Resuscitation after hemorrhagic shock: the effect on the liver—a review of experimental data

Abstract

The liver is currently considered to be one of the first organs to be subjected to the hypoxic insult inflicted by hemorrhagic shock. The oxidative injury caused by resuscitation also targets the liver and can lead to malfunction and the eventual failure of this organ. Each of the various fluids, vasoactive drugs, and pharmacologic substances used for resuscitation has its own distinct effect(s) on the liver, and the anesthetic agents used during surgical resuscitation also have an impact on hepatocytes. The aim of our study was to identify the specific effect of these substances on the liver. To this end, we conducted a literature search of MEDLINE for all types of articles published in English, with a focus on articles published in the last 12 years. Our search terms were "hemorrhagic shock," "liver," "resuscitation," "vasopressors," and "anesthesia." Experimental studies form the majority of articles found in bibliographic databases. The effect of a specific resuscitation agent on the liver is assessed mainly by measuring apoptotic pathway regulators and inflammation-induced indicators. Apart from a wide range of pharmacological substances, modifications of Ringer's Lactate, colloids, and pyruvate provide protection to the liver after hemorrhage and resuscitation. In this setting, it is of paramount importance that the treating physician recognize those agents that may attenuate liver injury and avoid using those which inflict additional damage.

New therapeutic strategy of hinokitiol in haemorrhagic shock‐induced liver injury

“…These models reveal that HS/R can cause multi‐organ injury, including kidney, lung and liver injury . Among the organs, the liver is currently considered to be most frequently affected by HS . Similar to their roles in other organs, NF‐κB activation and TNF‐α and IL‐6 production play crucial roles in HS/R‐induced liver injury …”

“…Notably, NF‐κB signalling related factors, such as IκBα and p65, has been shown to be involved in inflammatory responses caused by ischaemia/reperfusion injury . Moreover, HR‐induced hepatic injury has been reported to consist of two main stages . The primary injury occurs in the early phase of shock or ischaemia, whereas the secondary injury is attributed to the reperfusion phase.…”

“…6 Liver dysfunction following HS/ R results from a combination of ischaemia and reperfusion injury that has been reported to cause massive production of pro-inflammatory mediators and subsequent accumulation of neutrophils in the liver, which is directly correlated with mortality. 6 Thus, targeting inflammatory responses might be a potential strategy to ameliorate hepatic injury during HS/R. Hinokitiol (4-isopropyl-tropolone; β-thujaplicin, Figure 1A) is a bioactive tropolone-related compound found in the wood of cupressaceous plants.…”

The salutary effects of diphenyldifluoroketone EF24 in liver of a rat hemorrhagic shock model

“…In contrast, we employed a model of prolonged ischemia without any fluid resuscitation. It has been postulated that apoptotic cell death occurs mainly during the restoration of the circulation and oxygen supply, whereas ischemia associated with massive blood loss causes hepatocytes to undergo necrosis [ 45 ]. Presumably, the energy needs associated with the apoptosis process restrict it to occur only during the reperfusion phase because it depends on oxidative metabolism in the cells [ 46 ].…”

A case of canine hypoadrenocorticism needing blood transfusion for severe acute anemia due to gastrointestinal hemorrhage

“…Although using peroxidase-based tests to detect fecal occult blood may be useful, results are influenced by the diet [1,11]. Elevated liver enzymes were also present, possibly because hepatocytes are vulnerable to anoxia resulting from anemia [6], as is seen in hemolysis.…”