Thermoregulation Flashcards Preview

Infection & Immunity Block > Thermoregulation > Flashcards

Flashcards in Thermoregulation Deck (15):


An organism, tissue, or cell in which its internal conditions tend to parallel its external environment.



An organism, tissue, or cell that uses physiological, biochemical, or behavioral mechanisms to maintain homeostasis against the external environmental.


Thermoregulatory Control Center

Hypothalamus has pituitary gland extending from it
When fluid gets cooled down, then increase temperature

Pre-optic region (PO): in the anterior hypothalamus, maintains normal set temperature around 37/98.6; senses temperature and maintains



1. PO Hypothalmus: central nerve receptors
Cold sensitive neurons
Warm sensitive neurons

2. Spinal cord & muscle

3. Skin: skin temperature receptors
Cold pain (nocireceptor) - starts at 15C
Cold receptors - 8-42C
Warm receptors - 30-50
Heat pain (nocireceptor) - starts at 45C

Cold: firing decreases
Hot: firing increases


Central Nervous System Nerve Pathways

Somatic: fires motor neurons to nicotinic receptors and then causes production of heat (uses ACh)

Sympathetic: release ACh at nicotinic receptors and then norepinephrine or ACh (muscarinic for sweat glands only) to elicit response; short pre and long post

Parasympathetic: long pre and short post; nicotinic receptors (ACh) to muscarinic (ACh)

Adrenal medulla: short pre and post; releases ACh and then goes straight to the blood and secretes NE and E


Muscarinic and Nicotinic

Muscarinic: smooth muscle, glands, and sweat glands

Nicotinic: skeletal muscle and adrenal medulla


Set Point Equation

S = (Metabolism – work) +/- radiation heat waves, conduction to objects, conduction to air/convection - evaporation


Response to Cold Stress

Blood temperature starts to drop and pre-optic hypothalamus reduces firing rate
Behavior: minimize heat loss, trying to huddle to keep warm
Muscle thermogenesis “shivering”
Brown fat: mostly in infants because cannot shiver and use thermogenin in brown adipose to keep warm

For cold stress, you reduce sympathetic cholinergic to lose sweating and increase sympathetic adrenergic to decrease blood flow and venous volume to decrease heat loss from skin


Response to Heat Stress

Skin becomes red and sweating
Blood heats up and bathes the pre-optic hypothalamus and increases firing
Drink more water, get under shade, ice packs, etc. = behavioral
Efferent output sends motor nerves to say to stop shivering
Increase in cholinergic sympathetic takes over to induce sweat glands
Lose sympathetic adrenergic system to release constriction to increase venous blood volume and blood flow to increase heat circulation to lose heat
Shut down of brown adipose thermogenesis and it reduces sympathetic adrenergic and epinephrine


Mechanism of Sweat via Eccrine Glands

Eccrine sweat gland with secretory coil, duct, and acrosyringium to release out sweat for evaporative cooling
Input signal is sympathetic cholinergic output, these are all cholinergic terminals for eccrine sweat glands
Release ACh and then inside the cells ACh is received by M3 ACh receptors and then makes lipolipase C activated to elicit the intracellular cascade to increase Ca2+ and the sodium/K+/ 2Cl- transporter becomes activated
Main effect: increase in Cl- so as intracellular Cl- levels increase they get excreted out through Cl- channel, so as Cl- is excreted out then Na follows and the NaCl is followed by water aka sweat to get evaporative cooling


Max Skin Blood Flow

Max skin blood flow: changes over time
In cold stress is vasoconstriction from increase in sympathetic adrenergic and then skin flow decreases to maintain the heat
Heat stress: release of vasoconstriction causes the sympathetic adrenergic to kick in and increase sympathetic cholinergic output to increase blood flow to dissipate heat off the body



Cause: endogenous pyrogen interactions with the hypothalamus introduced via the central ventricular organs
Effect: There is a re-setting of the internal temperature set point to a new elevated temperature

This is a different SNS response compared to elevations in body temperature due to exercise or ambient heat exposure (heat stress)


Fever Induction

Get an infection, mediators of inflammation elicit immune response (monocytes/macrophages/endothelial cells, etc.) and produce pyrogenic cytokines and IL-1, TNF alpha, IL-6, and INF(not as potent)
All enter circulation and microbial toxins interact with endothelium and produce PGE2 and cAMP to regulate set point and cause heat conservation and shivering and behavioral changes to cause fever as the final result


Fever vs. Heat Stress

Heat stress: NEVER change the set point, but internal temp can change
Fever: set point CHANGES and so does internal temperature

When you have fever dissipation, does the body go to original set point? Once the infection is over, you no longer have pyrogens that interact with hypothalamic endothelium and the cytokines are not produced and the set point can go to normal
Block the system: PGE2 is produced through COX and you can use NSAIDs to block COX so PGE2 is not synthesized and this reduces the set point back to normal


Function of Fever

Function of fever: many theories; at a higher temp, it reduces proliferation of microbes in body, or helps body rid itself of infection through unknown means
Actual mechanism is still debatable, but proliferation is most common