Shattock M J, Manning A S, Hearse D J
Pharmacology. 1982;24(2):118-22. doi: 10.1159/000137585.
The effects of hydrogen peroxide on the normal and ischaemic myocardium were investigated using the isolated 'working' rat heart preparation. In the range 0-3 microM no changes in heart rate, aortic flow, coronary flow, or aortic pressure were observed. Between 3 and 30 microM, however, there was a dose-dependent fall in aortic flow and an accompanying increase in coronary flow, the total cardiac output remaining unchanged. At concentrations about 30 microM functional failure occurred. Following a 24-min ischaemic period during which time 6 microM hydrogen peroxide was infused via the aorta at a constant rate to remove any vasodilatory effect, all hearts failed to recover. In contrast, 50% of control hearts recovered pump function. In conclusion, therefore, hydrogen peroxide can reduce function in the aerobic working rat heart and may exert a vasodilatory effect. When this effect is eliminated hydrogen peroxide affords no protection during ischaemia and appears to exacerbate tissue injury.
使用离体“工作”大鼠心脏标本研究了过氧化氢对正常和缺血心肌的影响。在0至3微摩尔范围内,未观察到心率、主动脉流量、冠状动脉流量或主动脉压力的变化。然而,在3至30微摩尔之间,主动脉流量呈剂量依赖性下降,同时冠状动脉流量增加,总心输出量保持不变。在浓度约为30微摩尔时出现功能衰竭。在24分钟的缺血期内,以恒定速率通过主动脉注入6微摩尔过氧化氢以消除任何血管舒张作用,所有心脏均未能恢复。相比之下,50%的对照心脏恢复了泵功能。因此,综上所述,过氧化氢可降低有氧工作大鼠心脏的功能,并可能发挥血管舒张作用。当这种作用消除后,过氧化氢在缺血期间不能提供保护,反而似乎会加重组织损伤。