The protective effect of heat shock preconditioning on postischemic hepatic microcirculatory disturbances

Protective effects of heat shock (HS) preconditioning on postischemic hepatic microcirculatory disturbances were investigated by intravital fluorescence microscopy in two models: in situ warm ischemia (in situ model) and isolated liver perfusion (ILP model). Sprague-Dawley rats were divided into 3 groups: unstressed, ischemic, and MS-preconditioned ischemic groups. Ischemic insult was induced by clamping of the hepatoduodenal ligament for 20 minutes, followed by 120 minutes of reperfusion (in situ model), and by 30 minutes of no blood flow, followed by 120 minutes of flow-constant perfusion (ILP model). HS was induced by whole-body hyperthermia (42.0-42.5 degrees C for 15 min.) and the subsequent 48 hours recovery. The postischemic decrease of the sinusoidal perfusion rate and the postischemic increase of the numbers of stagnant leukocytes in sinusoids and sticking leukocytes in postsinusoidal venules were significantly suppressed by HS preconditioning.