Regional myocardial blood flow and segmental wall function after oxyfedrine administration in the ischaemic porcine heart

Summary: The effects of the cardiostimulant oxyfedrine on segmental myocardial wall function and regional myocardial blood flow were investigated in normally perfused and ischaemic regions in the porcine heart. Myocardial ischaemia was induced by reducing the left anterior descending coronary artery flow to approximately 40% of its baseline value. Six animals served as controls, while oxyfedrine (0.15 mg·kg-1) was administered to 11 animals after 10 min of flow reduction. The induction of ischaemia caused the maximum rate of rise of left ventricular pressure to decrease by 30 %, mean arterial blood pressure and cardiac output to decrease by 10%, while heart rate remained unchanged. Oxyfedrine increased the maximum rate of left ventricular pressure development to 25% above its baseline value, the mean arterial blood pressure to pre-occlusion values, and heart rate by 20%. Flow reduction resulted in a decrease in the flow to the central core of the ischaemic area from 1.27±0.19 to 0.67±0.15 cm3·min-1·g-1 and decreased the endo/epi-ratio from 0.96±0.03 to 0.65± 0.13 (P <0.001). Oxyfedrine increased the flow to the ischaemic area to 1.01 ±0.21 cm3·min-1·g-1 (P <0.05), but did not affect the endo /epi-ratio. The flow to the normally perfused region increased from 1.30±0.16 to 1.41 ±0.13 cm3·min-1·g-1. Without pronounced effects on the end-diastolic myocardial wall thickness (EDT), the mean velocity of systolic wall thickening, which declined to virtually zero during flow reduction, increased to 40% of the baseline value after drug administration. The systolic thickening itself returned to 18 ±5% of EDT; the values at the baseline and during flow reduction being 49 ±5 and 5.2 ±2.3% of EDT, respectively. The combined effect on the end-systolic thickness was a return to 78 % of the baseline value. It is concluded that oxyfedrine increases the blood flow to both the normal and the ischaemic myocardium, the velocity of systolic myocardial wall thickening and improves the ischaemic myocardial performance.

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