Abstract
In the course of an investigation of the possible role of diuresis as a contributing factor in the production of nonocclusive mesenteric infarction, blood flows were monitored in the superior mesenteric artery (SMA) and the thoracic aorta. Intravenous injection of the diuretic, furosemide, as a bolus at doses of 0.5 – 10.0 mg./kg. produced an early rise in SMA flow that peaked at about 2 minutes and lasted for 6–10 minutes. The ratio of SMA to thoracic aorta flow also increased. The increase in SMA flow and in the ratio were both dose dependent and statistically significant. Therefore, if furosemide administration is associated with nonocclusive mesenteric infarction, this is due to the secondary effects of vigorous diuresis and not to a primary action of the drug.
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