Konorev E A, Tarpey M M, Joseph J, Baker J E, Kalyanaraman B
Biophysics Research Institute, Medical College of Wisconsin, Milwaukee 53226, USA.
Free Radic Biol Med. 1995 Feb;18(2):169-77. doi: 10.1016/0891-5849(94)00112-w.
Nitronyl nitroxides have been used to trap nitric oxide (.NO) produced during visible irradiation of nitrovasodilators such as sodium nitroprusside (Joseph et al., Biochem. Biophys. Res. Commun. 192:926-934; 1993). We have also shown that nitrone and nitroso spin traps exert a potent vasodilatory effect in the isolated perfused rat heart (Konorev et al., Free Radic. Biol. Med. 14:127-137, 1993). The objective of this study was to investigate the effect of nitronyl nitroxides on the vasodilatory action of sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), alpha-(4-pyridyl-1-oxide)-N-tert-butyl nitrone (POBN) and 4-hydroxy-2,2,6,6-tetramethylpiperidinyloxy free radical (TEMPOL) in the isolated perfused rat heart model. In this study, we have used the following nitronyl nitroxides as nitric oxide traps: 2-(p-carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-3-oxide 1-oxyl (SLI) and 2(1',1'-dimethyl-2'-hydroxyethyl)-4,4,5,5-tetramethyl imidazoline-3-oxide 1-oxyl (SLII). Under in vitro conditions, both SLI and SLII trapped .NO released from SNP/light treatment and from spontaneous decomposition of SNAP, forming the corresponding imino nitroxides, which were characterized by electron spin resonance (ESR) technique. In isolated hearts, SNP (2 mumol/l) and SNAP (20 mumol/l) increased coronary flow rate to a maximum of 185% and 190%, respectively. SNP-induced vasodilation was inhibited by SLI (0.05-3 mmol/l) from 162% to 131% of baseline, and SNAP-induced vasodilation was inhibited by SLII (0.05-1.2 mmol/l) from 190% to 136% of baseline. In contrast, neither SLI nor SLII inhibited the vasodilatory action elicited by POBN or TEMPOL.(ABSTRACT TRUNCATED AT 250 WORDS)
硝酮氮氧化物已被用于捕获硝血管扩张剂（如硝普钠）在可见光照射过程中产生的一氧化氮（·NO）（约瑟夫等人，《生物化学与生物物理研究通讯》192:926 - 934；1993年）。我们还表明，硝酮和亚硝基自旋捕获剂在离体灌注大鼠心脏中发挥强大的血管舒张作用（科诺列夫等人，《自由基生物学与医学》14:127 - 137，1993年）。本研究的目的是在离体灌注大鼠心脏模型中研究硝酮氮氧化物对硝普钠（SNP）、S - 亚硝基 - N - 乙酰青霉胺（SNAP）、α -（4 - 吡啶基 - 1 - 氧化物）- N - 叔丁基硝酮（POBN）和4 - 羟基 - 2,2,6,6 - 四甲基哌啶氧基自由基（TEMPOL）血管舒张作用的影响。在本研究中，我们使用了以下硝酮氮氧化物作为一氧化氮捕获剂：2 -（对羧基苯基）- 4,4,5,5 - 四甲基咪唑啉 - 3 - 氧化物1 - 氧基（SLI）和2（1',1' - 二甲基 - 2' - 羟乙基）- 4,4,5,5 - 四甲基咪唑啉 - 3 - 氧化物1 - 氧基（SLII）。在体外条件下，SLI和SLII均捕获了SNP/光照处理以及SNAP自发分解释放的·NO，形成了相应的亚氨基氮氧化物，通过电子自旋共振（ESR）技术对其进行了表征。在离体心脏中，SNP（2 μmol/l）和SNAP（20 μmol/l）分别使冠状动脉血流速率最大增加至185%和190%。SLI（0.05 - 3 mmol/l）将SNP诱导的血管舒张从基线的162%抑制至131%，SLII（0.05 - 1.2 mmol/l）将SNAP诱导的血管舒张从基线的190%抑制至136%。相比之下，SLI和SLII均未抑制POBN或TEMPOL引发的血管舒张作用。（摘要截短至250字）
