Objective: To compare the differences in cardiac functions and myocardial injury between asphyxia and trans-oesophageal pacing induced rat cardiac arrest models.
Methods: Healthy adult male Sprague-Dawley (SD) rats were randomly divided into sham group, asphyxia group and electrical stimulation group by random number table. The rats in the latter two groups were randomly divided into two subgroups (24 hours and 72 hours) according to the sampling time after successful resuscitation, with 6 rats in each group. All rats were mechanically ventilated for 20 minutes, in electrical stimulation group, cardiac arrest was induced by trans-oesophageal cardiac pacing for about 3 minutes (intensity 30 V, frequency 50 Hz, pulse duration 2 ms), and in asphyxia group, cardiac arrest was induced by clipping trachea for about 3 minutes. Cardiopulmonary resuscitation (CPR) was initiated 4 minutes after cardiac arrest. Echocardiographic examination was performed at 2 hours after return of spontaneous circulation (ROSC) with cardiac color ultrasound apparatus. Cardiac tissues were harvested at 24 hours and 72 hours after ROSC, hematoxylin-eosin (HE) staining was performed, and myocardial damage was observed under light microscope. The levels of cardiac troponin I (cTnI) and B-type natriuretic peptide (BNP) in serum were determined by enzyme-linked immunosorbent assay (ELISA).
Results: There was no significant difference in ROSC rate between the asphyxia group and electrical stimulation group [94.4% (17/18) vs. 88.9% (16/18), P > 0.05]. The heart rate (HR), mean arterial pressure (MAP), left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) at 2 hours after ROSC in asphyxia group and electrical stimulation group were significantly lower than those in sham group [HR (bpm): 401.50±19.76, 370.67±18.63 vs. 430.17±18.38, MAP (mmHg, 1 mmHg = 0.133 kPa): 107.17±12.92, 92.50±9.35 vs. 125.67±5.72, LVEF: 0.60±0.02, 0.54±0.03 vs. 0.63±0.01, LVFS: (48.40±2.52)%, (40.33±3.32)% vs. (55.47±2.38)%, all P < 0.05], and the decrease in electrical stimulation group was more significant (all P < 0.05). Compared with sham group, the levels of cTnI and BNP in serum of electrical stimulation group were significantly increased at 24 hours after ROSC [cTnI (ng/L): 51.57±13.04 vs. 38.23±5.57, BNP (ng/L): 1 919.61±823.22 vs. 977.47±445.18, both P < 0.05], but there was no significant difference in cTnI or BNP of serum between asphyxia group and sham group [cTnI (ng/L): 46.84±11.04 vs. 38.23±5.57, BNP (ng/L): 1 144.13±390.05 vs. 977.47±445.18, both P > 0.05]. There was no significant difference in cTnI or BNP of serum at 72 hours after ROSC among all the groups. The results of HE stain showed that the pathological injury of myocardium in electrical stimulation group was more serious than that in asphyxia group, characterized by more severe myocardial edema and partial myocardial cell lysis.
Conclusions: The cardiac function after cardiac arrest-CPR was decreased in both asphyxia group and electrical stimulation group, but electrical stimulation had a heavier cardiac function injury than asphyxia.