ROLE OF PROSTAGLANDIN-E IN HEMODYNAMIC RESPONSE TO AORTIC CLAMPING AND DECLAMPING

  • 1 January 1976
    • journal article
    • research article
    • Vol. 80  (1) , 137-144
Abstract
The infrarenal aorta was occluded for 1 h in 11 control dogs and in 8 dogs in which biosynthesis of prostaglandin E (PGE) was inhibited by administration of indomethacin (2.5 mg/kg). The mean arterial pressure (MAP) in the indomethacin group was significantly (P < 0.001) higher than in the control group at the end of 60 min of aortic occlusion (187 .+-. 3 vs. 137 .+-. 4 mm. Hg, mean .+-. SEM) and remained higher (P < 0.001) after declamping. However, the decline in MAP at the time of aortic declamping was essentially the same for both groups. Total peripheral resistance (TPR) was higher in the indomethacin group than in the control group at the end of 1 h of occlusion (159 .+-. 13 vs. 124 .+-. 12%, P < 0.001) and remained higher throughout the period following occlusion. The plasma concentration of PGE in the control group increased significantly (P < 0.05) above control (630 .+-. 110 to .+-. 261 1299 pg/ml) during the 60 min period of occlusion with further increases to 1447 .+-. 389 and 1523 .+-. 256 pg/ml (P < 0.001) at 10 and 60 s after declamping, respectively. In the indomethacin group, PGE remained essentially unchanged throughout the clamping and declamping period and therefore was significantly (P < 0.05) lower than in the control group. A similar pattern was observed in the tissue levels of PGE. PGE is probably released during and after infrarenal aortic occlusion and may be responsible for maintaining reduced TPR and MAP. However, hypotension after declamping is not affected by inhibition of PGE biosynthesis.