Effect of amrinone on diaphragm blood flow

The purpose of the present study was to examaine the effect of amrinone, a drug known to augment cardiac output and dilate peripheral vascular beds, on diaphragm blood flow. Studies were performed on 12 anesthetized mechanically ventilated dogs in which strips of left costal diaphragm were developed in situ. Strip blood flow was assessed with a drop counter attached to a catheter tied into the phrenic veins' draining strips. Strip tension was measured with an isometric force transducer. Amrinone was administered as an intravenous bolus of 2 mg/kg followed by a continuous infusion of 25 μg.kg^-1.min^-1. Amrinone increased cardiac output and resting diaphragm blood flow [from 1.8 ± 0.1 to 3.2 ± 3 (SE) l/min and from 13 ± 2 to 29 ± 6 (SE) ml.100 g^-1.min^-1, respectively, P <0.001 for both comparisons]. Amrinone also increased blood flow during periods of rhythmic contraction (tension time indexes of 0.1-0.4, P <0.05 for comparisons of flow with and without amrinone at each tension time index) and increased the magnitude of the postcontraction hyperemia (P < 0.02 for comparisons of hyperemic flow with and without amrinone at tension time indexes of 0.3 and 0.4). Graded occlusion of the inferior vena cava produced reductions in arterial pressure, cardiac output, and diaphragm blood flow both before and after amrinone. Both cardiac output and diaphragm blood flow were greater after amrinone, however, at all levels of blood pressure examined. These findings indicate that amrinone can override diaphragm vasoregulatory systems and augment diaphragm blood flow. The fact that this agent increased, rather than reduced, the degree of postcontraction hyperemia suggests, however, that this drug may not decrease the metabolic debt accumulated during periods of strenuous contraction despite the higher levels of blood flow.