心臟停搏液灌注前注入Adenosine可有效改善缺血後心臟功能

Bolus Injection of Adenosine before Cardioplegia Induction Improves Postischemic Global Function in Coronary Artery Bypass Grafting

背景：進行冠狀動脈繞道手術的病患，在心肺體外循環的過程中，儘管有高鉀離子心臟停搏液的保護作用，心肌細胞仍然會因缺血及再灌注而導致細胞壞死與收縮不良，影響病患的手術預後。Adenosine為一內生性腺甘酸，臨床上被使用於心肌細胞缺血及再灌注而引起的損傷之防護。本研究即針對冠狀動脈繞道手術的病患，在主動脈被夾住後直接從主動脈注射adenosine，觀察其是否能強化傳統高鉀離子心臟停搏液的保護作用，而儘速恢復缺血後心臟功能。方法：三十位病患，隨機分為兩組：一組在夾住主動脈後，經由主動脈直接注射adenosine250|ig/kg;另一則使用等量之生理食鹽水經主動脈注射作為對照，隨後兩組再給予相同高滾度卸離子心臟停搏液使心跳停止。術中及術後檢驗troponinI的血清滾度，並根據強心劑的使用量及血行動力學的變化，評估心臟遭受缺血損傷的程度。結果：病患基本資料、平均心肺體外循環時間及平均缺血時間，兩組並無統計學差異。主動脈夾住後心臟顫動至完全停止的時間，實驗組（adenosine group）平均8.1秒，比對照組的79.0秒明顯為短。心肺體外循環結束及術後24小時，實驗組平均心輸出量指數從心肺體外循環前之2.1L/min/m2分別增加至2.6及3.2L/min/m2比對照組從2.3L/min/m2分別改變為2.0及2.5L/min/m2，呈現有義意之改善。此外，實驗組平均troponinI的分泌在術後24小時為7.9|ig/L，比對照組的23.2ug/L為低。接通血管再灌注之後，雖然實驗組比對照組較早恢復自發性心跳且較少使用電擊，但統計學上並無差異。結論：直接經由主動脈給予單一高劑量之adenosine250ug/kg，可以有效改善傳統高鉀離子心臟停搏液的心肌保護作用；能藉由有效縮短心臟顫動的時間，減少心臟能量的耗損，加速術後心臟功能之恢復。

Background: Alternative strategies to optimize preexisting cardioplegia during myocardial preservation are currently under extensive investigation. Adenosine, an endogenous purine nucleoside, has been approved for its cardioprotective potential against ischemic-reperfusion injury. Yet, little information is available with respect to the use of adenosine for cardioplegic induction in humans. The purpose of the present study was, therefore, to assess the clinical relevance of intra-aortic administration of adenosine following aortic cross-clamping with respect to the exertion of additional protection in routine coronary artery bypass surgery. Methods: Thirty patients to receive elective coronary artery bypass grafting under cardiopulmonary bypass (CPB) were prospectively randomized into two study groups. Immediate after aortic cross-clamping and just before the application of modified St. Thomas cardioplegic (20 mL/kg), adenosine solution (250 pg/kg) was injected into the aortic root in the study group (n = 15), while the same amount of normal saline injection was administered in the control group (n = 15). Anesthesia was carried out in all patients in a similar fashion, and all the surgeries were performed by the same team. Homodynamic change, cardiac enzyme assay, and post-bypass inotropic supplementation were recorded throughout the study period to evaluate the extent of myocardial ischemic injury. Results : The mean time to asystole after aortic cross-clamping was significantly shorter for the adenosine group compared with the control group (8.1 土 5.9 vs. 79.0 土 35.3 sec, respectively; P < 0.01). To compare with the baseline value, the mean cardiac index immediately post CPB and 24 hours postoperatively was increased significantly for the adenosine group (from 2.1 土 0.6 to 2.6 土 0.6 and 3.2 土 0.6 L/min/m2, respectively; P < 0.05), as contrasted with the control group (from 2.3 ± 0.5 to 2.0 土 0.4 and 2.5 ± 0.4 L/min/m2). Further, the requirement for inotropic sup-port after CPB and postoperative troponin I release were significantly less in the adenosine group. There appeared no adverse effects associated with adenosine administration. Conclusions: Immediate administration of 250 ug/kg adenosine via the aortic root following aortic cross-clamping could optimize the myocardial protective effect of conventional cardioplegia, quicken cardiac standstill, and offer better postoperative myocardial performance after CPB.