Induction of HSP70 shows differences in protection against I/R injury derived by ischemic preconditioning and intermittent clamping

Abstract Background Ischemic preconditioning (IP) and intermittent clamping (IC) increase the ischemic tolerance of the liver. The underlying mechanisms are not completely understood. Heat shock proteins protect cellular integrity in stress and have been discussed as mediators in preconditioning. IP and IC in rat livers were compared with respect to HSP induction and postischemic microcirculation. Methods All animals were exposed to 70 min of partial warm liver ischemia. Different clamping protocols were used: in control animals (C) 70 min continuous ischemia was applied. IP was performed by 5 min ischemia and 10 min reperfusion before the 70 min ischemia time. In IC-groups, ischemia time of 70 min was divided into four intervals. Each group included 21 animals with 3 different reperfusion intervals; either 30 min, 12 or 36 h. Intravital microscopy was performed after 30 min of reperfusion. AST-levels and HSP induction were analysed 90 min, 12 and 36 h after reperfusion. Results IP and IC significantly improved sinusoidal perfusion (IP: 83.4 ± 2.8%; IC: 84.4 ± 4.6% vs. C: 60.4 ± 3.9%; p 2 liver surface; p p  = 0.004). In the course of reperfusion HSP70 protein expression doubled between 90 min and 12 h in IC (0.529 ± 0.227 vs. 0.992 ± 0.246; p p Conclusion Microcirculation is similarly preserved by IP and IC. The early protection derived by IP prevents further induction of HSP70 in opposite to IC. Therefore, IP may offer a more comprehensive protection against I/R on a cellular and transcriptional level.