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Since the mechanism by which oxygen reduces infarct size is not yet completely understood, we tested the hypothesis that breathing 100% oxygen may alter regional myocardial blood flow. In 23 anaesthetised open-chest dogs with acute occlusions of the left anterior descending coronary artery or of its apical branch, regional myocardial blood flow was determined by the microsphere technique at 15 and 30 min following coronary artery occlusion. Fifteen treated dogs were ventilated with 100% oxygen beginning 17 min after occlusion (ie, after the first determination of regional myocardial blood flow) and continuing until the end of the experiment, while the other 8 dogs served as controls and were ventilated continuously with room air. In treated dogs, following the administration of 100% oxygen, transmural flow at sites remote from the distribution of the occluded vessel (nonischaemic sites) decreased from 121 +/- 5 before oxygen to 108 +/- 6 cm3 . min-1 . 100g-1 (P less than 0.05). However, in the ischaemic sites it increased from 28 +/- 3 before oxygen to 32 +/- 3 cm3 . min-1 . 100g-1 (P less than 0.05). In the control dogs transmural flow, 15 and 30 min after occlusion, was, in nonischaemic sites, 118 +/- 7 and 125 +/- 10 cm3 . min-1 . 100g-1 NS, and in the ischaemic sites 27 +/- 4 and 25 +/- 3 cm3 . min-1 . 100g-1 NS, respectively. Thus, ventilation with 100% oxygen can augment perfusion of the ischaemic myocardium and this may be, in part, the mechanism by which it reduces infarct size.

Colour flow Doppler maps the extent of the flow velocity disturbance of aortic regurgitation onto the two dimensional echocardiographic image of the left ventricular cavity. The spatial extent of this flow velocity disturbance expressed as a percentage of end diastolic left ventricular cavity area (CD%) was compared to regurgitant fraction (RF), measured volumetrically, in nine open chest dogs with varying degrees of surgically created aortic regurgitation (RF 0-85%). Right heart bypass controlled venous return to the left atrium and hence net left ventricular output, while total left ventricular output was measured with an aortic electromagnetic flow probe under various loading conditions, achieving mean diastolic transvalvular pressure gradients of 23-114 mm Hg, net left ventricular outputs of 750-3000 ml.min-1 and diastolic filling periods of 162-320 ms. A linear correlation between CD% and RF (r = 0.89) was demonstrated over this wide range of loading conditions. At a given transvalvular diastolic pressure gradient [68(SD9) mm Hg] CD% was linearly proportional to regurgitant aortic orifice area (r = 0.87). Thus CD% is proportional to the volumetric severity of aortic regurgitation under a wide range of haemodynamic conditions and varies appropriately with regurgitant aortic orifice area when diastolic transvalvular pressure gradient is held constant. The application of these principles to the non-invasive quantitation of valvular regurgitation by colour Doppler appears feasible.

In order to measure the protective effect of interventions following coronary artery occlusions in dogs, the creatine kinase activity of myocardial tissue was assayed after 24 h and related to the myocardial blood flow of that tissue measured with 85Sr labelled microspheres injected 15 min after occlusion. This assay showed normal levels when flow exceeded 50 cm3.min-1.100 g-1. In myocardium with flow reduced to 0 to 15 cm3. min-1.100g-1, creatine kinase activity was 7.6 +/- 0.6 IU.mg-1 protein in control dogs and 13.1 +/- 1.8 IU.mg-1 protein (P less than 0.01) in dogs given 500 NF units.kg-1 of hyaluronidase 20 min after occlusion. Where myocardial blood flow was reduced to 16 to 50 cm3. min-1. 100g-1, creatine kinase activity was increased from 14.1 +/- 1.1 to 20.5 +/- 1.4 IU.mg-1 protein by hyaluronidase. This method therefore assesses ischaemic damage independent of electrophysiological measurements and confirms myocardial preservation by hyaluronidase.