Depressed inotropic response to increased preload in rabbit hearts with left-ventricular dysfunction induced by chronic myocardial infarction

Chronic (8 weeks) coronary artery ligation caused marked left-ventricular dysfunction (LVD) in rabbits. The positive inotropic effect observed in vivo with intraventricular injection of saline in sham-operated (control) animals was reversed in rabbits with LVD. In vitro, a step increase in filling p...

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Bibliographic Details
Published in:Pflügers Archiv 2002-07, Vol.444 (4), p.513-522
Main Authors: Ng, G Andre, Hicks, Martin N, Cobbe, Stuart M, Smith, Godfrey L
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - physiology
Cardiac Output - physiology
Chronic Disease
Heart - physiopathology
Heart attacks
Male
Myocardial Contraction - physiology
Myocardial Infarction - physiopathology
Organ Culture Techniques
Rabbits
Ventricular Dysfunction, Left - physiopathology
Ventricular Function, Left - physiology
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Summary:Chronic (8 weeks) coronary artery ligation caused marked left-ventricular dysfunction (LVD) in rabbits. The positive inotropic effect observed in vivo with intraventricular injection of saline in sham-operated (control) animals was reversed in rabbits with LVD. In vitro, a step increase in filling pressure from 10 to 15 cm H(2)O caused an immediate increase, followed by a slow increase, in left-ventricular peak systolic pressure (LVP(max)) and cardiac output (CO) over 5-7 min in sham-operated hearts. No significant slow positive inotropic effect was observed in hearts with LVD in response to a standard increase in filling pressure. Progressive increases in filling pressure increased (LVP(max)) and CO to a maximum value at 20 cm H(2)O in control hearts. In the LVD group, progressive increases in filling pressure caused a negative inotropic response and reduced CO. Hearts from the LVD group were significantly dilated compared with control hearts but no significant changes in myocardial compliance were observed in beating or quiescent hearts. These studies reveal an impaired inotropic response to increased ventricular filling in LVD rabbit hearts; this defect included the depression of the slow inotropic response to an increased end-diastolic volume. These changes appear not to be accompanied by altered passive mechanical properties.
ISSN:0031-6768
1432-2013
DOI:10.1007/s00424-002-0848-3