Blood flow, oxygen consumption, and free fatty acid release in subcutaneous adipose tissue during hemorrhagic shock in control and phenoxybenzamine-treated dogs.

Dogs were anesthetized with a-D (+)-glucochloralose. After bleeding to a mean arterial pressure of 55 mm Hg, blood flow in subcutaneous adipose tissue decreased from 6 ± 0.9 (mean±SE) to 0.6 ± 0.21 ml/min/100 g (P < 0.001), and remained at that low level during bleeding to 35 mm Hg for an additional 90-minute period. In five out of nine experiments the blood flow ceased completely. Sixty minutes after reinfusion, the blood flow was significantly lower than control, and in two there was no blood flow after reinfusion. In animals previously treated with phenoxybenzamine (5 mg/kg), the decrease in blood flow was significant only at 35 mm Hg arterial pressure (2.6 ± 0.67 ml/min/100 g). After reinfusion blood flow increased to a mean above 10 ml/min/100 g, significantly higher than resting blood flow (P < 0.05). There was no significant change in arterial FFA concentration or FFA release in subcutaneous adipose tissue during bleeding and after reinfusion. In phenoxybenzamine-treated animals there was a tendency to have higher arterial FFA concentration and FFA release. The oxygen uptake fell from 0.47 ±0.07 to 0.13 ±0.05 ml/min/100 g (P<0.01) during 55 mm Hg arterial pressure and remained significantly lower also during 35 mm Hg arterial pressure. Previous treatment with phenoxybenzamine prevented a fall in O2 uptake in subcutaneous adipose tissue. The decrease in blood flow in subcutaneous adipose tissue during bleeding was more pronounced than found in other organs with same hemorrhagic shock procedure. After reinfusion, flow in subcutaneous adipose tissue could not be restored, indicating irreversible vascular damage, a-receptor activity seems to play a significant part in the development of vascular and metabolic changes in subcutaneous adipose tissue during bleeding. ADDITIONAL