Tumor necrosis factor suppression and microcirculatory disturbance amelioration in ischemia/reperfusion injury of rat liver after ischemic preconditioning^†

Abstract

The suppression of tumor necrosis factor-alpha and the subsequent amelioration of microcirculatory disturbances were observed, suggesting that the mechanism underlying the protective effect of ischemic preconditioning in hepatic ischemia/reperfusion injuries may involve tumor necrosis factor-alpha and microcirculatory regulation.

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

“…Indeed, PC attenuated morphological alterations and mucosal apoptosis partly by inhibiting the reactive oxygen species-mediated mitochondria-dependent pathway in the rat small intestine (19). Moreover, several studies showed that PC prevents intestinal ischemia-reperfusion injury by inhibiting leukocyte-endothelial cell interactions (2,33,47). The role of cell adhesion molecules like ICAM-1 and transmigration of neutrophils through the endothelial barrier is probably essential in gut barrier dysfunction (11).…”

A Bioartificial Liver Device Secreting Interleukin-1 Receptor Antagonist for the Treatment of Hepatic Failure in Rats

“…Formalin-fixed specimens were embedded in paraffin, and 5-mthick sections were cut and then stained with hematoxylin and eosin (H&E). Tissue sections were also analyzed using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), intercellular adhesion molecule-1 (ICAM-1) immunohistochemical staining, and vascular cell adhesion molecule-1 (VCAM-1) immunohistochemical staining following our protocols for rat liver [23]. For the TUNEL assay, a commercial apoptosis detection kit (Intergen, Purchase, NY) was used.…”

Beneficial Effects of Ischemic Preconditioning in Patients Undergoing Hepatectomy

“…However, intravital microscopic studies in rodents are in agreement with our clinical data because they showed that IPC significantly reduced leukocyte-endothelial cell adhesion and microvascular perfusion disturbances and, hence, improved parameters of hepatocellular energy metabolism. 56,57 However, to identify more specifically the relative importance of the down-regulation of cytotoxic neutrophil functions among other mechanisms of liver protection induced by IPC, it would be imperative to deplete the number of circulating neutrophils or to use PMNL-adhesion-blocking antibodies, experimental tools that both are not applicable in humans and have not been used to this end even in animal studies to date. …”