Protection of PEA in the rat isolated heart against ischaemia has been found in a preclinical study conducted by Lepicier and colleagues in 2003. It was already by that time known that endogenous compounds such as palmitoylethanolamide were protective for tissue in disstress.
PEA and 2-AG have been detected in rat cardiac tissue already by Schmid et al. in 2000 but at that time little was known about the role played by these lipid signal molecules played in the heart. It was reported that the ability of a prior exposure to lipopolysaccharide to limit infarct size in rats is blocked by a CB2-receptor antagonists. (Lagneux & Lamontagne, 2001). The first aim of their study was to evaluate the cardioprotective effect of endocannabinoids and PEA in the rat isolated heart. Secondly, the contribution of protein kinase C (PKC) and mitogen-activated protein kinases (MAP kinases) in this cardioprotective effect was assessed.
The results were impressive, as we can see in the graph. PEA could reduce the infarct size of an inschemic myocardium considerably.
Their conclusion was:
None of the untreated hearts recovered from ischaemia during the reperfusion period. Perfusion with either 300nm palmitoylethanolamide (PEA) or 300nm 2-arachidonoylglycerol (2-AG), but not anandamide (up to 1 mm), 15 min before and throughout the ischaemic period, improved myocardial recovery and decreased the levels of coronary CK and LDH. PEA and 2-AG also reduced infarct size.
Philippe Le ́picier, Jean-Franc ̧ois Bouchard et al Endocannabinoids protect the rat isolated heart against ischaemia British Journal of Pharmacology (2003) 139, 805–815