Li S Q, Zhao G, Li J, Qian W
Department of Pathophysiology, Kunming Medical College, China.
Zhongguo Yao Li Xue Bao. 1998 Sep;19(5):493-6.
To study the effect of histidine on cerebral thrombosis and possible mechanism.
Cerebral-cardiac stroke was produced by photochemically induced thrombotic cerebral ischemia in rats.
Platelet aggregation in whole blood increased markedly, peak heights at 4 and 24 h were (5.1 +/- 0.5) omega and (4.3 +/- 0.5) omega, respectively. Heart mitochondria volume (V), volume density (Vv), surface density (Nm), and surface density of outer membrane (Sv1) increased (8.2 +/- 5.5, 0.59 +/- 0.16, 0.11 +/- 0.03, and 0.22 +/- 0.05, respectively, P < 0.01), but numerical density (Nv), specific surface of inner membrane (delta 2) and of the cristae (delta 3) decreased (0.07 +/- 0.02, 2.8 +/- 0.8, and 2.4 +/- 0.7, respectively, P < 0.01) after cerebral thrombosis. The myocardial histopathologic characteristics were different from those of ischemic necrosis and myocardial damage caused by ischemic reperfusion. In rat treated with histidine after photochemical reaction, platelet aggregation decreased markedly [(2.93 +/- 1.08) omega, P < 0.01], reversible change often went with parameters related to the inner mitochondrial membrane but not the outer mitochondrial membrane.
Histidine depressed platelet aggregation and reduced myocardial mitochondrial damage resulted from cerebral ischemia.
研究组氨酸对脑血栓形成的影响及其可能机制。
采用光化学诱导血栓形成性脑缺血法制备大鼠脑心卒中模型。
全血中血小板聚集显著增加,4小时和24小时的峰值分别为(5.1±0.5)Ω和(4.3±0.5)Ω。脑血栓形成后,心脏线粒体体积(V)、体积密度(Vv)、表面密度(Nm)和外膜表面密度(Sv1)增加(分别为8.2±5.5、0.59±0.16、0.11±0.03和0.22±0.05,P<0.01),但数密度(Nv)、内膜比表面积(δ2)和嵴比表面积(δ3)降低(分别为0.07±0.02、2.8±0.8和2.4±0.7,P<0.01)。心肌组织病理学特征不同于缺血坏死和缺血再灌注引起的心肌损伤。光化学反应后用组氨酸处理的大鼠,血小板聚集显著降低[(2.93±1.08)Ω,P<0.01],线粒体膜相关参数常出现可逆性变化,但外膜无此变化。
组氨酸可抑制血小板聚集,并减轻脑缺血所致的心肌线粒体损伤。