Inhibition of thermoregulatory non‐shivering thermo‐genesis by trauma in cold‐acclimated rats

Abstract

1. Heat production and blood flow in the interscapular brown adipose tissue of 3° C acclimated rats have been measured by the heated thermo‐couple technique. 2. When the environmental temperature (Ta) was reduced from 30 to 3° C heat production by the brown adipose tissue began to increase at the lower limit of the thermoneutral zone and then increased linearly. 3. Blood flow also increased when Ta was reduced but was not so well correlated with Ta. There was however a good positive correlation between blood flow and heat production. 4. During the first hour after a 4 hr period of bilateral hind‐limb ischaemia in a 20° C environment the percentage of rats not producing heat in the interscapular brown adipose tissue increased and the tissue blood flow fell. 5. By varying the Ta of the injured rat it was found that the Ta at which heat transfer from the interscapular brown adipose tissue commenced was significantly lower than in the controls although the slope of the regression lines relating heat production and Ta was unaltered. 6. Blood flow also increased in the injured rat when Ta was lowered but the increase in the tissue blood flow per unit increase in heat production was less than in the controls. 7. In a 5° C environment heat production in the interscapular brown adipose tissue of the injured rat was further increased by the S. C. injection of L‐isoprenaline or L‐noradrenaline. 8. It is concluded that the central control of thermoregulatory non‐shivering thermogenesis is inhibited after injury in the rat.

Report of a Consensus Meeting on Human Brain Temperature After Severe Traumatic Brain Injury: Its Measurement and Management During Pyrexia

“…In the case for cerebral neuroprotection, results in rodents provide convincing evidence that if body (or brain) temperature is lowered such that animals are rendered hypothermic during a brief period of transient cerebral ischemia, infarct size is smaller compared to the “normothermic” or hyperthermic animal (Busto et al, 1987 ; Kim et al, 1996 ; Yanamoto et al, 1999 ). The starting point to begin hypothermic neuroprotection may well be a normal temperature (which in the rat under thermoneutral conditions is 38°C Stoner, 1974 ). Hypothermia holds promise as a neuroprotective therapy after ischemic stroke (Lyden et al, 2006 ) but as the role of ischemia remains controversial as a mechanism of brain damage after TBI (Coles, 2004 ; Vespa, et al, 2005 ) the benefit of hypothermia for neuroprotection in this patient group remains speculative (Abate et al, 2008 ).…”

An Effect of Injury on Thermoregulation in Man

“…In that species trauma inhibits both thermoregulatory heat production and loss, widening the temperature gap between the thresholds for the onset of thermoregulatory heat production and heat loss (Stoner, 1981). However, in this case the regression lines, against Tag showing the intensity of shivering (Stoner, 1971), total oxygen consumption (Stoner, 1969) and non-shivering thermogenesis (Stoner, 1974) were displaced to the left without change in slope.…”

Catecholaminergic alpha‐receptors and shivering in the rat.

“…Any study of thermoregulation should follow changes in the activity of a definite pathway such as the 'cold sensor to heat production' pathway. For this it would be fitting to measure non-shivering thermogenesis as heat production by brown adipose tissue (Stoner, 1974) or shivering thermogenesis as here. Our results indicate that a neurotransmitter could be said to have a specific effect on the cold sensor-shivering pathway only if there was no accompanying change in the systemic blood pressure.…”