C. J. Dunn

CYCLIC ADENOSINE 3′, 5′-MONOPHOSPHATE AND THE MECHANISM OF ACTION OF THREE COMMON ANTI-INFLAMMATORY DRUGS

1 The effects of indomethacin, dexamethasone and colchicine on cyclic adenosine 3′, 5′‐monophosphate (cyclic AMP) concentration in leucocytes during a crystal‐induced pleurisy in rats were studied. 2 Each of the drugs significantly increased leucocyte cyclic AMP content within 3 h of the injection of crystals. 3 By 6 h, leucocyte cyclic AMP levels were returning toward control levels and could not be sustained at the higher level by an additional administration of the respective anti‐inflammatory drug.

Leukocyte migration inhibition activity of nonimmune acute inflammatory pleural exudate

Material with leukocyte migration inhibition (LMI) activity has been demonstrated in various types of nonimmunologically induced acute pleural inflammatory exudates. This activity is present in inflammatory cell-free exudate and appears to involve the deposition of fibrin around the migrating leukocyte, resulting in “cell-trapping”. This is supported by the fact that removal or inhibition of fibrin formation leads to loss of exudate LMI activity. Both fibrinogen and complement as well as vitamin K-dependent clotting factors appear to be required for LMI activity. The mechanism involved in the LMI reaction and its significance in nonimmune and cell-mediated immune inflammation are discussed.

The role of kallikrein in leukocyte migration inhibition

Previous studies from this department have established the presence of leukocyte migration inhibition activity in acute nonimmune inflammatory rat pleural exudates, induced by different irritants, which involved coagulation phenomenon. In the present investigation we present evidence for a role of kallikrein in the leukocyte migration inhibition phenomenon exhibited by acute pleural exudate in rats depleted of kininogens by intravenous injection of cellulose sulfate.