Spillert C R, Sun S, Miller M A, Lazaro E J
Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103-2757.
J Natl Med Assoc. 1994 Sep;86(9):686-8.
Although hypertension is a major risk factor in acute myocardial infarction, concomitant hypercoagulability causing thrombosis leading to myocardial infarction remains unproven for lack of an appropriate coagulation test. This study was devised to determine whether a modified recalcification time (MRT) test can demonstrate that angiotensin II, a potent vasoconstrictor, also accelerates coagulation to promote thrombosis. The MRT incorporates blood cells and chemical coagulants for maximizing sensitivity. Four groups (A, B, C, and D) of aliquots of citrated human blood were incubated for 2 hours at 37 degrees C after adding to A--20 microL saline, to B--10 micrograms Escherichia coli endotoxin, to C--20 micrograms angiotensin II, and to D--a combination of E coli endotoxin and angiotensin II. The experiment was repeated with nonincubated aliquots. Modified recalcification time values +/- standard deviation in minutes were: A--5.5 +/- 1.5, B--4.6 +/- 1.1, C--4.9 +/- 1.0, and D--3.9 +/- 1.0. Significance (Student's t test) was as follows: B versus A P < .001; C versus A, P < .05; C versus D, P < .001; B versus C, P < .05; and B versus D, P < .001. No significant changes occurred in nonincubated blood. We conclude that angiotensin II has a hypercoagulable effect, as does endotoxin. The hypercoagulability in concert with vasospasm can explain the role of hypertension in acute myocardial infarction. This in vitro study excludes the role of other in vivo mechanisms in the development of angiotensin II-induced hypercoagulability.
尽管高血压是急性心肌梗死的主要危险因素，但由于缺乏合适的凝血检测方法，导致血栓形成进而引发心肌梗死的伴随高凝状态仍未得到证实。本研究旨在确定改良复钙时间（MRT）试验能否证明血管紧张素II（一种强效血管收缩剂）也会加速凝血以促进血栓形成。MRT纳入血细胞和化学凝血剂以最大化敏感性。将四组（A、B、C和D）枸橼酸化人血等分试样在37℃孵育2小时，其中A组加入20微升生理盐水，B组加入10微克大肠杆菌内毒素，C组加入20微克血管紧张素II，D组加入大肠杆菌内毒素和血管紧张素II的组合。对未孵育的等分试样重复该实验。改良复钙时间值（分钟）±标准差为：A组5.5±1.5，B组4.6±1.1，C组4.9±1.0，D组3.9±1.0。显著性（学生t检验）如下：B组与A组比较，P<0.001；C组与A组比较，P<0.05；C组与D组比较，P<0.001；B组与C组比较，P<0.05；B组与D组比较，P<0.001。未孵育的血液未发生显著变化。我们得出结论，血管紧张素II与内毒素一样具有促凝作用。高凝状态与血管痉挛共同作用可以解释高血压在急性心肌梗死中的作用。这项体外研究排除了其他体内机制在血管紧张素II诱导的高凝状态发生过程中的作用。
