Schubert T, Vetter H, Owen P, Reichart B, Opie L H
Department of Medicine, University of Cape Town, Republic of South Africa.
J Thorac Cardiovasc Surg. 1989 Dec;98(6):1057-65.
Adenosine is a potential cardioplegic agent by virtue of its specific inhibitory properties on nodal tissue. We tested the hypothesis that adenosine could be more effective than potassium in inducing rapid cardiac arrest and enhancing postischemic hemodynamic recovery. Isolated rat hearts were perfused with Krebs-Henseleit buffer or cardioplegic solutions to determine the time to cardiac arrest and the high-energy phosphate levels at the end of cardioplegia. Cardioplegic solutions contained adenosine 10 mmol/L, potassium 20 mmol/L, or adenosine 10 mmol/L + potassium 20 mmol/L and were infused at a rate of 2 ml/min for 3 minutes at 10 degrees C. Both time taken and total number of beats to cardiac arrest during 3 minutes of cardioplegia were reduced by adenosine 10 mmol/L and adenosine 10 mmol/L + potassium 20 mmol/L when compared with potassium 20 mmol/L alone (p less than 0.001). Tissue phosphocreatine was conserved by adenosine 10 mmol/L when compared with potassium 20 mmol/L, being 7.1 +/- 0.2 (mumol/gm wet weight (n = 7) and 6.0 +/- 0.3 mumol/gm wet weight (n = 5), respectively (p less than 0.05). Postischemic hemodynamic recovery was tested in isolated working rat hearts. After initial cardiac arrest, the cardioplegic solution was removed with Krebs-Henseleit buffer at a rate of 2 ml/min for 3 minutes at 10 degrees C, and thereafter total ischemia was maintained for 30 or 90 minutes at 10 degrees C before reperfusion. Adenosine 10 mmol/L enhanced recovery of aortic output when compared with potassium 20 mmol/L or adenosine 10 mmol/L + potassium 20 mmol/L, the percentage recovery after 30 minutes of ischemia being 103.0% +/- 4.4% (n = 6), 89.0% +/- 5.8% (n = 6), and 86.6% +/- 4.3% (n = 6), respectively (p less than 0.05 for comparison between adenosine 10 mmol/L and potassium 20 mmol/L). Thus adenosine cardioplegia caused rapid cardiac arrest and improved postischemic recovery when compared with potassium cardioplegia and with a combination of these two agents.
腺苷凭借其对节点组织的特定抑制特性,是一种潜在的心脏停搏剂。我们检验了这样一个假设,即腺苷在诱导快速心脏停搏和增强缺血后血流动力学恢复方面可能比钾更有效。用Krebs-Henseleit缓冲液或心脏停搏液灌注离体大鼠心脏,以确定心脏停搏时间和心脏停搏结束时的高能磷酸水平。心脏停搏液含有10 mmol/L腺苷、20 mmol/L钾或10 mmol/L腺苷 + 20 mmol/L钾,并在10℃以2 ml/min的速率输注3分钟。与单独使用20 mmol/L钾相比,10 mmol/L腺苷和10 mmol/L腺苷 + 20 mmol/L钾在心脏停搏3分钟期间使心脏停搏的时间和总心跳数均减少(p < 0.001)。与20 mmol/L钾相比,10 mmol/L腺苷可使组织磷酸肌酸得以保存,分别为7.1±0.2(μmol/g湿重,n = 7)和6.0±0.3 μmol/g湿重(n = 5)(p < 0.05)。在离体工作大鼠心脏中测试缺血后血流动力学恢复情况。初始心脏停搏后,在10℃以2 ml/min的速率用Krebs-Henseleit缓冲液去除心脏停搏液3分钟,此后在10℃维持完全缺血30或90分钟,然后再灌注。与20 mmol/L钾或10 mmol/L腺苷 + 20 mmol/L钾相比,10 mmol/L腺苷可增强主动脉输出的恢复,缺血30分钟后的恢复百分比分别为103.0%±4.4%(n = 6)、89.0%±5.8%(n = 6)和86.6%±4.3%(n = 6)(10 mmol/L腺苷与20 mmol/L钾比较,p < 0.05)。因此,与钾心脏停搏以及这两种药物的联合使用相比,腺苷心脏停搏可导致快速心脏停搏并改善缺血后恢复情况。