Blood-induced superoxide anion generation on the cerebral cortex of newborn pigs.
Blood-induced superoxide anion generation on the cerebral cortex of newborn pigs.
复制标题
血液诱导新生猪大脑皮层超氧阴离子的产生。
DOI：
10.1152/ajpheart.1989.257.5.h1560
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
C. Leffler
中科院分区：
文献类型：
--
作者：
R. Mirro;W. Armstead;J. Mirro;D. Busija;C. Leffler
猪被配备了关闭的颅窗，以测量放置在大脑皮层上的血液产生的超氧阴离子。在1)人工脑脊液(CSF)、2)同种异体非肝素化血液(血)和3)消炎痛处理后的血液中，测定超氧化物歧化酶(SOD)-可抑制的硝基蓝四氮唑(NBT)还原。与对照组相比，血液组超氧化物歧化酶可抑制的NBT还原显著增加，而吲哚美辛预处理的仔猪超氧化物歧化酶可抑制的NBT还原显著降低。这表明超氧阴离子是由血管外血液产生的，这种超氧阴离子的产生可以被吲哚美辛抑制。为了探讨超氧阴离子产生的细胞来源，在体外与仔猪全血或其成分孵育时，测定了超氧化物歧化酶抑制的NBT还原。非肝素化全血的超氧化物歧化酶抑制的NBT还原为30+/-5.7nmol.ml-1.20min-1。在吲哚美辛存在下，这一时间降至2.5+/-1.3nmol.ml-1.20min-1。ADP刺激的富血小板血浆中超氧化物歧化酶抑制的NBT还原为25.6+/-2.9nmol.400×10(6)细胞-1.20min-1，在吲哚美辛存在下显著降低(6.8+/-3.0nmol.400×10(6)细胞-1.20min-1)。粒细胞可显著降低超氧化物歧化酶抑制的NBT，但消炎痛对此无明显影响。同样，消炎痛不影响淋巴细胞和单核细胞对超氧化物歧化酶抑制的NBT还原。红细胞部分的减少很小。这些结果表明，大量的超氧阴离子是通过花生四烯酸代谢的血小板环氧合酶途径产生的。
Pigs were equipped with closed cranial windows to measure superoxide anion generation in response to blood placed on the cerebral cortex. Superoxide dismutase (SOD)-inhibitable nitro blue tetrazolium (NBT) reduction was measured in the presence of 1) artificial cerebrospinal fluid (CSF), 2) homologous nonheparinized blood (blood), and 3) blood after treatment with indomethacin. SOD-inhibitable NBT reduction was increased significantly in the blood group compared with control, whereas piglets pretreated with indomethacin had significantly less SOD-inhibitable NBT reduction. This suggests that superoxide anion is generated by extravascular blood and that this superoxide anion generation can be inhibited by indomethacin. To investigate the cellular origin of superoxide anion generation, SOD-inhibitable NBT reduction was measured during incubation with piglet whole blood or its components in vitro. The SOD-inhibitable NBT reduction of nonheparinized whole blood was 30 +/- 5.7 nmol.ml-1.20 min-1. This decreased to 2.5 +/- 1.3 nmol.ml-1.20 min-1 in the presence of indomethacin. SOD-inhibitable NBT reduction of ADP-stimulated platelet-rich plasma was 25.6 +/- 2.9 nmol.400 X 10(6) cells-1.20 min-1 and was decreased significantly (6.8 +/- 3.0 nmol.400 X 10(6) cells-1.20 min-1) in the presence of indomethacin. SOD-inhibitable NBT reduction by granulocytes was significant but unchanged by indomethacin. Similarly, SOD-inhibitable NBT reduction by lymphocytes and monocytes was unaffected by indomethacin. Reduction by the red cell fraction was small. These results suggest that substantial quantities of superoxide anion are generated via the platelet cyclooxygenase pathway of arachidonic acid metabolism.