Abstract:
OBJECTIVE:The aim was to investigate the ventricular/vascular coupling of the intact right heart under conditions of normal operation and acute pulmonary hypertension. METHODS:Right ventricular contractility was obtained by calculating the end systolic pressure-volume relationship (Ees) and the effective pulmonary arterial elastance (Ea), applying the Windkessel parameters of the pulmonary arterial input impedance. Coupling between the ventricle and its load could be determined in terms of Ees and Ea. Acute pulmonary hypertension was induced by injecting glass microspheres into the pulmonary vascular bed until a mean pulmonary arterial pressure of more than 35 mm Hg had been reached. Experimental subjects were Landras/Large white pigs (n = 11), studied under general anaesthesia. Ees was obtained by normalising the right ventricle pressure-diameter equivalent of Ees to stroke volume. The lumped element parameters of the Windkessel analogue were calculated from the pulmonary artery pressure and blood flow. Stroke work was calculated from the pressure-volume loop and oxygen consumption derived from the pressure-volume area. Efficiency was taken to be the ratio between stroke work and oxygen consumption. RESULTS:Ea increased significantly as mean pulmonary artery pressure rose, while Ees remained linear and constant. Stroke work, as well as efficiency, increased, with the maximum of the stroke work curve lying to the right of the efficiency maximum. At the control step (before pulmonary artery hypertension), Ees = 1.71 Ea (n = 11). CONCLUSIONS:Under control conditions, the right ventricle operates at maximum efficiency and submaximal work output. Compliance of the pulmonary artery is a significant factor in decoupling the right ventricle from its vascular load. As the compliance decreases with acute pulmonary hypertension, the maximum stroke work against load point shifted in such a manner that the right ventricle changed its operational status from a flow to a pressure pump, resulting in a decreased stroke volume.
journal_name
Cardiovasc Resjournal_title
Cardiovascular researchauthors
Fourie PR,Coetzee AR,Bolliger CTdoi
10.1093/cvr/26.9.839subject
Has Abstractpub_date
1992-09-01 00:00:00pages
839-44issue
9eissn
0008-6363issn
1755-3245journal_volume
26pub_type
杂志文章abstract::Regional myocardial anoxia was produced in dogs by perfusion of the left circumflex artery (LCA) with deoxygenated blood. Isolated sarcoplasmic reticulum fragments (cardiac relaxing system) showed decreased Ca2+ binding and uptake. The ability of isolated mitochondria to utilise long-chain fatty acids was markedly red...
journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/11.6.568
更新日期:1977-11-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(03)00330-4
更新日期:2003-06-01 00:00:00
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journal_title:Cardiovascular research
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更新日期:2001-02-16 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvaa288
更新日期:2020-12-01 00:00:00
abstract::To define the interactions between blood and endocardium damaged by lactic acid, the left ventricles of 48 isolated continuously perfused and beating hearts were exposed for 0-4 hours to Krebs Henseleit buffer (KHB) with or without 33 mumol.ml-1 of lactic acid (pH 6.4). After excising its apex, the left ventricle was ...
journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/23.6.478
更新日期:1989-06-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/23.5.400
更新日期:1989-05-01 00:00:00
abstract:OBJECTIVE:Inhibitors of poly (ADP-ribose) synthetase (PARS) activity reduce the infarct size caused by regional myocardial ischaemia and reperfusion in the rabbit and rat in vivo. The mechanism of action of these inhibitors is unclear. Here we investigate the effects of the PARS inhibitor 3-aminobenzamide (3-AB) on inf...
journal_title:Cardiovascular research
pub_type: 杂志文章
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更新日期:1999-01-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/17.6.344
更新日期:1983-06-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/28.3.312
更新日期:1994-03-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2003.11.009
更新日期:2004-02-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/21.5.337
更新日期:1987-05-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(97)00222-8
更新日期:1998-01-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvq061
更新日期:2010-08-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/17.12.767
更新日期:1983-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:
更新日期:1995-04-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(96)00167-8
更新日期:1996-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/24.6.456
更新日期:1990-06-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvq328
更新日期:2011-02-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(02)00243-2
更新日期:2002-05-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2005.04.034
更新日期:2005-09-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(00)00320-5
更新日期:2001-04-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2005.05.025
更新日期:2005-11-01 00:00:00
abstract::The mechanisms whereby glucose reduces fatty acid-induced release of enzyme from the coronary-ligated isolated perfused working rat heart are investigated. Alterations in the tissue contents of ATP, phosphocreatine, or glycogen could be excluded as possible mechanisms for the beneficial effect of glucose in this syst...
journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/13.12.693
更新日期:1979-12-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 临床试验,杂志文章
doi:10.1093/cvr/27.8.1477
更新日期:1993-08-01 00:00:00
abstract::Myocardial capillary permeability was determined in 20 dogs by applying a new method which resembles the tissue-uptake technique. The method consisted of a bolus injection of 51Cr-EDTA into the left atrium, determination of the average arterial tracer concentration and subsequent assay of myocardial tissue activity 10...
journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/18.5.277
更新日期:1984-05-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2006.10.003
更新日期:2007-03-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2005.11.021
更新日期:2006-03-01 00:00:00
abstract::Platelet-dependent thrombus formation is a key event in the pathogenesis of acute myocardial infarction (AMI). Platelets mediate both thrombotic occlusion of the entire epicardial coronary artery and also accumulate in the microcirculation resulting in impairment of microcirculation and provoking myocardial ischemia d...
journal_title:Cardiovascular research
pub_type: 杂志文章,评审
doi:10.1016/j.cardiores.2003.11.036
更新日期:2004-02-15 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvq296
更新日期:2011-02-01 00:00:00
abstract:BACKGROUND:The mechanism of defibrillation is controversial. Reentry appearing immediately after the shock has been shown to be responsible for defibrillation failure in some studies while other studies have demonstrated that a rapid train of focal activations with the first focus appearing >50 ms after the shock is re...
journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2003.10.009
更新日期:2004-01-01 00:00:00