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Glucose and lactate kinetics in burn shock
The American Journal of Physiology
|April 1, 1977
Summary
Burn shock causes early hyperglycemia due to increased glucose appearance and impaired glucose uptake. Lactate levels also rise significantly, indicating its crucial role in burn shock metabolism and substrate kinetics.
Area of Science:
- Biochemistry
- Physiology
- Trauma Medicine
Background:
- Burn injury triggers significant metabolic derangements.
- Understanding substrate kinetics is vital for managing burn shock.
Purpose of the Study:
- To investigate glucose and lactate kinetics during burn shock.
- To elucidate the metabolic alterations in burn injury.
Main Methods:
- Primed constant infusion of radiolabeled glucose ([6-3H]glucose) and lactate (Na-L-(+)-[U-14C]lactate).
- Measurement of substrate appearance (Ra) and disappearance (Rd) rates.
- Monitoring of plasma glucose and lactate concentrations.
Main Results:
- Early postburn hyperglycemia observed, driven by increased glucose Ra.
- Impaired tissue glucose extraction exacerbated hyperglycemia.
- Rapid rise in lactate Ra, with delayed increase in lactate Rd, leading to a 350% plasma lactate increase.
- Sustained elevated lactate Ra, Rd, and plasma concentrations post-30 minutes.
Conclusions:
- Lactate plays a critical role in the metabolic response to burn shock.
- Altered glucose and lactate kinetics are key features of burn shock pathophysiology.
- Findings highlight the importance of lactate in burn trauma substrate metabolism.