Hoffmeister H M, Storf R, Seipel L
Medizinische Klinik, Abt. III, Universität Tübingen, Federal Republic of Germany.
Cardiovasc Res. 1988 Dec;22(12):881-8. doi: 10.1093/cvr/22.12.881.
The effect of graded ischaemic injury on post-ischaemic myocardium was examined in rat hearts after three 4 min periods of asphyxia. Systolic function under steady state conditions and during isovolumic beats, the content of high energy phosphates and glycogen, and myocardial material properties were determined. Severity of the oxygen deficiency was varied by manipulating myocardial oxygen demand (MVO2) either by rapid atrial pacing or by vagal stimulation. After 20 min of post-asphyxial recovery, steady state haemodynamics were almost normal. In the high MVO2 group (atrial pacing) the dp/dtmax was reduced to 90%(NS). The isovolumic indices of function were decreased in all post-asphyxial groups. This was most pronounced in the high MVO2 group, with a reduction in peak left ventricular systolic pressure to 85.7 (SEM 3.4)% and a decrease in peak left ventricular systolic stress to 82.3(3.9)% (p less than 0.01). The post-asphyxial myocardial performance recovered better in the low MVO2 group (vagal stimulation). Material properties were altered only in the high MVO2 group. The decreased content of ATP and glycogen were comparable in all post-asphyxial groups. A phosphocreatine overshoot phenomenon was most marked in the high MVO2 group: 11.4(2.8) mumol.g-1 v 4.7(0.9) mumol.g-1 (control), p less than 0.01. The results indicate that post-ischaemic contractile dysfunction of reversibly injured is not closely related to the previous O2 deficit or to the functional impairment. We also obtained no correlation between ATP content and material properties in modestly injured post-ischaemic myocardium.
在大鼠心脏经历三次4分钟的窒息期后，研究了分级缺血性损伤对缺血后心肌的影响。测定了稳态条件下及等容搏动期间的收缩功能、高能磷酸盐和糖原含量以及心肌物质特性。通过快速心房起搏或迷走神经刺激来操纵心肌需氧量（MVO2），从而改变缺氧的严重程度。窒息后恢复20分钟后，稳态血流动力学几乎正常。在高MVO2组（心房起搏）中，dp/dtmax降至90%（无统计学意义）。所有窒息后组的功能等容指数均降低。这在高MVO2组中最为明显，左心室收缩压峰值降至85.7（标准误3.4）%，左心室收缩应力峰值降至82.3（3.9）%（p<0.01）。低MVO2组（迷走神经刺激）的窒息后心肌性能恢复较好。仅在高MVO2组中物质特性发生改变。所有窒息后组中ATP和糖原含量的降低程度相当。磷酸肌酸过冲现象在高MVO2组中最为明显：11.4（2.8）μmol·g-1 对比 4.7（0.9）μmol·g-1（对照组），p<0.01。结果表明，可逆性损伤的缺血后收缩功能障碍与先前的氧缺乏或功能损害没有密切关系。在轻度损伤的缺血后心肌中，我们也未发现ATP含量与物质特性之间存在相关性。
