ABSTRACT
Hepatic ischemia-reperfusion injury as a result of inflow obstruction is a major cause of morbidity and mortality associated with liver pathologies and surgery. Heat shock proteins, a family of stress-inducible proteins involved in maintaining cell homeostasis and regulating the immune system play a major role in liver regeneration. They serve as crucial indicators of ischemia-reperfusion injury in human liver and influence liver function and recovery. The primary objectives of this article are to review the potential role of heat shock proteins as a diagnostic marker for liver diseases and therapeutic target in critical illness. The review will start by focusing on the essentials of heat shock proteins as an endogenous system as it relates to hepatic injury. It will elucidate the influence of heat shock protein-70 on hepatic diseases and ischemia-reperfusion. It will then look at their potential diagnostic role and finally highlights its activities as a possible therapeutic tool. Orv. Hetil., 2016, 157(42), 1659-1666.
Subject(s)
HSP70 Heat-Shock Proteins/metabolism , Liver/blood supply , Myocardial Reperfusion Injury/metabolism , Humans , Liver/surgery , Myocardial Reperfusion Injury/bloodABSTRACT
Tissue capnometry may be suitable for the indirect evaluation of regional hypoperfusion. We tested the performance of a new sublingual capillary tonometer in experimental hemorrhage. Thirty-six anesthetized, ventilated mini pigs were divided into sham-operated (n = 9) and shock groups (n = 27). Hemorrhagic shock was induced by reducing mean arterial pressure (MAP) to 40 mmHg for 60 min, after which fluid resuscitation started aiming to increase MAP to 75% of the baseline value (60-180 min). Sublingual carbon-dioxide partial pressure was measured by tonometry, using a specially coiled silicone rubber tube. Mucosal red blood cell velocity (RBCV) and capillary perfusion rate (CPR) were assessed by orthogonal polarization spectral (OPS) imaging. In the 60 min shock phase a significant drop in cardiac index was accompanied by reduction in sublingual RBCV and CPR and significant increase in the sublingual mucosal-to-arterial PCO2 gap (PSLCO2 gap), which significantly improved during the 120 min resuscitation phase. There was significant correlation between PSLCO2 gap and sublingual RBCV (r = -0.65, p < 0.0001), CPR (r = -0.64, p < 0.0001), central venous oxygen saturation (r = -0.50, p < 0.0001), and central venous-to-arterial PCO2 difference (r = 0.62, p < 0.0001). This new sublingual tonometer may be an appropriate tool for the indirect evaluation of circulatory changes in shock.
