| The mechanism of nitrous oxide-induced changes in pulmonary vascular resistance in a dog model of left atrial outflow obstruction. | |
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MedLine Citation:
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PMID: 2520935 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Nitrous oxide has been reported to increase pulmonary vascular resistance (PVR) in patients with pulmonary hypertension secondary to mitral stenosis. Additional data suggest this response involves sympathetic stimulation because the increase in PVR can be prevented by alpha-adrenergic and ganglionic blockade. Whether or not active pulmonary vasoconstriction occurs remains unclear. This study was designed to more fully characterize the influence of N2O on pulmonary hemodynamics during left atrial outflow obstruction (LAO). Responses in an in situ blood-perfused lung lobe were compared with those in the remaining intact lung of six dogs anesthetized with pentobarbital, 30 mg/kg, and morphine, 1.5 mg/kg, and prepared for measurement of peak left ventricular (LV) pressure, LV end-diastolic pressure (LVEDP), LV dP/dt, systemic arterial and pulmonary arterial (PA) pressures, and cardiac output (CO). The pulmonary artery branch supplying the left middle lung lobe was cannulated and perfused at a constant rate with warmed blood. LAO was produced by filling the balloon of a Foley catheter positioned in the left atrium (LA) with enough saline to increase PA pressure by 50%; the balloon was subsequently left filled for the entire protocol. Measurements were first obtained during ventilation with 67% N2, and 33% O2. The inspired gas was then changed to 67% N2O and 33% O2 for 10 minutes, and then returned to the N2/O2 mixture. Once baselines had been reestablished (about 10 minutes), phentolamine, 0.75 mg/kg, was administered, and the response to 10 minutes of N2O again observed. N2O did not change vascular resistance in the isolated lobe, but increased intact-lung PVR.(ABSTRACT TRUNCATED AT 250 WORDS) |
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Authors:
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P M Heerdt; R W Caldwell |
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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: Journal of cardiothoracic anesthesia Volume: 3 ISSN: 0888-6296 ISO Abbreviation: J Cardiothorac Anesth Publication Date: 1989 Oct |
Date Detail:
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Created Date: 1992-08-18 Completed Date: 1992-08-18 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8709732 Medline TA: J Cardiothorac Anesth Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 568-73 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, University of Tennessee, Memphis. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anesthesia, Inhalation* Animals Atrial Function, Left / drug effects Blood Pressure / drug effects Cardiac Output / drug effects Dogs Lung / blood supply* Nitrous Oxide / pharmacology* Phentolamine / pharmacology Pulmonary Artery / physiopathology Pulmonary Circulation / drug effects Stroke Volume / drug effects Vascular Resistance / drug effects* Ventricular Function, Left / drug effects Ventricular Outflow Obstruction / physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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HBLI-17796/HB/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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10024-97-2/Nitrous Oxide; 50-60-2/Phentolamine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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