Objective

To investigate the effects of different target hypothermia on the cardiovascular function and prognosis of rats after cardiopulmonary resuscitation.

Methods　

A total of 44 male SD rats were induced with electrical stimulation to ventricular fibrillation (VF) for 8 minutes, then cardiopulmonary resuscitation (CPR) was performed for 8 minutes followed by electric defibrillation (DF). Totally 28 SD rats survived VF, and randomized into either 37 ℃ normothermia group, 35 ℃ hypothermia group, 33 ℃ hypothermia group or 28 ℃ hypothermia group (7 each) after restoration of autonomic circulation (ROAC). Hypothermia was immediately induced with surface cooling to the target temperature. The target temperature was maintained for 4 hours before rewarming to (37±0.2) ℃. Survived animals were observed for up to 72 hours. Mean aortic pressure (MAP), ejection fraction (EF), heart rate (HR), blood lactate level (Lac), microcirculation of buccal flow (MBF), duration of survival, survival rate and neurological deficit score (NDS) were measured during hypothermia and post-rewarming.

Results　

During CPR, there were no difference in coronary perfusion pressure (CPP), times of DF, duration of VF-ROAC (P>0.05). During hypothermia treatment, the slowest HR was observed in the 28 ℃ hypothermia group, and the highest HR was observed in the 37 ℃ normothermia group; The levels of MAP and EF were higher in hypothermia groups than in normothermia group, among which the EF level (%) was obviously higher in 33 ℃ hypothermia group and 28 ℃ hypothermia group than in 35 ℃ hypothermia group [(63.8±6.1, 67.8±8.4)% vs. (54.0±5.2)%, P<0.05]; the Lac level was markedly lower in 33 ℃ hypothermia group and 35 ℃ hypothermia group than in 37 ℃ normothermia group and 28 ℃ hypothermia group (P<0.05); the MBF levels were lower in hypothermia groups than in normothermia group, while no statistical significant difference existed in MBF level among the 3 hypothermia groups (P>0.05). After rewarming, the EF level was markedly higher in 35 ℃ hypothermia group than in the 33 other groups [(52.9±3.3)% vs. (46.9±6.2, 38.5±7.5, 35.8±7.3)%, P<0.05]; MBF was obviously recovered in 33 ℃ and 35 ℃ hypothermia groups compared with that in 28 ℃ hypothermia group [(2.8±0.4, 2.4±0.5) vs. (1.6±0.6), P<0.05], but no difference existed between 33 ℃ and 35 ℃ hypothermia group. The duration of survival, survival rate and NDS score were much better in 33 ℃ and 35 ℃ hypothermia groups than in 28 ℃ hypothermia groups and 37 ℃ normothermia group, but no difference between 33 ℃ and 35 ℃ hypothermia groups (P<0.05).

Conclusions　

Hypothermia therapy with 33 ℃ and 35 ℃ target temperature may protect the blood circulation function of rats after CPR, reduce nerve function injury and improve prognosis. Hypothermia therapy with 35 ℃ target temperature might be a new choice for treatment of patients with clinical cardiac arrest after recovery.