Journal of Applied Physiology, Vol 59, Issue 1 180-182, Copyright © 1985 by American Physiological Society
Regulation of increase in anastomotic blood flow following pulmonary arterial occlusion
S. K. Jindal, S. Lakshminarayanan, W. Kirk and J. Butler
We have previously shown that there is an acute increase in anastomotic
bronchial blood flow (Qbr) after pulmonary arterial obstruction in dogs. We
examined the role of arachidonic acid metabolites in mediating this
increase. The left lower lobe (LLL) was isolated and perfused (zone 2) with
autologous blood in open-chested anesthetized dogs (n = 19). Qbr was
measured from the amount of blood that overflowed from the closed vascular
circuit of the suspended LLL and changes in its weight. In the control
animals, there was a prompt and significant increase in Qbr following
pulmonary arterial obstruction. Pretreatment with indomethacin (n = 6) or
sodium salicylate (n = 4) almost completely blocked this rise in Qbr.
Following pulmonary arterial occlusion, there was a rise in both
thromboxane and a prostacyclin metabolite (6-keto-PGF1 alpha) in the blood
of the pulmonary circulation of the LLL, although the 6-keto-PGF1 alpha
rose relatively more. Pretreatment with indomethacin caused a fall in both
thromboxane and prostacyclin levels (n = 3), which no longer rose after
pulmonary arterial occlusion. These findings suggested that the balance of
the vasodilator (prostacyclin) and vasoconstrictor (thromboxane)
prostaglandins may play an important role in mediating the rise in Qbr that
follows pulmonary arterial obstruction.
