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Updated: May 27, 2026

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Oxygen blood transport during experimental sepsis: effect of hypothermia*
Karelle Léon1, Karine Pichavant-Rafini, Eric Quéméner
1Laboratoire ORPHY EA 4324, Université Européenne de Bretagne, Université de Brest, France. Karelle.Leon@univ-brest.fr
Objectives:
The aim of this study was to highlight the link between induced hypothermia and increased survival duration as observed in the septic model developed by the laboratory. To reach this objective, survival duration and blood oxygen transport capacity were measured at two temperatures-38 °C (induced normothermia) and 34 °C (induced hypothermia)-in septic rats.
Design:
A prospective, randomized, experimental animal study.
Setting:
University laboratory.
Subjects:
Forty-four male Sprague-Dawley rats (median weight, 232 g; range, 200-303 g).
Interventions:
After anesthesia and obtention of the temperature goal, sepsis was induced by cecal ligation and perforation.
Measurements And Main Results:
Sepsis induction led to death 5 hrs 11 mins ± 0 hr 36 mins after cecal ligation and perforation at 38 °C. At this temperature, significant changes in blood oxygen transport capacity were observed in septic rats; Hill number decreased from 2.36 ± 0.10 (baseline group) to 1.99 ± 0.17 (septic group) (p = .008) and oxygen-hemoglobin affinity decreased and P50 increased from 41.40 ± 2.4 Torr (baseline group) to 51.17 ± 14.07 Torr (septic group). Furthermore, in normothermia, a significant increase of creatinine and albumin plasmatic concentrations was observed 4 hrs after sepsis induction. Survival duration was significantly higher in induced hypothermia (7 hrs 22 mins ± 0 hr 12 mins at 34 °C) compared with induced normothermia. At 34 °C, no significant change in blood oxygen transport capacity was observed. In the same way, exposure to 34 °C induced no change in measured plasmatic parameters except an increase in albumin concentration in septic rats compared with the baseline group.
Conclusions:
Sepsis led to a decrease of both oxygen hemoglobin cooperativity and affinity at 38 °C. By contrast, no change in these parameters was observed when sepsis was induced during hypothermia. Taken together, these results could be interpreted in normothermia septic rats as an adaptive mechanism that could enhance the release of oxygen at the tissue level. Hypothermia by slowing down sepsis evolution could increase survival duration.
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