This study hypothesizes that induced hypothermia (IH) can safely extend aortic cross-clamp (ACC) time, significantly reducing metabolic burden and end-organ injury, thereby enabling more comprehensive aortic arch reconstructions and offering distinct advantages.

In this experimental animal research, 62 New Zealand white rabbits were randomized into normothermia (39°C) and mild hypothermia (35°C) groups. Animals in each group underwent proximal aortic arch (PAA) clamping for 20, 30, or 40 minutes. Serial blood samples measured biochemistry, oxidative stress biomarkers, arterial and mixed venous blood gases, and lactate levels. Kidney and liver tissues were harvested for histopathological evaluation of ischaemic changes.

Normothermic rabbits experienced significant increases in oxidative stress, metabolic acidosis, and end-organ injury (renal, hepatic, and exclusively, spinal cord injury) with prolonged clamping. Conversely, IH markedly attenuated these adverse effects, preserving acid-base balance and reducing histological injury. Notably, the metabolic burden and end-organ injury observed after 30 minutes of hypothermic ischaemia were comparable with those after 20 minutes of normothermic ischaemia, suggesting a substantial extension of safe clamping time.

Induced hypothermia during ACC provides significant protection against ischaemia-reperfusion injury by minimizing oxidative damage, preserving antioxidant capacity, and maintaining metabolic balance, thereby enhancing haemodynamic function post-surgery. This approach allows for safely extended ACC times, with a safety margin appearing to correspond to 30 minutes under hypothermia, facilitating complex aortic arch reconstructions and enabling safer surgical training. Clinical trials are warranted to confirm these findings in humans.