Prostaglandin release and mechanical perfromance in the isolated rabbit heart during induced changes in the internal environment.

The isolated rabbit heart was perfused according to the Langendorff technique. Prostaglandins in the effluent from the organ were identified by use of thin layer chromatography and assayed on the rat stomach strip. The effect of alterations of the physical and chemical conditions of the perfusion medium on the overflow of prostaglandins from the heart was studied. In addition, the capacity of noradrenaline and acetylcholine to release prostaglandins was tested. Acidosis, hyperthermia, hypothermia, hypotension, hyperosmoaarity and increased [K+] OR [Ca++] levels, while all inducing marked changes in the mechanical activity of the heart, did not induceporstaglandin release. Hypoxia, on the other hand, stimulated the liberation of prostaglandins. Noradrenaline was a potent agent for stimulation of prostaglandin release, in the absence of alpha- and betaadrenergic receptor blockade. Acetylcholine was also found to liberate prostaglandins, by activation of muscarinic receptors. The prostaglandin releasing capacity of acetylcholine was about 3 times weaker than that of noradrenaline. It is concluded that the release of prostaglandins from the rabbit heart is not dependent on the mechanical activity of the organ. Furthermore, it is suggested that prostaglandins released by hypoxia may play an important roli in the development of reactive hyperemia. Finally it is stated that the release of prostaglandins from the heart caused by acetylcholine may constitute the negative link in an endogenous prostaglandin mediated feed-back inhibition of the release of acetycholine from parasympathetic nerve endings.