Propranolol and vagal nerve stimulation do not affect postsystolic shortening during acute myocardial ischaemia in the dog.

Changes in myocardial segment length (ultrasonic crystals) and myocardial blood flow (15(3) microns microspheres) were studied during 5 min occlusions of the left anterior descending coronary artery in open chest anaesthetised dogs, and the effects of occlusion without intervention were compared with those of occlusion during bilateral vagal nerve stimulation (n = 11) and occlusion after administration of 1 mg.kg-1 propranolol (n = 9) in the same dogs. Delineation of the perfusion beds of occluded and non-occluded arteries at necropsy verified placement of the crystals at the centres and immediately within the borders of the ischaemic areas. In untreated animals (n = 6) systolic shortening during occlusion decreased by 160(2)% (dyskinesis) in the centre zone and by 61(1)% (hypokinesis) in the border zone of ischaemia, myocardial blood flow decreased by 96(2)% in the centre and 81(2)% at the border, and the changes were reproducible over three successive occlusions. Postsystolic shortening (after peak decline of left ventricular pressure) was reproducible in control animals over three occlusions, was similar in magnitude to the magnitude of dyskinesis (centre zone) or to the degree of hypokinesis (border zone), and persisted after the release of occlusion. Vagal stimulation and propranolol decreased dyskinesis during occlusion but did not affect postsystolic shortening or collateral blood flow within the ischaemic zones. If postsystolic shortening of dyskinetic centre zone segments represents residual active shortening of these segments, as is suggested by other evidence, these results suggest that the oxygen sparing effects for very ischaemic myocardium of vagal stimulation and propranolol do not include a significant reduction in residual active shortening.