title: Reversal of dyskinesis by increased end diastolic segment length in ischaemic-reperfused myocardium.
abstract: Persistent dyskinesis is universally observed after reperfusion of a severely ischaemic segment. Although inotropic stimulation shows a latent contractile reserve, it is not known whether this reserve can be recruited by increasing end diastolic segment length (local length-tension relation). To investigate this, six anaesthetised open chest dogs were placed on right heart bypass to increase end diastolic segment length independently of mean arterial pressure. Instantaneous left ventricular pressure-segment length relations and fractional systolic shortening were determined by sonomicrometry in the centre of the region perfused by the left anterior descending coronary artery during sequential increases in end diastolic segment length. Measurements were made before occlusion of the left anterior descending coronary artery, during 1 h of occlusion, and after 2 h of reperfusion. Before ischaemia, segmental shortening increased from 11.0(SEM 1.6)% to 23.5(1.5)% (p less than 0.05) as end diastolic segment length increased. Dyskinesis developed during occlusion of the left anterior descending coronary artery [12.1(2.6)% control v -7.2(1.6)% occlusion, p less than 0.05] and was present over the entire range of end diastolic segment lengths. Following reperfusion, segmental dyskinesis [-2.5(2.4)%] persisted at the lower end of the range of end diastolic segment length, but was progressively replaced by active shortening, averaging 7.3(3.2)% (p less than 0.05) as end diastolic segment length was sequentially increased. We conclude that segmental function following reperfusion is sensitive to changes in end diastolic segment length, and that active shortening is recruited from an apparently dyskinetic segment as end diastolic segment length progressively increases.
authors.affiliation: Department of Cardiothoracic Surgery, Bowman Gray School of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.
authors.forename: J
authors.initials: J
authors.lastname: Vinten-Johansen
authors.forename: P J
authors.initials: PJ
authors.lastname: Carroll
authors.forename: W E
authors.initials: WE
authors.lastname: Johnston
authors.forename: W C
authors.initials: WC
authors.lastname: Little
authors.forename: V
authors.initials: V
authors.lastname: Chiantella
authors.forename: J S
authors.initials: JS
authors.lastname: Julian
authors.forename: A R
authors.initials: AR
authors.lastname: Cordell
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002315:Cardiopulmonary Bypass; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000601:surgery; D004285:Dogs; D008026:Ligation; D009200:Myocardial Contraction; D015425:Myocardial Reperfusion; D013997:Time Factors