title: [The effects of mild hypothermia on cardiac function and myocardial structure in a rabbits model of ventricular fibrillation after restoration of spontaneous circulation].
abstract: OBJECTIVE
  To examine the impact of mild hypothermia on cardiac function, myocardial tissue integrity, and 48 hours mortality in a rabbits model of ventricular fibrillation after restoration of spontaneous circulation (ROSC).
  
  
  METHODS
  The rabbits were randomly divided into four groups: normothermic post ROSC (NTPR, n = 10), mild hypothermia post ROSC (HTPR, n = 10), normothermic control (NTC, n = 8) and mild hypothermia control (HTC, n = 8). Ventricular fibrillation was induced by trans-epicardium electric-shook with alternating current in all the animals and ROSC was achieved through administration of adrenaline (i.v.) and artificial ventilation in group NTPR and HTPR. The body temperature of the animals was kept either at (39.0 ± 0.5) centigrade (NTPR and NTC) or (33.5 ± 0.5) centigrade (HTPR and HTC) for 4 hours after surgery for hemodynamic index data collection 0.5, 1, 2, 3 and 4 hours after surgery, 48 hours later, the mortality in the animals was recorded, and myocardial tissue samples were collected from survived animals for morphological examination by light and electric microscopy and analysis of apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The content of ATP, ADP and AMP in the tissue samples was measured by high performance liquid chromatography (HPLC) for the calculation of energy charges (EC).
  
  
  RESULTS
  (1)Hemodynamic indexes: as compared to the NTC group, HTC group exhibited significantly lower levels of heart rate (HR) and -dp/dt max in all the time points. No significant difference between the two groups in the levels of +dp/dt max and mean artery pressure (MAP) was found in all the time points but 0.5 hour. There was no significant difference in the levels of left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP), and femoral artery blood pressure between the two groups.(2) In comparison with NTPR group, HTPR group exhibited significantly (all P < 0.05) lower levels of HR (bpm) and -dp/dt max in all time points (ROSC 0.5, 1, 2, 3, 4 hours: HR 216.5 ± 33.3 vs. 292.9 ± 38.4, 218.2 ± 28.0 vs. 294.3 ± 37.0, 227.5 ± 25.4 vs. 291.4 ± 25.3, 232.4 ± 27.4 vs. 278.1 ± 30.8, 230.6 ± 22.0 vs. 285.1 ± 38.2; -dp/dt max 1847.1 ± 241.2 vs. 2383.3 ± 470.9, 1860.7 ± 167.8 vs. 2154.6 ± 319.5, 1822.3 ± 389.7 vs. 2239.7 ± 379.0, 1950.6 ± 412.9 vs. 2229.6 ± 392.4, 1875.7 ± 555.6 vs. 2396.7 ± 420.1). There was no significant difference between the two groups in the levels of LVEDP, +dp/dt max, LVESP, and femoral artery blood pressure. (3)Optical and electron microscopy revealed myocardium injury in samples from animals underwent ROSC. However, in comparison with the NTPR group, samples from HTPR group exhibited less damage to the myocardium structure. (4) Apoptosis index (AI) of myocardium was significantly (P < 0.05) higher in NTPR group (42.02%) than in HTPR group (26.39%). (5) Tests of myocardial energy: ATP level (μmol/g) in HTPR was significantly (P < 0.05) higher than NTPR (0.97 ± 0.26 vs. 0.65 ± 0.16). EC in NTPR was significant lower than it in two control groups [(0.33 ± 0.13)% vs. (0.52 ± 0.12)%, (0.55 ± 0.06)%, both P < 0.05], whereas no such difference was found between HTPR [(0.41 ± 0.12)%] and two control groups. (6) 48 hours survival rate in HTPR group was significantly higher (P = 0.043) as compared to NTPR group (100% vs. 60%).
  
  
  CONCLUSIONS
  Myocardial dysfunction and myocardium tissue injury both develop in post-resuscitation rabbits with ventricular fibrillation. In these animals, reducing body temperature to the level of mild hypothermia after ROSC may improve the 48 hours survival rate, probably via mechanisms that suppress myocardial cell apoptosis. In our study, such intervention produced no obvious negative impact neither on the cardiac function nor hemodynamics.
authors.affiliation: Emergency Department, Capital Medical University, Beijing, China.
authors.forename: Yin-ping
authors.initials: YP
authors.lastname: Li
authors.forename: Jian
authors.initials: J
authors.lastname: Qin
authors.forename: Zhen-xing
authors.initials: ZX
authors.lastname: Fan
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.forename: Wen-qiang
authors.initials: WQ
authors.lastname: Chen
authors.forename: Chun-lin
authors.initials: CL
authors.lastname: Hu
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
mesh_terms: D000818:Animals; D007036:Hypothermia, Induced; D008297:Male; D009206:Myocardium / Q000473:pathology*; D011817:Rabbits; D012151:Resuscitation; D014693:Ventricular Fibrillation / Q000473:pathology* / Q000503:physiopathology*