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Biochemical changes after surgical stress in rabbits
Summary
Surgical stress causes distinct biochemical changes in normal and diabetic rabbits. These changes, particularly in the subacute phase, support a two-phase model of stress response involving catecholamine and pituitary-adrenal activity.
Area of Science:
- Biochemistry
- Endocrinology
- Physiology
Background:
- Surgical stress induces significant physiological and biochemical alterations.
- Understanding these changes in both normal and diabetic states is crucial for managing patient outcomes.
- Bessman's two-phase theory of stress response provides a framework for interpreting these metabolic shifts.
Purpose of the Study:
- To investigate and compare the biochemical responses to surgical stress in normal and diabetic rabbits.
- To analyze these responses across acute and subacute phases post-surgery.
- To evaluate the role of insulin in modulating these stress-induced metabolic changes.
Main Methods:
- Normal and diabetic rabbits were subjected to laparotomy under anesthesia.
- Blood samples were collected to measure glucose, ketone bodies, lactate, protein, blood urea nitrogen (BUN), and free alanine.
- Animals were studied in two phases: acute (0-180 minutes) and subacute (1-3 days post-surgery).
Main Results:
- Diabetic rabbits exhibited higher glucose, ketones, lactate, BUN, and alanine, with lower protein levels compared to normal rabbits.
- In the acute phase, both groups showed similar responses to surgical stress.
- In the subacute phase, normal rabbits showed increased ketone bodies and BUN, while diabetics displayed increased glucose, lactate, and alanine.
Conclusions:
- The observed biochemical changes support Bessman's two-phase stress response model (catecholamine and pituitary-adrenal phases).
- Acute phase response is attributed to glycogenolysis and lipolysis (catecholamine-mediated).
- Subacute phase response involves ketogenesis and gluconeogenesis from protein, with ketonemia prominent in normal rabbits, suggesting insulin's limited direct role in stress-induced lipolysis and ketogenesis.