Adenosine in hemorrhagic shock: possible role in attenuating sympathetic activation.
Changes in plasma purine nucleoside level, autonomic activity and hemodynamic reactions were studied in pentobarbital anesthetized rabbits during hemorrhagic shock. Shock was elicited by bleeding the animals to a mean blood pressure of 40 mmHg and maintained until 60% of the maximum bleeding volume in the reservoir had been taken up spontaneously. The remaining shed blood was reinfused thereafter. Norepinephrine (NE), epinephrine (E), adenosine (AD) and uric acid were measured by HPLC with electrochemical detection, fluorometry or UV absorbance. The results showed hemorrhagic shock caused a significant rise in plasma NE, E, AD, and uric acid levels, but the magnitudes and time profiles were different among them. Plasma NE and E increased during the shock compensatory period then declined in the decompensation period whereas adenosine and its metabolite uric acid were elevated persistently during both periods. It is concluded that a balance between autonomic activity and tissue metabolism is important in the maintenance of hemodynamics during shock.
D000241:Adenosine / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011817:Rabbits; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D014527:Uric Acid / Q000097:blood
D014527:Uric Acid; D000241:Adenosine; D009638:Norepinephrine; D004837:Epinephrine