Tian G, Biro G P, Xiang B, Butler K W, Deslauriers R
Department of Physiology, Faculty of Medicine, University of Ottawa, Ontario.
Basic Res Cardiol. 1992 Jul-Aug;87(4):356-65. doi: 10.1007/BF00796521.
This study investigated whether increasing the magnesium concentration during secondary cardioplegia improves postischemic myocardial recovery. Twenty-four isolated pig hearts were divided into four groups. All hearts were initially subjected to control perfusion with modified Krebs-Henseleit solution for 30 min, followed by a single infusion of St. Thomas' solution #2. The hearts were then maintained without perfusion at 12 degrees C for 4 h. Following this hypothermic preservation, the hearts in group I were reperfused with modified Krebs-Henseleit solution for 50 min, while hearts in group II and III were reperfused with a secondary cardioplegic solution containing 16 or 0 mmol/L magnesium, respectively, for 20 min followed by 30 min of perfusion with modified Krebs-Henseleit solution. In group IV, the hearts were initially reperfused with Krebs-Henseleit solution containing 16 mmol/L potassium for 20 min, followed by 30 min of reperfusion with modified Krebs-Henseleit solution. The changes in high-energy phosphates and intracellular pH were monitored throughout the experiments using 31P nuclear magnetic resonance (NMR) spectroscopy. Heart rate, left-ventricular systolic developed pressure, and rates of pressure increase and decrease were measured during control perfusion and reperfusion to calculate the percent contractile functional recovery. Needle biopsies for measurement of energy metabolites with high performance liquid chromatography were performed at the end of preservation and reperfusion to confirm the NMR measurements. All six hearts in group I showed significantly less recovery of contractile function during reperfusion when compared to the hearts in groups II, III, IV (p less than 0.05). There was no difference in either recovery of metabolism or mechanical function among the latter three groups of hearts. None of hearts in groups II, III, and IV showed ventricular fibrillation, which occurred in all six hearts of group I upon reperfusion. The results suggest that a short period of re-arrest perfusion following ischemia ("secondary cardioplegia") improves postischemic contractile functional recovery and prevents reperfusion-induced ventricular fibrillation. Increased magnesium concentration in the secondary cardioplegia did not provide additional benefit to the ischemic myocardium, possibly due to the low permeability of the sarcolemmal membrane to magnesium.
本研究调查了在二次心脏停搏期间增加镁浓度是否能改善缺血后心肌恢复。24个离体猪心脏被分为四组。所有心脏最初均用改良的Krebs-Henseleit溶液进行对照灌注30分钟，随后单次输注圣托马斯溶液#2。然后将心脏在12℃下无灌注保存4小时。在这种低温保存后，I组心脏用改良的Krebs-Henseleit溶液再灌注50分钟，而II组和III组心脏分别用含16或0 mmol/L镁的二次心脏停搏溶液再灌注20分钟，随后用改良的Krebs-Henseleit溶液灌注30分钟。在IV组中，心脏最初用含16 mmol/L钾的Krebs-Henseleit溶液再灌注20分钟，随后用改良的Krebs-Henseleit溶液再灌注30分钟。在整个实验过程中，使用31P核磁共振（NMR）波谱监测高能磷酸盐和细胞内pH的变化。在对照灌注和再灌注期间测量心率、左心室收缩压以及压力上升和下降速率，以计算收缩功能恢复百分比。在保存和再灌注结束时进行针吸活检，用高效液相色谱法测量能量代谢物，以确认NMR测量结果。与II、III、IV组心脏相比，I组的所有六个心脏在再灌注期间收缩功能恢复明显较少（p小于0.05）。后三组心脏在代谢恢复或机械功能方面没有差异。II、III和IV组中没有心脏出现心室颤动，而I组的所有六个心脏在再灌注时均出现心室颤动。结果表明，缺血后短时间的再停搏灌注（“二次心脏停搏”）可改善缺血后收缩功能恢复并预防再灌注诱导的心室颤动。二次心脏停搏中增加镁浓度对缺血心肌没有额外益处，这可能是由于肌膜对镁的通透性较低。
