Key result
Warmer hypothermic circulatory arrest at 28°C yields similar cognition to deeper cooling despite increased neuronal injury.
Why the study?
Postoperative neurologic injury remains prevalent after hypothermic circulatory arrest (HCA) for aortic and cardiac operations, and there is no consensus on the optimal HCA temperature.
Does hypothermic circulatory arrest at 24°C or 28°C compared to 18°C affect postoperative neurologic outcomes, biomarkers, mitochondrial function, and neuropathology in a canine model?
Does hypothermic circulatory arrest at 24°C or 28°C compared to 18°C affect postoperative neurologic outcomes, biomarkers, mitochondrial function, and neuropathology in a canine model?
In a canine model of prolonged hypothermic circulatory arrest with antegrade cerebral perfusion, temperatures of 18, 24, and 28°C yielded similar overall neuropathologic and cognitive outcomes, but elevated serum enolase and two cases of neurologic deficits at 28°C suggest caution and need for further safety evaluation of warmer temperatures.
Answers are grounded in this paper and cite their sources.
May support avoiding 28°C targets in arrest; leaves open human trial validation of neurologic risks.
Objective Hypothermic circulatory arrest (HCA) is required for certain aortic and cardiac operations, but postoperative neurologic injury remains prevalent. There is currently no consensus on the optimal temperature. We used a canine model to investigate neurologic outcomes after HCA at 18, 24, and 28°C. Methods Eighteen canines underwent peripheral bypass followed by prolonged HCA (90 min) at 18, 24, or 28°C (n=6, 5, and 7, respectively) with antegrade cerebral perfusion at 10 mL/kg/min. After HCA, animals were rewarmed, weaned from bypass, and extubated. Over three postoperative days (POD), behavior, cognition, and biomarkers were assessed. On POD 3, brains were removed for mitochondrial function testing and neuropathology. Results There were no significant differences between groups in behavior scores on POD 1-3. However, two 28°C animals had notable neurologic deficits, with none in the other groups. Cognition, assessed by novel object recognition, was not different between groups (all p>0.1). The 28°C group had increased serum enolase levels on POD 1 and 2 (both p<0.05). There were no significant differences in cellular respiration (all p>0.15). Prominent brain damage was noted without differences in regional or global neuropathologic injury between groups (all p>0.2). Conclusions Temperatures of 18, 24, and 28°C for prolonged HCA with cerebral perfusion yielded similar results for behavior, cognition, mitochondrial function, and neuropathology in this model after excluding one 28°C animal with severe injury. Neurologic deficits (n=2) and increased serum enolase in 28°C animals suggest that continued investigation of the safety of warmer temperatures for prolonged HCA is warranted.
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Bradshaw et al. (2026) studied Hypothermic circulatory arrest (n=18). Hypothermic circulatory arrest at 28°C with antegrade cerebral perfusion vs. Hypothermic circulatory arrest at 18°C or 24°C was evaluated on Neurologic outcomes including behavior, cognition, serum enolase biomarkers, cellular respiration, and neuropathology (p=>0.1). Hypothermic circulatory arrest at 28°C vs 18°C and 24°C showed similar cognition and neuropathology, but higher serum enolase and 2/7 neurologic deficits.
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