[Surgical stress and organ dysfunction: liver].
Tatsuya Nakatani, Kiyonori Kobayashi
Abstract
Tatsuya Nakatani, Kiyonori Kobayashi
Abstract
Various kinds of neuroendocrine responses occur to an extensive surgical stress such as major operation and severe trauma. Studies of the details of this response have focused on many endocrine systems for decades. Hypersecretion of the hormones results in metabolic and cardiovascular changes, particularly in catabolic condition. As hepatic circulation is affected by catecholamines such as norepinephrine, hepatic mitochondrial redox status highly reduced due to tissue hypoxia and to shortage in the energy substrate, even in the cases without apparent blood loss. This results in hepatic energy crisis. Although most of the conventional hepatic biochemical parameters failed to reveal, the crisis is often unexpectedly severe if one estimate it by measuring arterial ketone body ratio (AKBR), which reflects hepatic mitochondrial redox status. The energy crisis results in the disturbance of excretion of conjugated bilirubin from hepatocyte to bile canaliculi that has to occur against bilirubin concentration gradient. This explains one of the mechanisms of posttraumatic as well as postoperative hyperbilirubinemia. Recently, numerous studies focused on various kinds of physiologically active substances, such as monokines, eicosanoids, and oxygen radicals. They are released from various kinds of cell strains as humoral mediators in response to many kinds of stimuli and affect hepatic function. Studies to modulate the activity of such mediators are going on.
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Various kinds of neuroendocrine responses occur to an extensive surgical stress such as major operation and severe trauma. Studies of the details of this response have focused on many endocrine systems for decades. Hypersecretion of the hormones results in metabolic and cardiovascular changes, particularly in catabolic condition. As hepatic circulation is affected by catecholamines such as norepinephrine, hepatic mitochondrial redox status highly reduced due to tissue hypoxia and to shortage in the energy substrate, even in the cases without apparent blood loss. This results in hepatic energy crisis. Although most of the conventional hepatic biochemical parameters failed to reveal, the crisis is often unexpectedly severe if one estimate it by measuring arterial ketone body ratio (AKBR), which reflects hepatic mitochondrial redox status. The energy crisis results in the disturbance of excretion of conjugated bilirubin from hepatocyte to bile canaliculi that has to occur against bilirubin concentration gradient. This explains one of the mechanisms of posttraumatic as well as postoperative hyperbilirubinemia. Recently, numerous studies focused on various kinds of physiologically active substances, such as monokines, eicosanoids, and oxygen radicals. They are released from various kinds of cell strains as humoral mediators in response to many kinds of stimuli and affect hepatic function. Studies to modulate the activity of such mediators are going on.
Key concepts: Medicine, Ketone bodies, Endocrine system, Hormone, Norepinephrine, Internal medicine, Hypoxia (environmental), Surgical stress