Valen G, Kaszaki J, Szabo I, Nagy S, Vaage J
Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.
Agents Actions. 1993 Sep;40(1-2):37-43. doi: 10.1007/BF01976749.
Release of histamine (H) by ischemia-reperfusion injury was investigated in isolated rat hearts (Langendorff model). The effect of 10, 15, 20, 25, 30, 40 and 60 min ischemia (n = 10 each) on H in the coronary effluent and in cardiac tissue was studied after 4 min reperfusion. Release of creatine kinase and lactate dehydrogenase in the coronary effluent increased with time of ischemia. Tissue H increased from 95 +/- 10 ng/g rat heart (mean +/- SEM) before ischemia to max 148 +/- 10 ng/g after 20 min ischemia (p < 0.002), and increased also after 15 (p < 0.01), 25 (p < 0.01), and 30 min (p < 0.045). H in the coronary effluent increased after 15 (from 16 +/- 3 to 26 +/- 2 pmol/min, p < 0.044), 30 (26 +/- 6 pmol/min, p < 0.027), and 60 min ischemia (47 +/- 6 pmol/min, p < 0.0044). Release of H during ischemia-reperfusion is neither dependent on the severity of the ischemic insult, nor on the level of tissue H.
在离体大鼠心脏（Langendorff模型）中研究了缺血再灌注损伤引起的组胺（H）释放。在4分钟再灌注后，研究了10、15、20、25、30、40和60分钟缺血（每组n = 10）对冠脉流出液和心脏组织中H的影响。冠脉流出液中肌酸激酶和乳酸脱氢酶的释放随缺血时间增加。组织H从缺血前的95±10 ng/g大鼠心脏（平均值±标准误）增加到缺血20分钟后的最高148±10 ng/g（p < 0.002），在15分钟（p < 0.01）、25分钟（p < 0.01）和30分钟（p < 0.045）后也增加。冠脉流出液中的H在缺血15分钟（从16±3至26±2 pmol/分钟，p < 0.044）、30分钟（26±6 pmol/分钟，p < 0.027）和60分钟（47±6 pmol/分钟，p < 0.0044）后增加。缺血再灌注期间H的释放既不依赖于缺血损伤的严重程度，也不依赖于组织H的水平。
