Effects of Lactate Administration on Postcardiac Arrest Myocardial Dysfunction: An Ex Vivo Study

In vivo studies have reported cardiovascular benefits of lactate administration after cardiac arrest (CA). However, it remains unclear whether these improvements are due to direct or indirect myocardial effects of lactate. Therefore, we investigated the effects of lactate administration in an ex vivo CA model.

Isolated rat hearts were subjected to 20 minutes of nonshockable CA followed by 40 minutes of reperfusion. Four groups were analyzed: Control (n = 9), reperfused with standard Krebs buffer; lactate (n = 9), reperfused with Krebs containing 20 mmol/L L-lactate; Lact 5min (n = 5), reperfused with Krebs for 5 minutes and then with Krebs containing 20 mmol/L L-lactate; Lact Hyper (n = 6), reperfused with hypertonic (Na + 163 mmol/L) Krebs containing 20 mmol/L L-lactate. Endpoints included rate-pressure product, left ventricular end-diastolic pressure, coronary flow, and arrhythmia incidence. Troponin and creatine kinase release, mitochondrial calcium retention capacity, and mitochondrial respiration were assessed.

Rate-pressure product recovery at the end of reperfusion was 47% ± 4% of baseline in Control versus 45% ± 4%, 40% ± 3%, and 42% ± 3% in Lactate, Lact 5min , and Lact Hyper ( P = ns). Left ventricular end-diastolic pressure and coronary flow were comparable across the groups. Ventricular arrhythmias occurred in 44%, 33%, 40%, and 50% of hearts, respectively ( P = ns). Troponin and creatine kinase levels were similar ( P = ns) between Controls and Lactate-treated hearts. Mitochondrial functions, which were significantly impaired by CA, did not differ significantly between the two groups.

Lactate administration did not improve post-CA myocardial function and was not deleterious. These findings suggest that the in vivo benefits of lactate administration are unlikely due to direct myocardial effects.