Cerebral Inflammation in an Animal Ischemia–Reperfusion Model Comparing Histidine-Tryptophan-α-Ketoglutarate and Del Nido Cardioplegia

Brain injury and cerebral inflammation are frequent complications following cardiopulmonary bypass (CPB) resulting in neurocognitive dysfunction, encephalopathy, or stroke. We compared cerebral inflammation induced by del Nido and histidine-tryptophan-α-ketoglutarate (HTK) cardioplegia in a porcine model. Pigs underwent 90 min cardiac arrest using HTK (n = 9) or Jonosteril^®-based del Nido cardioplegia (n = 9), followed by a 120 min reperfusion. Brain biopsies were collected and analyzed for the mRNA and protein expression of hypoxia-inducible factor-1α (HIF-1α) and cytokines. HTK induced a decrease in blood sodium, chloride, and calcium concentration (cross-clamp aorta: <i>p</i>_sodium < 0.01, <i>p</i>_chloride < 0.01, <i>p</i>_calcium < 0.01; 90 min ischemia: <i>p</i>_sodium < 0.01, <i>p</i>_chloride < 0.01, <i>p</i>_calcium = 0.03) compared to the more stable physiological electrolyte concentrations during del Nido cardioplegia. Hyponatremia and hypochloremia persisted after a 120 min reperfusion in the HTK group (<i>p</i>_sodium < 0.01, <i>p</i>_chloride = 0.04). Compared to del Nido, a higher mRNA expression of the proinflammatory cytokine IL-1β was detected in the frontal cortex (HTK: ∆Ct 6.5 ± 1.7; del Nido: ∆Ct 8.8 ± 1.5, <i>p</i> = 0.01) and the brain stem (HTK: ∆Ct 5.7 ± 1.5; del Nido: ∆Ct 7.5 ± 1.6, <i>p</i> = 0.02) of the HTK group. In conclusion, we showed comparability of HTK and del Nido for cerebral inflammation except for IL-1β expression. Based on our study results, we conclude that del Nido cardioplegia is a suitable and safe alternative to the conventional HTK solution.