Chad E. Johnston

Clonidine decreases vasoconstriction and shivering thresholds, without affecting the sweating threshold

PurposeThis study was conducted to test the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold and dose-dependent decreases in vasoconstriction and shivering thresholds.MethodsSix healthy subjects (two female) were studied on four days after taking clonidine in oral doses of either 0 (control). 3. 6 or 9 μg · kg. The order followed a balanced design in a double-blind fashion. Oesophageal temperature and mean skin temperature (from 12 sites) were measured. Subjects were seated in 37°C water which was gradually warmed until sweating occurred (sweat rate increased above 50 g · m 2 · h−1). The water was then cooled gradually until thresholds for vasoconstnction (onset of sustained decrease in fingertip blood flow) and shivering (sustained elevation m metabolism) were determined. Thresholds were then referred to as the core temperature, adjusted to a designated mean skin temperature of 33°C.ResultsHigh dose clonidine similarly decreased the adjusted core temperature thresholds for vasoconstriction by 1. 16 ± 0.30°C and for shivenng by 1.63 ± 0.23°C (P< 0.01). The dose response effects were linear for both cold responses with vasoconstriction and shivenng thresholds decreasing by 0.13 ± 0.05 and 0.19 ± 0.09°C · μg−1 respectively (P < 0.0001). The sweating threshold was unaffected by clonidine, however the interthreshold range between sweating and vasoconstnction thresholds increased from control (0.19 ± 0.48°C) to high dose donidine (1.31 ±0.54°C).ConclusionThe decreases in core temperature thresholds for cold responses and increased interthreshold range are consistent with the effects of several anaesthetic agents and opioids and is indicative of central thermoregulatory inhibition.RésuméObjectifVérifier si la clonidine provoque une augmentation du seuil de sudation et une diminution des seuls de vasoconstnction et de fnsson proportionnellement à la dose.MéthodesSix patients en bonne santé (dont deux femmes) qui avaient reçu des doses orales de clonidine de 0 (contrôle). 3. 6 et 9 μg· kg ont été étudiés pendant quatre jours. Létude suivait un plan équilibré et en double insu. Les températures moyennes oesophagiennes et cutanées (à 12 endroits) ont été mesurées. Les sujets étaient assis dans l’eau à 37°C réchauffée graduellement jusqu’à l’apparition de la sudation (un taux de sudation à50 g · m2 · h−1). Leau était par la suite refroidie progressivement jusqu’aux seuils de vasoconstnction (début de la diminution du flux sanguin à l’extrémité des doigts) et de frissonnement. Ces seuils ont été reconnus comme la température centrale ajustée à une température cutanée désignée de 33°C.RésultatsLes hautes doses de clonodine abaissent également les seuils de vasoconstriction ajustés à la température centrale de 1. 16 ± 0.30°C et du frissonnement de 1,63 ± 0.23C (P < 0,01). Les effets dose-réponse sont linéaires pour les deux réponses au froid avec des seuils de vasoconstnction et de frissonnement diminuant respectivement de 0,13 ± 0,05 et de 0.19 ± 0.09°C μg−1 (P < 0,0001). Le seuil de sudation n’est pas affecté par le donodine; toutefois l’écart entre les seuils de sudation et de vasoconstriction s’élargit entre le contrôle (0,19 ± 0,48°C) et la clonodine à haute dose (1.31 ± 0.54°C).ConclusionLa baisse des seuils de la température centrale pour les réponses au froid et l’augmentation de l’écart entre les seuils sont consistants avec les effets de plusieurs agents anesthésiques et morphmiques et démontrent une inhibition de la thermorégulation centrale.

Intense exercise increases the post-exercise threshold for sweating

Abstract We demonstrated previously that esophageal temperature (Tes) remains elevated by ≈0.5°C for at least 65 min after intense exercise. Following exercise, average skin temperature (Tavg) and skin blood flow returned rapidly to pre-exercise values even though Tes remained elevated, indicating that the Tes threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, Tw = 42°C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, Ta = 24°C). At a Ta of 24°C, 15 min of cycle ergometry (70% VO2max) (Exercise) was then followed by 30 min of recovery. Subjects were then immersed again (Tw = 42°C) until onset of sweating (Immersion 2). Baseline Tes and Tskavg were 37.0 (0.1)°C and 32.3 (0.3)°C, respectively. Because the Tskavg at the onset of sweating was different during Exercise [30.9 (0.3)°C] than during Immersion 1 and Immersion 2 [36.8 (0.2)°C and 36.4 (0.2)°C, respectively] a corrected core temperature, Tes (calculated), was calculated at a single designated skin temperature, Tsk(designated), as follows: Tes(calculated) = Tes + [β/(1−β)][Tskavg−Tsk(designated)]. The Tsk(designated) was set at 36.5°C (mean of Immersion 1 and Immersion 2 conditions) and β represents the fractional contribution of Tskavg to the sweating response (β for sweating = 0.1). While Tes(calculated) at the onset of sweating was significantly lower during exercise [36.7 (0.2)°C] than during Immersion 1 [37.1 (0.1)°C], the threshold of sweating during Immersion 2 [37.3 (0.1)°C] was greater than during both Exercise and Immersion 1 (P < 0.05). We conclude that intense exercise decreases the sweating threshold during exercise itself, but elicits a subsequent short-term increase in the resting sweating threshold.

Alcohol lowers the vasoconstriction threshold in humans without affecting core cooling rate during mild cold exposure

Elevated blood alcohol levels are often seen in hypothermia and hyperthermia related deaths, leading to the belief that alcohol renders humans poikilothermic. We examined the core temperature (TCO) thresholds for sweating, vasoconstriction and shivering as well as core cooling rates of seven subjects immersed in 28 °C water. On two separate days, subjects exercised on an underwater cycle ergometer to elevate TCO above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects drank orange juice (7 ml·kg−1) prior to immersion during the control trial and 1 ml·kg−1 absolute ethanol, added to orange juice in a 1:6 ratio, during the alcohol trial. Mean blood alcohol concentration (breath analysis) was 0.097 ± 0.010 g% at the start of cooling and 0.077 ± 0.008 g% at the end of the cooling period. Alcohol lowered the vasoconstriction threshold by 0.32 ± 0.2 °C and elevated finger tip blood flow, but had no effect on thresholds for sweating and shivering or core cooling rate. Considering these minor effects it is unlikely that moderate alcohol consumption predisposes individuals to hypothermia or hyperthermia via impaired thermoregulation, but rather likely due to behavioral factors.