Effect of Severe Injury and Critical Illness on High-energy Phosphates in Human Liver and Muscle

Liaw, Koung-Yi; Wei, Tzu-Tang; Hsu, Shu-Chien; Lin, Jyh-Woei

doi:10.1097/00005373-198507000-00009

Cited by 16 publications

(9 citation statements)

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“…The muscle specimens taken for determinations of energy‐rich phosphagens were not frozen immediately, which was the case in the investigations by Liaw et al . (1980, 1985) and Bergström et al . (1976).…”

Section: Methodsmentioning

confidence: 93%

The effect of unloading on protein synthesis in human skeletal muscle

Gamrin¹,

Berg

Essén³

et al. 1998

Acta Physiologica Scandinavica

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Atrophy of skeletal muscle is observed in response to immobilization and lack of weight-bearing. The aim of this study was to investigate the effect of immobilization on muscle protein synthesis and associated biochemical parameters in skeletal muscle of healthy volunteers employing a standardized model of lower limb unloading. One leg was unloaded for 10 days, and percutaneous muscle biopsies were taken before and at the end of the unloading period. The capacity for protein synthesis, as reflected by the concentration of RNA, decreased by 16% (P < 0.05) although the fractional synthesis rate (FSR) of protein was not significantly changed after 10 days of unloading. Furthermore there was an increase in the concentration of the free branched chain amino acids in muscle by 48% (P < 0.05).

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Section: Methodsmentioning

confidence: 93%

The effect of unloading on protein synthesis in human skeletal muscle

Gamrin¹,

Berg

Essén³

et al. 1998

Acta Physiologica Scandinavica

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“…Several studies on critical illness point towards a disturbance in the levels of these high-energy phosphates in skeletal muscle. In limb muscle of critically ill patients, especially with sepsis, a low-energy charge potential with reductions in ATP, ADP, and/or PCr and a rise in AMP and free creatine has been described in the presence of high lactate levels and an increased lactate-to-pyruvate ratio (210,425,426,444). In rats with hemorrhagic shock, ATP, ADP, and PCr levels already dropped after 1 h in diaphragm (continuously working muscle) and after 2 h in soleus muscle (more sedentary or resting muscle) (115).…”

Section: A Disturbances In Energy-rich Phosphates In Critical Illnessmentioning

confidence: 99%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

293

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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“…The muscle specimens taken for determinations of energy-rich phosphagens were not frozen immediately, which was the case in the investigations by Liaw et al (1980Liaw et al ( , 1985 and Bergstro Èm et al (1976). So Èderlund and Hultman have demonstrated that the phosphocreatine content in muscle after a 1-min delay of freezing corresponds better to the level in fresh muscle, than immediately frozen muscle specimens.…”

Section: Muscle Biopsymentioning

confidence: 99%

The effect of unloading on protein synthesis in human skeletal muscle

GAMRIN¹,

BERG

ESSEN³

et al. 1998

Acta Physiol Scand

View full text Add to dashboard Cite

Atrophy of skeletal muscle is observed in response to immobilization and lack of weight-bearing. The aim of this study was to investigate the effect of immobilization on muscle protein synthesis and associated biochemical parameters in skeletal muscle of healthy volunteers employing a standardized model of lower limb unloading. One leg was unloaded for 10 days, and percutaneous muscle biopsies were taken before and at the end of the unloading period. The capacity for protein synthesis, as reflected by the concentration of RNA, decreased by 16% (P < 0.05) although the fractional synthesis rate (FSR) of protein was not signi®cantly changed after 10 days of unloading. Furthermore there was an increase in the concentration of the free branched chain amino acids in muscle by 48% (P < 0.05).

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Effect of Severe Injury and Critical Illness on High-energy Phosphates in Human Liver and Muscle

Cited by 16 publications

References 0 publications

The effect of unloading on protein synthesis in human skeletal muscle

The effect of unloading on protein synthesis in human skeletal muscle

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The effect of unloading on protein synthesis in human skeletal muscle

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