Summary
While insulin induced hypoglycemia is the principle method of producing a hypothalmic-pituitary-adrenal
stress response, the mechanism by which this occurs may be different from that produced
by other stressors. In a pilot study, we explored ways to standardize lower body negative
pressure (LBNP), as a simulator of hemorrhage, to determine its utility for future
studies of hypothalamic-pituitary-adrenal (HPA) axis function. Reduced atmospheric
pressure of -40 mmHg applied at the level of the iliac crests during LBNP rapidly
lowers blood pressure in most subjects, simulating acute hemorrhage. In 6 normal subjects,
ACTH and cortisol values were measured before, during and after the application LBNP
at 0800, 1600 and 2300 hours in the basline state and at 1600 hours on the day following
1 mg of dexamethasone. Peak ACTH values of 60-250 pg/ml occurred 2 to 10 minutes after
the cessation of the stimulus in subjects experiencing presyncope or having a systolic
or diastolic blood pressure decrease of > 20 mmHg with a rise in pulse of 30 beats
per minute or more. There was no significant difference between ACTH responses at
different times of day. Peak cortisol values of 25-30 μg/dl occurred 15-20 minutes
after cessation of the stimulus. In all subjects, administration of dexamethasone
greatly attenuated the ACTH response and decreased but did not ablate the cortisol
response.
In conclusion, these data indicate that LBNP may be used to simulate hemorrhage as
a stimulus of the HPA axis. HPA axis changes occur only when physiologic evidence
of hypovolemic stress is present. Dexamethasone may be used to modulate the response
to this stress paradigm.
Key words
LBNP - Neuroendocrine - Hemorrhage - HPA Axis - Stress
