The Adrenergic Response to Mild Core Hypothermia

Higgins, Michael S.; Frank, Steven M.; Breslow, Michael J.; Fleisher, L. A.

doi:10.1097/00000542-199409001-00234

Cited by 3 publications

(3 citation statements)

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“…Thirdly, our volume of cold infusion in protocol 1 may have been sufficient to change cardiopulmonary volumes and pressures. However, a similar volume of warm saline was not shown to change blood pressure, heart rate or H RV [31]. Therefore, it is unlikely that the effect we observed was due to the fluid infusion, but rather due to the change in core temperature.…”

Section: Protocol 2: Skin-surface Coolingmentioning

confidence: 60%

“…The response to cold challenge involves afferent input of temperature information to the hypothalamic centres, central processing of this information and an efferent response [30]. This efferent response is characterized by peripheral sympathetic activation as indicated by increased noradrenaline, but no adrenal medullary or cortical activation as determined by adrenaline and cortisol [24,31]. The peripheral sympathetic activation is marked by profound vasoconstriction, as demonstrated by an increase in the forearmfingertip temperature gradient [23].…”

Section: Protocol 2: Skin-surface Coolingmentioning

confidence: 99%

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Thermoregulation and Heart Rate Variability

et al. 1996

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1. Heart rate variability is modulated by multiple control systems, including autonomic and hormonal systems. Long-term variability, i.e. the very low-frequency band of the power spectra, has been postulated to reflect thermoregulatory vasomotor control, based upon thermal entrainment experiments. However, the relationship between thermoregulatory responses (vasoconstriction and shivering) and heart rate variability has not been studied. 2. We performed two distinct protocols in a series of human subjects. In the first protocol, core temperature was reduced by intravenous infusion of cold saline, while skin temperature was unchanged. The second protocol involved skin-surface warming and cooling until shivering developed. Power spectral analysis was performed using a fast Fourier transformation, and the area in three distinct band-widths was determined. 3. Very low-frequency power (0.0039-0.04 Hz) increased significantly in response to core cooling, peripheral vasoconstriction and shivering, while both very low- and low- (0.04-0.15 Hz) frequency power increased in response to skin-surface cooling. Heart rate decreased during core cooling-induced vasoconstriction, suggesting a direct thermal response, and increased in relation to the metabolic demands associated with shivering. 4. Our results suggest that very low-frequency power is modulated by thermal stimuli which result in core hypothermia and thermoregulatory activity, while skin-surface cooling without core hypothermia does not selectively modulate this frequency band.

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Section: Protocol 2: Skin-surface Coolingmentioning

confidence: 60%

Section: Protocol 2: Skin-surface Coolingmentioning

confidence: 99%

Thermoregulation and Heart Rate Variability

et al. 1996

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“…The a-adrenergic antagonist-induced 'selective' inhibition of vasomotor tone in the absence of changes in metabolic heat production suggests that the two thermoregulatory responses occur by different mechanisms. Previous studies have shown that vasoconstriction [17][18][19] and non-shivering thermogenesis [20] are mediated by catecholamines. There is some evidence for an adrenergic mechanism contributing to the metabolic response during cold challenge, with adrenaline contributing more than noradrenaline to the shivering response [21].…”

Section: Variablementioning

confidence: 98%

α-Adrenoceptor Mechanisms of Thermoregulation during Cold Challenge in Humans

et al. 1996

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1. Previous studies on the thermoregulatory effects of alpha-adrenoceptor antagonists have been performed primarily in animals and the findings have been inconsistent. There is evidence for thermoregulatory impairment by alpha-adrenergic antagonists in humans not exposed to cold, but the effects of alpha-adrenergic blockade during cold challenge have not been investigated. 2. Fourteen healthy human volunteers (seven elderly, aged 55-68 years and seven young, aged 19-27 years) were studied on three separate days and received three randomly assigned treatments; (i) control (no drug), (ii) low-dose phentolamine and (iii) high-dose phentolamine. On each day cold intravenous saline (4 degrees C) was given until both vasoconstriction and shivering were triggered or a maximum fluid volume (40 ml/kg) was delivered. Core temperature, peripheral vasoconstriction and metabolic heat production were measured. 3. The alpha-adrenoceptor antagonist caused a dose-dependent inhibition of vasoconstriction in the elderly but did not impair vasoconstriction in the young subjects at the doses that were given. Shivering and metabolic heat production were unaffected by alpha-adrenergic blockade in the elderly or in the young. 4. These findings illustrate the selective inhibition of vasoconstriction (but not shivering) by alpha-adrenoceptor antagonism in elderly individuals. Compared with the young, the elderly are more sensitive to the effects of alpha-antagonists, perhaps due to downregulation of the alpha-adrenoceptor. These findings lead us to conclude that thermoregulatory vasoconstriction is alpha-adrenergically mediated, and this response is attenuated by alpha-adrenoceptor blockade in elderly humans.

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