Warm nondepolarizing adenosine and lidocaine cardioplegia: Continuous versus intermittent delivery
Received 20 October 2006; received in revised form 6 December 2006; accepted 18 December 2006.
Objective
Continuous infusion of warm to normothermic cardioplegia may limit the surgeon’s visual field, increase coronary vascular resistance, and lead to potassium-exacerbated ischemia-reperfusion damage. Our aim was to examine the versatility of a new normokalemic, nondepolarizing adenosine–lidocaine cardioplegia during continuous or intermittent infusion at 33°C and compare it with lidocaine cardioplegia.
Methods
Isolated, perfused rat hearts (n = 6 each group) were arrested at 33°C for 40 or 60 minutes with 200 μm of adenosine and 500 μm of lidocaine in Krebs-Henseleit buffer (10 mmol/L glucose, pH 7.6-7.7 at 37°C) or 500 μm of lidocaine in Krebs–Henseleit buffer for 60 minutes delivered at 60 mm Hg.
Results
Times to arrest were 7 to 10 seconds for the adenosine–lidocaine groups and 102 seconds for the lidocaine group (P < .05). Total cardioplegia volumes for intermittent (2 minutes every 18 minutes) and continuous deliveries were 122 to 159 mL and 699 to 922 mL for the 40- and 60-minute adenosine–lidocaine arrest protocols, respectively, and 136 mL for the 60-minute intermittent lidocaine group. In the last 2 minutes of the 40- and 60-minute arrest protocols, the coronary vascular resistance was not significantly different for the hearts arrested with adenosine and lidocaine (0.27–0.32 megadyne/sec/cm−5). Significantly higher coronary vascular resistance was found in the lidocaine cardioplegia group (0.38 megadyne/sec/cm−5). No significant differences were found between the continuous or intermittent adenosine–lidocaine delivery protocols. Hearts arrested with adenosine and lidocaine recovered 88% to 89% of aortic flow and 109% of coronary flow at 60 minutes of reperfusion after 40-minute arrest, and 77% to 86% of aortic flow and 98% to 109% of coronary flow at 60 minutes of reperfusion after 60-minute arrest. Lidocaine cardioplegia led to significantly lower aortic and coronary flows after 60-minute arrest compared with the intermittent adenosine–lidocaine group.
Conclusions
We conclude that adenosine–lidocaine cardioplegia can be delivered intermittently or continuously with similar functional recoveries after a 40- or 60-minute arrest at 33°C. Hearts receiving lidocaine cardioplegia took a significantly longer time to arrest, showed higher coronary vascular resistance, and achieved lower functional recovery than the 60-minute adenosine–lidocaine cardioplegia groups. Intermittent or continuous delivery of adenosine–lidocaine cardioplegia may offer an alternative to current surgical hyperkalemic cardioplegia at warm to normothermic temperatures.
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