Key result
Fed nutritional status compared to 24-30 h starvation altered the hormonal response to hypovolemic stress during 90 minutes of hemorrhagic hypotension in rats.
Why the study?
Does nutritional status alter the hormonal response to hypovolemic stress in rats?
Does nutritional status alter the hormonal response to hypovolemic stress in rats?
Changing nutritional status alters the hormonal response to hypovolemic stress in a rat model of hemorrhagic hypotension.
Answers are grounded in this paper and cite their sources.
Nutritional status must be controlled in rodent hemorrhage models; leaves open translation to clinical hypovolemic shock.
Hyperglycemia-inducing hyperosmolality has recently been proven beneficial in the maintenance of blood volume and extracellular fluid volume during early hemorrhagic hypotension. Fed animals benefitted from better plasma refill compared with starved ones when subjected to equal blood loss. Using lightly sedated fed and 24-30 h starved rats, hormones with relevance to glucose homeostasis were studied during 90 min of hemorrhagic hypotension of 70 mmHg (1 mmHg = 133.32 Pa). Marked differences in the overall hormonal developments were found between the two groups. In fed rats, insulin and glucagon responses were initially attenuated, while somatostatin increased to an early peak level at 30 min, returning to basal at 90 min. In starved rats, somatostatin increased gradually during the 90 min. Adrenaline release was massive in both groups. Corticosterone showed no increase from basal levels in the fed group during hemorrhage, while starved rats increased their basal level fourfold already at 30 min. These data are presented as evidence that changing nutritional status alters hormonal response to hypovolemic stress.
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Ljungqvist et al. (1986) studied Hemorrhagic hypotension. Fed nutritional status vs. 24-30 h starved was evaluated on Hormonal response (insulin, glucagon, somatostatin, adrenaline, corticosterone). Fed nutritional status compared to 24-30 h starvation altered the hormonal response to hypovolemic stress during 90 minutes of hemorrhagic hypotension in rats.
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