Concepedia

Publication | Closed Access

Adrenergic, respiratory, and cardiovascular effects of core cooling in humans

430

Citations

0

References

1997

Year

TLDR

The study induced mild core hypothermia in awake humans by infusing cold saline (4 °C) at 30 or 40 ml/kg on two separate days, with a warm saline control, and measured adrenergic, respiratory, and cardiovascular responses. Core cooling raised norepinephrine by up to 700 %, increased oxygen consumption by 112 %, caused peripheral vasoconstriction and higher mean arterial pressure without affecting heart rate, while epinephrine and cortisol remained unchanged, indicating a peripheral sympathetic response without significant adrenal activation.

Abstract

The adrenergic, respiratory, and cardiovascular responses to isolated core cooling were assessed in awake human subjects. Mild core hypothermia was induced by intravenous infusion of 30 or 40 ml/kg of cold saline (4 degrees C) on 2 separate days. A warm intravenous infusion (30 ml/kg, 37 degrees C) was given on a third day as a control treatment. Mean norepinephrine concentration increased 400% and total body oxygen consumption increased 30% when core temperature decreased 0.7 degrees C. Mean norepinephrine concentration increased 700% and total body oxygen consumption increased 112% when core temperature decreased 1.3 degrees C. Core cooling was associated with peripheral vasoconstriction and increased mean arterial blood pressure, whereas heart rate was unchanged. Plasma epinephrine and cortisol concentrations were unchanged during core cooling. There were no changes in any measured parameter with the warm infusion. These findings suggest that mild hypothermia induced by isolated core cooling is associated with an adrenergic response characterized by peripheral sympathetic nervous system activation without a significant adrenocortical or adrenomedullary response. The respiratory and cardiovascular responses to core cooling are characterized by a shivering-induced increase in metabolic rate, norepinephrine-mediated peripheral vasoconstriction, and increased arterial blood pressure.