These results do not rule out the role of AVP during antipyresis but rather suggest that several endogenous antipyretics may be involved in the febrile response (Moltz, 1993).
These findings suggest that AVP is centrally released during osmotic stimuli and hypovolemia and that 24-hour water deprivation, resulting in a combination of hypovolemia and hyperosmolality, would also be expected to release central AVP and, therefore, induce antipyresis.
During endotoxin fever, AVP-V1 antagonists infused within the ventral septum block salicylate antipyresis but had no effect on the antipyretic action of acetaminophen (Wilkinson & Kasting, 1990).
Thus, it has been recommended that the lowest therapeutic dose that provides sufficient antipyresis should be used in order to prevent potential toxicity or adverse side effects in children (AAP, 2001).
If these three factors are guaranteed, the child is likely to achieve adequate antipyresis. However, if the use of either acetaminophen or ibuprofen is not effective and if additional nonpharmacological methods of fever reduction have also failed, the practitioner is encouraged to proceed with caution when recommending alternating antipyretic therapy.
Maximum antipyresis was reached at approximately 3-4 hours after administration for both drugs (Kauffman & Nelson, 1992; Kelley et al, 1992; Wilson et al, 1991).
The more rapid antipyresis in younger children has been attributed to their greater body surface, which allows for more rapid heat loss via the skin (Kauffman & Nelson, 1992).