Study on carbon monoxide toxicity independent of hypoxia

1.碳单氧化物（CO）中毒在3000 ppm的CO暴露中导致40分钟刺激的羟基自由基（·OH）产生。（1）CO诱导的OH生成被一个电压依赖的Na^+通道阻断剂四氯毒素（TTX）抑制。（2） CO中毒增加了提取物谷氨酸（Glu）水平，但Glu受体拮抗剂（MK-801和NBQX）对OH一代没有影响。（3） α-甲基对酪氨酸、氯基林（DA合成和氧化物代谢的抑制剂，负责任地）和二美替氮21-磷酸盐（磷酸酶A2抑制剂）对CO-诱导的OH产生没有影响。（4）氮氧化物（NO）合成酶抑制剂和NO预催化剂、L-精氨酸（L-Arg）及其映体、D-Arg，对CO-诱导的OH产生有复杂效应。（这可能至少是部分原因，因为它的性质可能具有较低的能力，以增强无生产，由exogenous L-Arg使用。）（5）CO-诱导的OH一代被诱导得更慢，而CO中毒在提取物中的存在比提取物猫的缺失更少。The ·OH generation in the absence of extracellular Ca^<2+> was suppressed by dantrolene （an inhibitor of Ca^<2+> release from sarcoplasmic reticulum）。（6） Hypoxic hypoxia （HH; 5%O_2 for 40 min） stimulated ·OH generation in the striatum， though more wearly than the CO poisoning. 2。一氧化碳（3000 ppm，40分钟）和HH （5%O_2，40分钟）在O_2含量和氧红细胞水平中诱导了类似变化，但不是pO_2，在动脉血液和提取物氨基酸（Glu、姜黄和丙氨酸）中，血液流动和pO_2在结构中。

1. Carbon monoxide (CO) poisoning caused by CO exposure at 3000 ppm for 40 min stimulated hydroxyl radical (・OH) generation in rat striatum.(1) The CO-induced ・OH generation was suppressed by a voltage-dependent Na^+ channel blocker, tetrodotoxin (TTX).(2) CO poisoning increased the extracellular glutamate (Glu) level, but Glu receptor antagonists (MK-801 and NBQX) had no effect on the ・OH generation.(3) α-Methyl-p-tyrosine, clorgyline (Inhibitors of DA synthesis and oxidative metabolism, respectively) and dexamethazone 21-phosphate (a phospholipase A2 inhibitor) had no effect on the CO-induced ・OH generation.(4) Nitric oxide (NO) synthase inhibitors and an NO precursor, L-arginine (L-Arg), and its enantiomer, D-Arg, had complex effects on the CO-induced ・OH generation. (This might be at least partly due to the nature of the striatum that may have a low ability to enhance NO production by utilising exogenous L-Arg.)(5) The CO-induced ・OH generation was more slowly induced by the CO poisoning in the absence of extracellular Cat than in the presence of extracellular Ca^<2+>. The ・OH generation in the absence of extracellular Ca^<2+> was suppressed by dantrolene (an inhibitor of Ca^<2+> release from sarcoplasmic reticulum).(6) Hypoxic hypoxia (HH; 5% O_2 for 40 min) stimulated ・OH generation in the striatum, though more wearly than the CO poisoning.2. CO (3000 ppm for 40 min) and HH (5% O_2 for 40 min) induced similar changes in O_2 contents and oxyhemoglobin levels, but not pO_2, in arterial blood and extracellular amino acids (Glu, taurine and alanine), the blood flow and pO_2 in the striatum.