Fifth congress of the international xenotransplantation associationAttenuation of hepatic microcirculatory failure during in situ xenogeneic rat liver perfusion by heat shock preconditioning
Section snippets
Materials and methods
The liver of Sprague-Dawley rats (200 to 250 g) was perfused in situ via the portal vein with diluted fresh human blood at a constant flow rate. Heat shock preconditioning was given by whole-body hyperthermia in a water bath (42°C for 15 minutes), followed by a recovery of 18 hours. The animals were assigned to two groups: heat shock-treated group (HS group; n = 6) and non-treated group (XENO group; n = 6). Hepatic microcirculation was evaluated by using intravital fluorescence microscope. The
Results
Xenogeneic microvascular failure observed in XENO group, decrease of sinusoidal perfusion rate, and increase of the stagnant leukocyte number in sinusoids were significantly attenuated in HS group (P < .05), while sinusoidal diameter was comparable in both groups. The increase of wet-to-dry ratio of the liver tissue observed in XENO group was also significantly suppressed in HS group (P < .05). A marked expression of HSP70 and HO-1/HSP32 proteins was correlatively observed at 18 hours after
Discussion
The current study demonstrates that nonimmunologic stress preconditioning therapy can attenuate xenogeneic organ injury, especially xenogeneic microvascular disturbances. The protective mechanism of heat shock preconditioning may be associated with the induction of HSPs. HSP70 promotes a correct refolding of denatured proteins as molecular chaperone,3 suggesting that HSP70 may prevent the intracellular accumulation of damaged proteins during xenoperfusion. HO-1/HSP32 is an inducible form of HO
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