The low oxygen-carrying capacity of Krebs buffer causes a doubling in ventricular wall thickness in the isolated heart
The low oxygen-carrying capacity of Krebs buffer causes a doubling in ventricular wall thickness in the isolated heart
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DOI：
10.1139/y04-138
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发表时间：
2005-02-01
影响因子：
2.1
通讯作者：
Garlick, PB
中科院分区：
文献类型：
--
作者：
Southworth, R;Blackburn, SC;Garlick, PB
与体内心脏相比，缓冲液灌注的 Langendorff 心脏明显血管舒张。在这项研究中，我们利用超声波来确定这种血管舒张是否会转化为左心室壁厚度（LVWT）的变化，以及当这些心脏切换到“工作”模式时这种效应是否持续存在。为了研究灌注压、血管张力和氧利用率对心脏尺寸的影响，我们在 Langendortf 模式下以 80、60 和 40 cm H2O 压力灌注心脏（来自雄性 Wistar 大鼠），并向更多组的心脏灌注血管收缩剂内皮素-1 (ET-1) 或血液替代品 FC-43。与体内相同心脏相比，缓冲液灌注引起舒张期 LVWT 加倍（5.4 +/- 0.2 mm 与 2.6 +/- 0.2 mm，p < 0.05），并且通过将心脏切换到“工作”模式不会逆转这种情况。 60 和 40 cm H2O 的灌注压导致舒张期 LVWT 增加。 ET-1输注导致舒张期LVWT呈剂量依赖性下降（浓度为10(-9) mol/L时为6.6 +/- 0.4至4.8 +/- 0.4 mm，p < 0.05），同时冠状动脉流量下降。 FC-43 将舒张期 LVWT 从 6.7 +/- 0.5 降低至 3.8 +/- 0.7 mm (p < 0.05)，冠脉流量从 16.1 +/- 0.4 降至 8.1 +/- 0.4 mL/min (p < 0.05)。我们得出的结论是，在缓冲液灌注的心脏中观察到的舒张期 LVWT 增加是由于缓冲液的携氧能力低于体内血液而引起的血管舒张，并且 ET-1 在 Langendorff 心脏中的正性肌力作用可能是这种壁增厚逆转的结果。讨论了这些发现的含义。
The buffer-perfused Langendorff heart is significantly vasodilated compared with the in vivo heart. In this study, we employed ultrasound to determine if this vasodilation translated into changes in left ventricular wall thickness (LVWT), and if this effect persisted when these hearts were switched to the "working" mode. To investigate the effects of perfusion pressure, vascular tone, and oxygen availability on cardiac dimensions, we perfused hearts (from male Wistar rats) in the Langendortf mode at 80, 60, and 40 cm H2O pressure, and infused further groups of hearts with either the vasoconstrictor endothelin-1 (ET-1) or the blood substitute FC-43. Buffer perfusion induced a doubling in diastolic LVWT compared with the same hearts in vivo (5.4 +/- 0.2 mm vs. 2.6 +/- 0.2 mm, p < 0.05) that was not reversed by switching hearts to "working" mode. Perfusion pressures of 60 and 40 cm H2O resulted in an increase in diastolic LVWT. ET-1 infusion caused a dose-dependent decrease in diastolic LVWT (6.6 +/- 0.4 to 4.8 +/- 0.4 mm at a concentration of 10(-9) mol/L, p < 0.05), with a concurrent decrease in coronary flow. FC-43 decreased diastolic LVWT from 6.7 +/- 0.5 to 3.8 +/- 0.7 mm (p < 0.05), with coronary flow falling from 16.1 +/- 0.4 to 8.1 +/- 0.4 mL/min (p < 0.05). We conclude that the increased diastolic LVWT observed in buffer-perfused hearts is due to vasodilation induced by the low oxygen-carrying capacity of buffer compared with blood in vivo, and that the inotropic effect of ET-1 in the Langendorff heart may be the result of a reversal of this wall thickening. The implications of these findings are discussed.