Responses of the Canine Splenic Vascular Bed to Various Biogenic and Foreign Substances

Responses of dog splenic vascular bed to various compounds administered into the splenic artery were investigated under a constant perfusion pressure. Adrenergic drugs; epinephrine, norepinephrine and dopamine produced a marked vasoconstriction which was followed by a vasodilation. Phenylephrine, tyramine, methoxamine and ephedrine produced only vasoconstriction. Isoproterenol dilated the splenic vascular bed. Cholinergic drugs; cholinesters and pilocarpme caused a vasodilation, while physostigmine produced a vasoconstriction. Ganglion stimulants; McN-A-343, TMA and lobeline produced a vasodilation, while DMPP and nicotine caused a vasoconstriction. TEA, one of ganglion blockers, caused a vasoconstriction. Angiotensin II, lys-vasopressin, oxytocin and 5-hydroxytryptamine produced a vasoconstriction. Bradykinin, kallikrein and histamine caused a vasodilation. Various nucleosides and nucleotides, i.e., adenosine, AMP, ADP, ATP, uridine, UMP, UDP, UTP, DPN and TPN induced peculiar oscillatory vascular responses. Vasodilators including nitroglycerin, papaverine, verapamil, dipyridamole, hydralazine and caffeine dilated the splenic vascular bed, while cocaine, guanethidine and ergotamine constricted it. Procaine, morphine, bretylium, tolazoline showed a vasodilation. These results indicated that the splenic vascular bed has a very characteristic behavior.