ABSTRACT
Objective To detemine the value of cardiac troponin in early diagnosis of severe myocardial contusion in the dog.Methods Twelve dogs weighing (11.4 ± 1.5) kg were subjected to severe myocardial contusion by impacting the chest area with BIM-Ⅱ biological impact machine.Electrocardiogram,cTnT and cTnI were measured before,immediately,and 2,4,6 and 8 hours after injury.Animals were then killed and the serum was separated for gross examination and triphenyl tetrazolium chloride (TTC) staining.Results Supraventricular tachycardia,ventricular tachycardia,ventricular premature beat,myocardial ischemia,atrial fibrillation,and ventricular fibrillation were seen on the electrocardiogram 2,4,6 and 8 hours after the injury,which suggested a high sensitivity but low specificity.cTnT and cTnI levels revealed no specific changes at postoperative 2 and 4 hours,but cTnT and cTnl were significantly increased to (0.130 ± 0.052) ng/ml and (1.615 ± 0.371) ng/ml at postoperative 8 hours,significantly higher than that immediately after operation (P ＜ 0.01).Sensitivity and specificity of cTnT and cTnI were both 100％,while the specificity of the TTC staining was (39.78 ± 9.07)％.Conclusion Cardiac troponin is of high sensitivity and specificity in early diagnosis of severe myocardial contusion and has good correlation with pathological changes,which exhibits great potential in clinical application.
ABSTRACT
Objective To establish an animal model of dog severe myocardial contusion (MC) .Methods 12 dogs with the body weight of (11 .36 ± 1 .50)kg were selected .The BIM‐Ⅱ type biological impact machine was adopted to directly impact the bare area of the left chest by the driving pressure of 800 kPa ,the impact area was 16 .61 cm2 and the chest wall was inward compressed within 4-6 cm ,the severe myocardial contusion model was established .The pathological examination was taken at 8 h after injury and grading was performed according to the Abbreviated Injury Scale (AIS ,update in 2005) .Results The scattered large area bleeding spots appeared in the epicardium and endocardium of wound area .No obvious abnormality was found in the non - wound area .The pathological examination was performed based on the coronal plane of the left ventricular cross section .The percentage of the section 8 h necrosis area to the total area was (39 .78 ± 9 .07)% .Conclusion The established dog severe myocardial contusion model is stable and reproducible ,which can accurately simulate the temporary MC mode .
ABSTRACT
AIM: To explore the effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction.METHODS: The mouse model of heart failure was established by ligating the left anterior descending coronary to produce acute myocardial infarction.Thirty-two mice were divided into 4 groups: sham group and groups of post-operation at time points of 2,4 or 6 weeks,respectively.The ventricular dilatation and left ventricular functions were assessed by echocardiography.The expression of GRP78,CHOP,caspase-12,cleaved caspase-12,JNK and phosphorylated-JNK was detected by Western blotting.The cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL).RESULTS: The cardiac expression of endoplasmic reticulum chaperones GRP78 was significantly increased in the hearts with functional failure.The upregulated expression of CHOP,phosphorylated-JNK and cleaved caspase-12 illuminated that the CHOP-JNK-caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis were activated in the heart with functional failure by myocardial infraction.CONCLUSION: These findings suggest that the congestive heart failure induced by myocardial infraction is associated with endoplasmic reticulum stress and activation of CHOP,JNK,caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis.