Caty M G, Schmeling D J, Friedl H P, Oldham K T, Guice K S, Till G O
Department of Surgery, University of Michigan Medical School, Ann Arbor.
J Pediatr Surg. 1990 Feb;25(2):218-22; discussion 222-3. doi: 10.1016/0022-3468(90)90406-y.
Xanthine oxidase (XO)-derived oxygen radicals are thought to play an important role in the intestinal injury resulting from ischemia and reperfusion. In vitro data shows enhanced XO activity in the presence of histamine. Histamine is known to be released during intestinal ischemia and reperfusion. The purpose of this study was to evaluate the relationship between histamine and XO in vivo in intestinal ischemia/reperfusion injury. Using an established model of gut ischemia and reperfusion, portal venous plasma was obtained and assayed for histamine levels, XO activity, and xanthine dehydrogenase (XD) activity following injury. Intestinal ischemia for 120 minutes resulted in a 200% increase in plasma histamine levels (263.4 +/- 36.9 nmol/mL control, v 548.7 +/- 35.1 nmol/mL experimental, P less than .05). Reperfusion for 15 minutes resulted in a further increase in plasma histamine (to 658.3 +/- 33.9 nmol/mL), compared with 120 minutes of ischemia alone. No significant change in plasma XO activity resulted after simple ischemia for 120 minutes. However, XO activity doubled within 15 minutes of reperfusion of the ischemic intestine (6.37 +/- 0.53 nmol O2- per milliliter per minute v 3.12 +/- 0.25 nmol O2- per milliliter per minute, P less than .05). Reperfusion for 60 minutes resulted in the maximal observed increase in plasma XO activity (9.49 +/- 0.67 nmol O2- per milliliter per minute). Analysis of XD activity demonstrated no significant decrease compared with controls until 120 minutes of ischemia and 60 minutes of reperfusion (1.62 +/- 0.49 nmol uric acid per milliliter per minute at 60 minutes of reperfusion, versus 5.02 +/- 0.52 nmol uric acid per milliliter per minute control, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
黄嘌呤氧化酶（XO）衍生的氧自由基被认为在缺血再灌注引起的肠道损伤中起重要作用。体外数据显示，在组胺存在的情况下，XO活性增强。已知组胺在肠道缺血再灌注期间会释放。本研究的目的是评估在肠道缺血/再灌注损伤的体内情况下，组胺与XO之间的关系。使用已建立的肠道缺血再灌注模型，在损伤后获取门静脉血浆，检测组胺水平、XO活性和黄嘌呤脱氢酶（XD）活性。肠道缺血120分钟导致血浆组胺水平增加200%（对照组为263.4±36.9 nmol/mL，实验组为548.7±35.1 nmol/mL，P<0.05）。再灌注15分钟导致血浆组胺进一步增加（达到658.3±33.9 nmol/mL），与单纯缺血120分钟相比。单纯缺血120分钟后，血浆XO活性无显著变化。然而，缺血肠道再灌注15分钟内XO活性增加了一倍（6.37±0.53 nmol O2-每分钟每毫升对3.12±0.25 nmol O2-每分钟每毫升，P<0.05）。再灌注60分钟导致血浆XO活性出现观察到的最大增加（9.49±0.67 nmol O2-每分钟每毫升）。对XD活性的分析表明，直到缺血120分钟和再灌注60分钟，与对照组相比才出现显著下降（再灌注60分钟时为1.62±0.49 nmol尿酸每分钟每毫升，对照组为5.02±0.52 nmol尿酸每分钟每毫升，P<0.05）。（摘要截选至250字）
