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Cellular glucose utilization during hemorrhagic shock in the pig
Surgery
|September 1, 1975
Summary
Injury causes hyperglycemia in pigs by inhibiting glucose use in cells and increasing liver glucose production. This study clarifies the complex metabolic response to hemorrhagic shock.
Area of Science:
- Physiology
- Metabolism
- Endocrinology
Background:
- Understanding glucose homeostasis after injury is crucial for effective treatment.
- Hemorrhagic shock significantly alters metabolic processes.
- Pigs serve as a relevant model for studying human physiological responses to trauma.
Purpose of the Study:
- To investigate the mechanisms behind glucose dysregulation following hemorrhagic shock in pigs.
- To determine the roles of cellular glucose utilization and hepatic glucose production in injury-induced hyperglycemia.
Main Methods:
- Pigs were subjected to controlled hemorrhagic shock.
- Measurements included plasma glucose, intracellular free glucose in red blood cells and muscle, portal and systemic plasma glucose levels, and plasma insulin and phosphate concentrations.
Main Results:
- Increased free glucose in red blood cells and muscle indicated inhibited glucose phosphorylation.
- Systemic plasma glucose exceeded portal plasma glucose, with decreased liver free glucose, suggesting hepatic glucose mobilization.
- Plasma insulin and phosphate levels rose during the shock period.
Conclusions:
- Hyperglycemia following injury in this model is a result of both reduced cellular glucose uptake (due to impaired phosphorylation) and increased glucose release by the liver.
- These findings highlight a dual mechanism contributing to elevated blood glucose levels after trauma.