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心脏停搏液对低温缺血性停搏后肥厚大鼠心脏舒张功能的保护作用。

Protective effects of cardioplegia on diastolic function of hypertrophied rat hearts after hypothermic ischaemic arrest.

作者信息

Grousset C, Menasche P, Apstein C S, Mouas C, Marotte F, Piwnica A

出版信息

Eur Heart J. 1984 Dec;5 Suppl F:347-53. doi: 10.1093/eurheartj/5.suppl_f.347.

Abstract

This study was undertaken to assess the effects of hypothermia and chemical cardioplegia on the functional recovery of hypertrophied non-failing rat hearts subjected to an extended period of global ischaemia. Left ventricular hypertrophy was produced by constriction of the abdominal aorta. Hearts were studied an average of 8 weeks following this procedure. Sham-operated animals served as controls. Twenty-nine isolated isovolumic perfused rat heart preparations were then subjected to 2 h of ischaemic arrest at 15-18 degrees C followed by 45 min of normothermic reperfusion. In one series of hearts (8 sham, 8 hypertrophied), myocardial protection consisted of hypothermia alone. In another series (6 sham, 7 hypertrophied), repeated infusions of cardioplegic solution at 30-min intervals throughout arrest were added to hypothermia. Hypothermia alone resulted in a similar preservation of contractility as evidenced by the recovery of dp/dtmax/left ventricular (LV) systolic pressure after 45 min of reperfusion (91.6 +/- 5.9% of control values in sham vs 78.6 +/- 6.5% in hypertrophied hearts). Conversely, the recovery of compliance was much more impaired in hypertrophied hearts as indicated by a significantly higher percentage of increase in post-ischaemic LV diastolic pressure (DP) (at 45 min of reperfusion: 243.8 +/- 27.5% of control values vs 167.1 +/- 23.8% in sham, P less than 0.05). The addition of cardioplegia improved the preservation of contractility in both groups but its major effect was to normalize the recovery of compliance in hypertrophied hearts so that post-ischaemic LVDP values were no longer different from those recorded in normal hearts (at 45 min of reperfusion: 102.1 +/- 32.8% vs 98.5 +/- 14.2% of pre-ischaemic values respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在评估低温和化学心脏停搏对经历长时间全心缺血的肥厚性非衰竭大鼠心脏功能恢复的影响。通过腹主动脉缩窄诱导左心室肥厚。在此操作后平均8周对心脏进行研究。假手术动物作为对照。然后将29个离体等容灌注大鼠心脏标本在15 - 18℃下进行2小时的缺血性停搏,随后进行45分钟的常温再灌注。在一组心脏(8个假手术,8个肥厚性)中,心肌保护仅包括低温。在另一组(6个假手术,7个肥厚性)中,在停搏期间每隔30分钟重复输注心脏停搏液并联合低温。单独低温导致收缩性得到类似程度的保留,再灌注45分钟后dp/dtmax/左心室(LV)收缩压的恢复情况证明了这一点(假手术组为对照值的91.6±5.9%,肥厚性心脏组为78.6±6.5%)。相反,肥厚性心脏的顺应性恢复受损更严重,缺血后左心室舒张压(DP)升高的百分比显著更高(再灌注45分钟时:对照值的243.8±27.5%,假手术组为167.1±23.8%,P<0.05)。添加心脏停搏液改善了两组的收缩性保留,但它的主要作用是使肥厚性心脏的顺应性恢复正常,使得缺血后左心室舒张压值与正常心脏记录的值不再有差异(再灌注45分钟时:分别为缺血前值的102.1±32.8%和98.5±14.2%)。(摘要截断于250字)

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