Snoeckx L H, van der Vusse G J, Coumans W A, Reneman R S
Department of Physiology, Cardiovascular Research Institute Maastricht, University of Limburg, The Netherlands.
J Mol Cell Cardiol. 1990 Dec;22(12):1439-52. doi: 10.1016/0022-2828(90)90987-d.
Abdominal aorta constriction was performed in 10-week-old Lewis rats (Aoband). Ten weeks later the hearts were isolated and attached to a non-recirculating perfusion apparatus. The hearts could eject against a diastolic aortic pressure of either 60 or 100 mmHg. The functional recovery was compared with that of hearts of sham-operated (Sham) rats. After 45 min of global ischemia, Sham hearts regained cardiac output up to 75% and 70% of the pre-ischemic levels at 60 and 100 mmHg, respectively. At 60 mmHg Aoband hearts showed a minor recovery of ejection function. However, at 100 mmHg the recovery of Aoband hearts was completely comparable with that of Sham hearts. At 60 mmHg but not at 100 mmHg, the pre-ischemic and post-ischemic coronary flow was lower in Aoband than in Sham hearts (P less than or equal to 0.05). During the initial reperfusion phase Sham hearts, perfused at 60 mmHg, released more degradation products of adenine nucleotides and lactate dehydrogenase (LDH) than Aoband hearts (P less than or equal to 0.05), while the Aoband hearts lost more degradation products and LDH than the Sham hearts later during the reperfusion phase (P less than or equal to 0.05). In the groups perfused at 60 mmHg, higher tissue levels of ATP were found in Sham than in Aoband hearts at the end of the reperfusion period (P less than or equal to 0.05). However, at 100 mmHg comparable levels were found in the Sham and Aoband hearts. It is concluded that the height of the coronary perfusion pressure is of critical importance for the post-ischemic functional recovery of the compensated hypertrophied heart. At sufficiently high perfusion pressure levels, the functional and biochemical recovery of the hypertrophied heart is at least as good as in the non-hypertrophied heart. However, in the hypertrophied heart a coronary perfusion pressure which is too low leads to relative underperfusion during the initial reperfusion period which is associated with severely depressed cardiac performance and delayed wash-out of metabolites and intracellular enzymes.
对10周龄的Lewis大鼠（Aoband）进行腹主动脉缩窄术。10周后，分离心脏并连接到非循环灌注装置上。心脏能够在60或100 mmHg的舒张期主动脉压力下射血。将其功能恢复情况与假手术（Sham）大鼠的心脏进行比较。在45分钟全心缺血后，Sham心脏在60和100 mmHg时的心输出量分别恢复到缺血前水平的75%和70%。在60 mmHg时，Aoband心脏的射血功能有轻微恢复。然而，在100 mmHg时，Aoband心脏的恢复情况与Sham心脏完全相当。在60 mmHg而非100 mmHg时，Aoband心脏缺血前和缺血后的冠状动脉血流量低于Sham心脏（P≤0.05）。在最初的再灌注阶段，以60 mmHg灌注的Sham心脏比Aoband心脏释放更多的腺嘌呤核苷酸降解产物和乳酸脱氢酶（LDH）（P≤0.05），而在再灌注后期，Aoband心脏比Sham心脏损失更多的降解产物和LDH（P≤0.05）。在以60 mmHg灌注的组中，再灌注期结束时，Sham心脏的组织ATP水平高于Aoband心脏（P≤0.05）。然而，在100 mmHg时，Sham和Aoband心脏的ATP水平相当。结论是，冠状动脉灌注压的高度对代偿性肥厚心脏缺血后的功能恢复至关重要。在足够高的灌注压力水平下，肥厚心脏的功能和生化恢复至少与非肥厚心脏一样好。然而，在肥厚心脏中，过低的冠状动脉灌注压力会导致最初再灌注期的相对灌注不足，这与心脏功能严重受损以及代谢产物和细胞内酶的清除延迟有关。
