bioguy wrote:dowjunk wrote:
Fever is a response of hypothalamus against an exo/endo pyretic substance. This response is PGE2................PGE2 will favour an ischemic attack, especially in the presence of platelets: more TXA2 will be formed, as the cor art constricts!
I will be needing your opinion whether its the constriction (more of what i think) in coronary arteries, becuase i am confused as i read somewhere that its the pGE2 influenced reperfusion of myocardial cells thats more threatening?
I thought PGE2 is a vasodilator. In the case of fever, I was thinking more in terms of hemodynamic changes that demand an increased cardiac output - increasing O2 demand of myocardium - relative ischemia - MI I am not sure - what are the hemodynamic changes in Fever? (if there are any)
Yes all changes in the body are somehow regulated by a 'mechanism'; this includes hemodynamic changes! During fever, the body is conserving body heat  by the vasoconstriction effect of skin vessels thru hypothal control. May be what you are discussing is this rise in body heat causing all metabolic activties to increase considerably....hence a reiased hemodynamic function. Definetely this leads to more heart work! But I would still think that its the prostaglandins and interleukins involved in ischemic pain if any! Research favors this concept. Although the hemodynamic load would exacerbate the phenomenon. Any way.....a topic that is very much studied by the researchers these days than the physicians  ......so no worries
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And thanks GG.....made things clear regarding the central influence of cyanosis in TOF!
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