Mechanisms to preserve and increase heat

• Behavioural patterns: seek shelter, increase clothing, curl up
• Ingestion of food
• Increase activity
• Vasoconstriction and piloerection
• Shivering
• Non-shivering thermogenesis

Cutaneous vasoconstriction via a1 (alpha one) receptors acting on arterioles, reduces heat loss caused by radiation and convection.

A countercurrent exchange mechanism transfers heat from the warm arterial blood going to the limbs, to the cold venous blood returning.

Shivering doubles heat production but can increase metabolic activity by up to 600% in adults. It does not occur in children until they are several years old.

Ondansetron given before induction of anesthesia reduces shivering after general anesthesia.

Reference
Ondansetron given before induction of anesthesia reduces shivering after general anesthesia.
Powell RM, Buggy DJ
Anesth Analg. 2000; 90: 1423-7

Non-shivering thermogenesis doubles heat production in infants, but probably has little significance in adults. It is mediated via ß3 (beta three) adrenergic receptors located in brown fat. Brown fat is more abundant in infants and is located between the scapula, at the nape of the neck and along the great vessels. It contains many mitochondria (giving its colour), which increase lipid oxidation to generate ATP production and heat. An uncoupling protein called UCP1 short-circuits the process by uncoupling oxidative phosphorylation.

Fever

Fever is perhaps one of the oldest and most universally known hallmarks of disease. The thermoregulatory mechanisms behave as if they were adjusted to maintain body temperature at a higher than normal level, i.e. “as if the thermostat has been reset”. Temperature-raising mechanisms are activated in response to temperature receptors that signal that body temperature is below the new set point. This usually produces chilly sensations due to cutaneous vasoconstriction, and occasionally enough shivering to produce rigors.

It is due to the production of endogenous pyrogens, which are cytokines produced by monocytes, macrophages and Kupffer cells in response to toxins. These cytokines, such as interleukins, interferons and tumour necrosis factor (TNF), act on the hypothalamus and cause the local release of prostaglandins. Drugs which inhibit cyclo-oxygenase (COX), such as aspirin, paracetamol and non steroidal anti-inflammatory drugs (NSAIDs), therefore have anti-pyretic effects.