[Fever as a homeostatic process accompanying infection].
After a survey of experimental data the author considers the notion that elevated (febrile) temperature acts as an adaptive factor buffering against the disordering of biomembrane homeostasis during infection. Impendance of the membrane homeostasis under infectious conditions occurs due to the certain disturbance of membrane structure caused by pyrogen-induced activation of phospholipases and liberation of arachidonic acid from phospholipid deposits. A consequence of liberation and oxygenation of the arachidonic acid is an outflow of double bonds from the overall pool embedded in the structure of membrane. This in turn leads to an increase of membrane bulk phase transition temperature and to depletion of membrane fluidity at normal (non-febrile) temperature.
Kozak
W
W
Katedra i Zakład Fizjologii AM, Bydgoszczy.
D000890:Anti-Infective Agents / Q000627:therapeutic use; D001095:Arachidonic Acids / Q000378:metabolism; D001833:Body Temperature Regulation / Q000187:drug effects / Q000502:physiology*; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D005334:Fever / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007239:Infections / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D007375:Interleukin-1 / Q000378:metabolism; D008560:Membrane Fluidity / Q000187:drug effects / Q000502:physiology
D000890:Anti-Infective Agents; D001095:Arachidonic Acids; D007375:Interleukin-1
Goraczka jako proces homeostatyczny towarzyszacy infekcji.