We hypothesized that
intraperitoneal injections of anaesthetics or fluid per se might evoke a delayed preconditioning-like response in mice hearts isolated and Langendorff perfused 24 h later. To test this, mice were given
opioid anaesthesia by
intraperitoneal injections or
sham treated and the hearts were harvested and subjected to global ischaemia and reperfusion 24 h later in series 1. In series 2, mice were subjected to
intraperitoneal injection of Ringer,
sham needle prick procedure, or no intervention 24 h before heart isolation. In series 3, intraperitoneal Ringer injection 24 h earlier was compared with the effects of classic preconditioning or no pretreatment of the isolated heart or no treatment. Heart function was measured in all series. At the end of reperfusion, hearts in series 1 and 2 were frozen and
infarct size was estimated by
triphenyltetrazolium chloride solution. In series 3, separate hearts were frozen for immunoblotting to detect phosphorylation of
mitogen-activated
protein (MAP)
kinases. Cardiac activation of
nuclear factor kappa B (NFkappaB) was measured using a NFkappaB
luciferase firefly reporter mouse. The ischaemia-induced impairment of left ventricular function was attenuated by
opioid anaesthesia injected 24 h earlier, which also reduced
infarct size. Injection of fluid, but not the
sham needle prick procedure, reduced
infarct size. The functional protection afforded by classic preconditioning and Ringer pretreatment was comparable. Neither cardiac MAP
kinases nor NFkappaB were influenced by the interventions. In conclusion, this study demonstrates a delayed preconditioning-like effect of the heart caused by intraperitoneal administration of
opioid anaesthetics and of fluid only in the mouse. The mechanism of protection remains to be determined.