Respiratory and acid-base parameters during salicylic intoxication in XXXX .

@entity825 @entity2697 @entity4486 @entity235 @entity11141 @entity4774 @entity221 @entity3945 @entity10441
This paper examines the mechanism responsible for @entity10441 and accompanying @entity3945 during acute salicylism. @entity11141 (250 mg/kg) was administered to 8 spontaneously breathing anesthetized @entity235 ( @entity4486 , 50 mg/kg, and @entity4774 , 500 mg/kg, iv). The @entity825 was sectioned and connected to a pneumotachograph. A catheter was placed in the cisterna magna for sampling cerebrospinal fluid (CSF) and a femoral artery was cannulated for blood sampling and pressure determinations. Once the cardiorespiratory steady-state was obtained, air flow, tidal volume, arterial pressure, ECG and rectal temperature were measured for baseline control. The measurements were repeated 8 times during 100 min after @entity2697 infusion. Simultaneous determinations of CSF and plasma @entity2697 showed that plasmatic levels were maximal just after infusion, diminishing with time. CSF concentration increased gradually as the @entity2697 diffused through the blood-brain barrier. Minute ventilation increased to more than 600% of control values and was maximal between 60-100 min after @entity2697 infusion. @entity3945 and @entity221 (up to 40.3 degrees C) followed the time-course of @entity10441 . Only a small part of @entity10441 can be attributed to the temperature increase. A high correlation coefficient (r = 0.974) was obtained by regression analysis of the values for ventilation and CSF @entity2697 . We conclude that the central action of @entity2697 is much more important for increasing ventilation than effects related to oxidative phosphorylation uncoupling.
