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心率与体温过低对离体兔心整体心肌收缩的相互作用。

Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart.

作者信息

Mattheussen M, Mubagwa K, Van Aken H, Wusten R, Boutros A, Flameng W

机构信息

Centre for Experimental Surgery and Anaesthesiology, University of Leuven, Belgium.

出版信息

Anesth Analg. 1996 May;82(5):975-81. doi: 10.1097/00000539-199605000-00015.

DOI:10.1097/00000539-199605000-00015
PMID:8610909
Abstract

We studied the effects of mild hypothermia on cardiac contractility in isolated rabbit hearts perfused with Krebs-Henseleit solution according to the technique of Langendorff. Isovolumetric left ventricular pressure (LVP) was measured with a fluid-filled balloon. Hearts were paced after induction of atrioventricular block. At low heart rates ( < 30 bpm) mild hypothermia (cooling to 30 degrees C) induced a 32% increase in LVp (146.5 +/- 10 mm Hg at 30 degrees C vs 110.7 +/- 13 mm Hg at 37 degrees C) but this positive inotropic response was progressively lost by increasing heart rate. At pacing rates > or = 90 bpm, lower systolic LVP, higher diastolic LVP, and lower positive and negative LV dP/dt were obtained in hypothermic (93 +/- 12 mm Hg, 55 +/- 18 mm Hg, 584 +/- 137 mm Hg/s, and 323 +/- 57 mm Hg/s at 210 bpm, respectively) compared to normothermic hearts (123 +/- 4 mm Hg, 10 +/- 4 mm Hg, 1705 +/- 145.5 mm Hg/s, and 1155 +/- 78 mm Hg/s at 210 bpm, respectively.) The duration of mechanical diastole was reduced or suppressed in these hearts. Exposure to the beta-adrenoreceptor agonist, isoproterenol, improved this diastolic dysfunction during hypothermia and pacing at high rates, suggesting that the sarcoplasmic reticulum Ca2+ uptake might be involved. Our data are also consistent with an increase in myofilament Ca2+ sensitivity that is opposed by isoproterenol during hypothermia.

摘要

我们根据Langendorff技术,研究了轻度低温对用Krebs-Henseleit溶液灌注的离体兔心脏心肌收缩力的影响。用充满液体的球囊测量等容左心室压力(LVP)。在诱导房室传导阻滞之后对心脏进行起搏。在低心率(<30次/分钟)时,轻度低温(冷却至30℃)使左心室压力增加32%(30℃时为146.5±10mmHg,37℃时为110.7±13mmHg),但随着心率增加,这种正性肌力反应逐渐消失。在起搏频率≥90次/分钟时,与正常体温的心脏相比,低温心脏(在210次/分钟时分别为93±12mmHg、55±18mmHg、584±137mmHg/s和323±57mmHg/s)的收缩期左心室压力较低、舒张期左心室压力较高,左心室压力的正负变化率较低。这些心脏的机械舒张持续时间缩短或受到抑制。暴露于β-肾上腺素能受体激动剂异丙肾上腺素可改善低温及高频率起搏期间的这种舒张功能障碍,提示肌浆网Ca2+摄取可能参与其中。我们的数据还与低温期间肌丝Ca2+敏感性增加一致,而异丙肾上腺素在低温期间对此有拮抗作用。

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