)) from 2.0 +/- 0.2 to 3.3 +/- 0.2 mmHg min/mL but decreased characteristic impedance (Z(C)) from 0.21 +/- 0.02 to 0.18 +/- 0.01 mmHg min/mL (both p < 0.05). Sodium nitroprusside only slightly decreased Z(0) but increased Z(C) in normal lungs (p < 0.05) and did not affect Z(C) and decreased Z(0) in hypertensive lungs (p < 0.05). Serotonin increased Z(C) in normal and hypertensive lungs but decreased Z(0) in hypertensive lungs (p < 0.05). There was an inverse correlation between mean pulmonary artery pressure and Z(C) in all circumstances. These findings demonstrate that vasoactive interventions can have different sites of action (i.e., proximal vs. distal segments) in the normal and chronically hypoxic pulmonary vasculature, and the pressure-dependency of Z(C) and R(W). The measurement of PVZ in isolated lungs allows for an improved understanding of the modes of action of drugs and hypoxia on the pulmonary circulation. |
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Authors:
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Rebecca R Vanderpool; Robert Naeije; Naomi C Chesler |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-02-17 |
Journal Detail:
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Title: Annals of biomedical engineering Volume: 38 ISSN: 1521-6047 ISO Abbreviation: Ann Biomed Eng Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-01 Completed Date: 2010-06-29 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0361512 Medline TA: Ann Biomed Eng Country: United States |
Other Details:
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Languages: eng Pagination: 1854-61 Citation Subset: IM |
Affiliation:
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Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI 53706-1609, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia / physiopathology Blood Vessels / physiopathology Cardiovascular Agents / pharmacology* Electric Impedance Hypertension, Pulmonary / physiopathology Lung / blood supply*, physiopathology Male Mice Mice, Inbred C57BL Nitroprusside / pharmacology* Pulmonary Circulation / drug effects* Pulsatile Flow / drug effects Vascular Resistance / drug effects* |
| Grant Support | |
ID/Acronym/Agency:
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1UL1RR025011/RR/NCRR NIH HHS; R01 HL086939-01A1/HL/NHLBI NIH HHS; R01 HL086939-02/HL/NHLBI NIH HHS; R01 HL086939-03/HL/NHLBI NIH HHS; R01 HL086939-03S1/HL/NHLBI NIH HHS; R01 HL086939-04/HL/NHLBI NIH HHS; R01 HL086939-05/HL/NHLBI NIH HHS; R01HL086939/HL/NHLBI NIH HHS; UL1 RR025011-01/RR/NCRR NIH HHS; UL1 RR025011-02/RR/NCRR NIH HHS; UL1 RR025011-03/RR/NCRR NIH HHS; UL1 RR025011-03S1/RR/NCRR NIH HHS; UL1 RR025011-03S2/RR/NCRR NIH HHS; UL1 RR025011-04/RR/NCRR NIH HHS; UL1 RR025011-05/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cardiovascular Agents; 15078-28-1/Nitroprusside |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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