Inhibition of glycogen synthase kinase (GSK)-3-β improves liver microcirculation and hepatocellular function after hemorrhagic shock.

Ischemia and reperfusion may cause liver injury and are characterized by hepatic microperfusion failure and a decreased hepatocellular function. Inhibition of glycogen synthase kinase (GSK)-3β, a serine-threonine kinase that has recently emerged as a key regulator in the modulation of the inflammatory response after stress events, may be protective in conditions like sepsis, inflammation and shock. Therefore, aim of the study was to assess the role of GSK-3β in liver microcirculation and hepatocellular function after hemorrhagic shock and resuscitation (H/R).

Endothelin-1 contributes to hemoglobin glutamer-200-mediated hepatocellular dysfunction after hemorrhagic shock.

Hemoglobin glutamer-200 (HbG) might be an alternative to human blood. However, artificial oxygen carriers are initially successful to restore oxygen supply but may induce organ dysfunction and increase mortality several days after application in terms of delayed side effects. Impairment of microcirculation and an inflammatory cytokine response through induction of endothelin (ET) 1 may contribute.

Hemin arginate-induced heme oxygenase 1 expression improves liver microcirculation and mediates an anti-inflammatory cytokine response after hemorrhagic shock.

Microvascular failure is a major determinant for the development of hepatocellular dysfunction after hemorrhagic shock. Induction of heme oxygenase (HO) 1 may confer hepatocellular protection. Hemin arginate (HAR) induces HO-1 and protects against shock-induced organ failure.

Melatonin pretreatment improves liver function and hepatic perfusion after hemorrhagic shock.

Exogenous administration of pineal hormone melatonin (MEL) has been demonstrated to attenuate organ damage in models of I/R and inflammation by antioxidative effects. However, specific organ-protective effects of MEL with respect to hemorrhagic shock have not been investigated yet. In the present study, we evaluated the role of MEL pretreatment for hepatic perfusion, redox state, and function after hemorrhage and resuscitation, with emphasis on MEL receptor activation.

Dobutamine improves liver function after hemorrhagic shock through induction of heme oxygenase-1.

Rationale: Induction of heme oxygenase-1 (HO-1) protects the liver against reperfusion injury after hemorrhagic shock. Previous data suggest that the beta(1)-adrenoceptor agonist dobutamine induces HO-1 in hepatocytes.

Objectives: To investigate the functional significance of dobutamine pretreatment for liver function after hemorrhagic shock in vivo.

Age-associated loss of immunomodulatory protection by granulocyte-colony stimulating factor in endotoxic rats.

Elderly patients have a higher incidence of morbidity and mortality due to infectious diseases. Because most immune functions in the elderly differ compared with those in younger subjects, we studied the effect of the immunomodulating agent G-CSF on endotoxic liver injury and cytokine release in an aging animal model of acute sepsis. Young (3-month-old), mature (12-month-old), and senescent (24-month-old) male Sprague-Dawley rats (n = 6 each) were treated with bacterial endotoxin for 6 h.

In vivo quantification of ageing changes in the rat liver from early juvenile to senescent life.

Aims/method: Using high resolution multifluorescence in vivo microscopy, the present study was undertaken to determine the changes in rat hepatic tissue architecture and microvasculature during the growth associated with juvenile maturation and adult senescence, i.e. the age of 1, 3, 12 and 24 months.