Nakamura K, Ichihara K, Abiko Y
Department of Pharmacology, Asahikawa Medical College, Japan.
Eur J Pharmacol. 1989 Oct 10;169(2-3):259-67. doi: 10.1016/0014-2999(89)90023-x.
The effect of lidocaine on the accumulation of non-esterified fatty acids (NEFA) was investigated in the isolated, perfused working rat heart. Ischemia was induced by lowering the afterload pressure to 0 mm Hg for 20 min, and reperfusion was induced by raising the pressure to the pre-ischemic value (60 mm Hg) for 20 min. The heart was frozen for biochemical studies immediately after ischemia or reperfusion. Ischemia decreased the mechanical function, increased the levels of palmitoleic, arachidonic and linoleic acids, left unchanged the levels of oleic, lauric, myristic, palmitic and stearic acids, decreased the levels of adenosine triphosphate (ATP), creatine phosphate (CrP), decreased the energy charge potential (ECP) and increased the level of lactate. Lidocaine (10(-5) or 3 x 10(-5) M) improved the mechanical function and attenuated the changes in NEFA, ATP, CrP, and ECP caused by ischemia. These findings suggest that lidocaine attenuates the ischemia- and reperfusion-induced metabolic changes in the myocardium.
