Silverman N A, Schmitt G, Levitsky S, Feinberg H
J Thorac Cardiovasc Surg. 1984 Sep;88(3):424-31.
Metabolic evidence of improved delivery of cardioplegic solutions by adjuvant use of nitroglycerin (NTG) and reinfusing these solutions distal to an obstructed coronary artery was sought in 40 dogs subjected to cold cardioplegic arrest. The left anterior descending coronary artery was occluded prior to initiating arrest by intra-aortic root infusion. Cardioplegic solution was reinfused with the left anterior descending occluded throughout ischemia (Group I), or with this artery reopened, to simulate a completed distal anastomosis (Group II). Serial biopsy specimens of the left ventricular apex were assayed for adenosine triphosphate and creatine phosphate, while specimens from the posterior left ventricular wall served as controls. Regional myocardial temperatures were recorded throughout ischemia. Half of the hearts in each group received 300 micrograms of nitroglycerin in the cardioplegic solution. Adenosine triphosphate was preserved in myocardium distal to a patent coronary artery whether nitroglycerin was added to the cardioplegic solution or not (control, control + NTG). Moreover, nitroglycerin did not prevent the 26% to 34% (p less than 0.05) decline in adenosine triphosphate levels when the left anterior descending remained obstructed throughout ischemia (Group I, I + NTG). However, opening the left anterior descending for reinfusion of cardioplegic solution allowed adenosine triphosphate to be preserved at end-ischemia (Group II, II + NTG). In addition, the metabolic reperfusion injury manifested by a 37% (p less than 0.01) decline in adenosine triphosphate levels after aortic unclamping (Group II) was obviated when nitroglycerin was added to the cardioplegic solution delivered in this manner (II + NTG). The depletion of cardioplegic solution stores during ischemia was more severe in the experimental groups than in controls (p less than 0.05). These metabolic changes did not correlate with regional myocardial temperature gradients. The data indicate that myocardium jeopardized by coronary stenoses can be preserved as well as myocardium supplied by a patent coronary artery by adjuvant use of nitroglycerin and varying the mode of delivery of the cardioplegic solution.
在40只接受冷心脏停搏的犬中,研究了辅助使用硝酸甘油(NTG)改善心脏停搏液输送以及在冠状动脉阻塞远端重新输注这些溶液的代谢证据。在通过主动脉根部输注开始心脏停搏之前,阻塞左前降支冠状动脉。在整个缺血期间,在左前降支阻塞的情况下重新输注心脏停搏液(I组),或者在该动脉重新开放的情况下重新输注,以模拟完成的远端吻合(II组)。对左心室心尖的系列活检标本进行三磷酸腺苷和磷酸肌酸检测,而左心室后壁的标本作为对照。在整个缺血期间记录局部心肌温度。每组一半的心脏在心脏停搏液中接受300微克硝酸甘油。无论是否在心脏停搏液中添加硝酸甘油,在有通畅冠状动脉的远端心肌中三磷酸腺苷均得以保存(对照组、对照组+NTG)。此外,当左前降支在整个缺血期间保持阻塞时(I组、I+NTG),硝酸甘油并不能阻止三磷酸腺苷水平下降26%至34%(p<0.05)。然而,开放左前降支以重新输注心脏停搏液可使三磷酸腺苷在缺血末期得以保存(II组、II+NTG)。此外,当以这种方式输送的心脏停搏液中添加硝酸甘油时(II+NTG),可避免主动脉松开后三磷酸腺苷水平下降37%(p<0.01)所表现出 的代谢性再灌注损伤。在缺血期间,实验组心脏停搏液储备的消耗比对照组更严重(p<0.05)。这些代谢变化与局部心肌温度梯度无关。数据表明,通过辅助使用硝酸甘油和改变心脏停搏液的输送方式,受冠状动脉狭窄危及的心肌与由通畅冠状动脉供血的心肌一样可以得到保存。