Ott I, Neumann F J, Schömig A
First Medizinische Klinik, Technische Universität München, Germany.
Coron Artery Dis. 1995 Jul;6(7):525-32.
Previous studies have suggested an increased risk of myocardial infarction associated with physical exercise. Activated neutrophils may contribute to the triggering mechanisms.
Fifteen patients with stable angina pectoris underwent symptom-limited bicycle ergometry. In neutrophils obtained from serial blood samples, superoxide anion production (SOP) was determined by superoxide dismutase-inhibited reduction of cytochrome C and chemotactic mobility in the microchemotaxis chamber. The same ergometry was repeated after successful balloon angioplasty [percutaneous transluminal coronary angioplasty (PTCA)].
Rate-pressure products and systemic lactate concentrations were similar in both ergometries. Angina was induced in all exercise tests before PTCA, but in none after PTCA. Before the ergometries, systemic neutrophil counts, SOP and chemotactic mobility were essentially the same. Compared with baseline, exercise-induced angina immediately after the first ergometry was associated with an increase in neutrophil count by 0.8 +/- 0.1 nl-7 (P < 0.01), an increase in N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated SOP by 2.44 +/- 0.49 nmol/15 min/5000 cells (P < 0.01) and an increase in chemotaxis by 10.28 +/- 1.65 cells per vision field (P < 0.01). In the ergometry after PTCA this increase in SOP and in chemotaxis disappeared (0.26 +/- 0.39 nmol/15 min/5000 cells and 2.15 +/- 1.52 cells per vision field; NS), whereas the increase in neutrophil count was not significantly different from that in the ergometry before PTCA.
This study reveals that neutrophil hyper-reactivity after exercise-induced angina can be attributed to myocardial ischaemia.
先前的研究表明，体育锻炼会增加心肌梗死的风险。活化的中性粒细胞可能参与触发机制。
15例稳定型心绞痛患者接受了症状限制的自行车测力计运动试验。从连续采集的血样中获取中性粒细胞，通过超氧化物歧化酶抑制的细胞色素C还原法测定超氧阴离子生成（SOP），并在微量趋化性室中测定趋化运动性。在成功进行球囊血管成形术[经皮腔内冠状动脉成形术（PTCA）]后重复相同的测力计运动试验。
两次测力计运动试验中的心率-血压乘积和全身乳酸浓度相似。PTCA前的所有运动试验均诱发心绞痛，但PTCA后均未诱发。在测力计运动试验前，全身中性粒细胞计数、SOP和趋化运动性基本相同。与基线相比，第一次测力计运动试验后立即出现的运动诱发心绞痛与中性粒细胞计数增加0.8±0.1 nl⁻¹（P<0.01）、N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）刺激的SOP增加2.44±0.49 nmol/15分钟/5000个细胞（P<0.01）以及趋化性增加10.28±1.65个细胞/视野（P<0.01）相关。在PTCA后的测力计运动试验中，SOP和趋化性的这种增加消失（0.26±0.39 nmol/15分钟/5000个细胞和2.15±1.52个细胞/视野；无显著性差异），而中性粒细胞计数的增加与PTCA前的测力计运动试验相比无显著差异。
本研究表明，运动诱发心绞痛后中性粒细胞的高反应性可归因于心肌缺血。
