[Surgical stress and organ dysfunction: liver]

Area of Science:

• Neuroendocrinology
• Hepatology
• Metabolic response to stress

Context:

• Extensive surgical stress (major operations, severe trauma) induces significant neuroendocrine responses.
• These responses involve hormone hypersecretion, leading to metabolic and cardiovascular changes, particularly in a catabolic state.
• Hepatic circulation is impacted by catecholamines, causing reduced hepatic mitochondrial redox status due to hypoxia and energy substrate shortage.

Purpose:

• To investigate the mechanisms underlying hepatic energy crisis following surgical stress.
• To explain the development of posttraumatic and postoperative hyperbilirubinemia.
• To highlight the utility of the arterial ketone body ratio (AKBR) in assessing hepatic mitochondrial redox status.

Summary:

• Surgical stress causes neuroendocrine hypersecretion, impacting hepatic circulation and leading to reduced mitochondrial redox status and energy crisis.
• This hepatic energy crisis disrupts conjugated bilirubin excretion, contributing to hyperbilirubinemia, a phenomenon often underestimated by conventional biochemical markers.
• The arterial ketone body ratio (AKBR) serves as a sensitive indicator of hepatic mitochondrial redox status, revealing the severity of the energy crisis.

Impact:

• Provides a deeper understanding of the pathophysiology of hyperbilirubinemia after trauma and surgery.
• Identifies the arterial ketone body ratio (AKBR) as a critical diagnostic tool for assessing hepatic mitochondrial dysfunction.
• Suggests potential targets for therapeutic interventions by exploring the role of physiologically active substances like monokines and oxygen radicals.