Thrombin-induced vasodilation in the hindlimb (dog).

The objective of this study is to test the hypothesis that the vasodilation produced by intra-arterial injection of thrombin to the hindlimb of a dog may be caused by the secondary release or production of some vasodilating substance. The vasodilator response to thrombin was compared with the vasodilator response to acetylcholine, isoproterenol, histamine and serotonin before and after blockade with atropine, propranolol, phenergan or methyl-D-lysergic acid butanolamide (UML-491), respectively. Though the appropriate blocking agent blocked the vasodilator response to the respective drug, the thrombin-induced vasodilation was not blocked. These data support the hypothesis that thrombin-induced vasodilation is a response to the thrombin moiety.

Vasodilator effect of thrombins prepared from normal or deficient human or canine plasmas.

Thrombins prepared from plasmas deficient in various clotting factors are capable of inducing vasodilator response to the hindlimb of the dog and this response proved to be similar to that produced by thrombins prepared from normal plasmas. Thus the vascular effect of thrombin is not mediated by any other clotting factor which might be present in small amounts in the thrombin preparations. Thrombin prepared from canine normal plasma exerted a more potent vasodilator response, indicating a species specificity for the vascular response to thrombin. Since the vasodilating effect of thrombin is not mediated by (i) a nervous mechanism, (ii) any known vasodilating substance or (iii) any other clotting factor, it is concluded that the thrombin moiety possesses vasodilating properties.