Katsumata Y, Aoki M, Sato K, Oya M, Yada S, Suzuki O, Yoshino M
Forensic Sci Int. 1981 Jul-Aug;18(1):1-4. doi: 10.1016/0379-0738(81)90132-8.
The effect of carbon monoxide (CO) inhalation on plasma levels of uric acid and hypoxanthine in rats was investigated. Exposure to 3% CO caused respiratory arrest within about 2 minutes. The plasma uric acid level of CO-treated rats increased to 157% above that of ether-treated rats. When rats were exposed to 1% or 0.8% CO, the exposure periods until the onset of respiratory arrest were prolonged, and plasma uric acid levels at respiratory arrest were further elevated. Plasma uric acid levels at respiratory arrest increased with prolongation of the exposure periods. Under our experimental conditions, hypoxanthine or xanthine was not detected in plasma of CO-treated rats. These results are discussed in relation to the hyperuricemia in hemorrhagic shock or hypoxemia: CO-induced hyperuricemia can be attributed to the stimulated degradation of adenine nucleotides under tissue anoxia, and thus could be an excellent parameter of tissue anoxia.
研究了吸入一氧化碳（CO）对大鼠血浆尿酸和次黄嘌呤水平的影响。暴露于3%的CO中约2分钟内会导致呼吸停止。经CO处理的大鼠血浆尿酸水平比经乙醚处理的大鼠高出157%。当大鼠暴露于1%或0.8%的CO中时，直至呼吸停止开始的暴露时间延长，且呼吸停止时的血浆尿酸水平进一步升高。呼吸停止时的血浆尿酸水平随暴露时间的延长而增加。在我们的实验条件下，未在经CO处理的大鼠血浆中检测到次黄嘌呤或黄嘌呤。结合失血性休克或低氧血症中的高尿酸血症对这些结果进行了讨论：CO诱导的高尿酸血症可归因于组织缺氧时腺嘌呤核苷酸降解的刺激，因此可能是组织缺氧的一个良好指标。
