The Short-Term Effects of Isolated Traumatic Brain Injury on the Heart in Experimental Healthy Rats

• Published in: Neurocritical care 2020-10, Vol.33 (2), p.438-448
• Main Authors: Lee, Yao-Lin, Lim, Sher-Wei, Zheng, Hong-Xiang, Chang, Wei-Ting, Nyam, Tee-Tau Eric, Chio, Chung-Ching, Kuo, Jinn-Rung, Wang, Che-Chuan
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Biomarkers; Contusions; Critical Care Medicine; Heart rate; Intensive; Internal Medicine; Investigations; Ketamine; Medicine; Medicine & Public Health; Neurology; Original Work; Physiology; Trauma; Traumatic brain injury
• ISSN: 1541-6933; 1556-0961
• DOI: 10.1007/s12028-019-00902-5

Background To date, cardiac dysfunction after traumatic brain injury (TBI) has not been consistent. In this study, we hypothesized that TBI may play a role in the development of new-onset cardiac dysfunction in healthy experimental rats. Materials and Methods Anesthetized healthy male Sprague–Dawley rats were divided into two groups: a sham-operated control group and a TBI group. The brain was injured with 2.4 atm percussion via a fluid percussion injury model. During the 120 min after TBI, we continuously measured brain parameters, including intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and cardiac parameters, such as heart rate (HR), inter-ventricular septum dimension (IVSD), left ventricular internal dimension diastole (LVIDd), end-diastolic volume (EDV), ejection fraction (EF), fractional shortening (FS), and LV mass diastole (LVd mass) by cardiac echo. On days 1, 3, 7, and 14 after TBI, the brain damage volume was evaluated with triphenyltetrazolium chloride; the physiological parameters of the heart, including HR, IVSd, LVIDd, EDV, EF, FS, and LVd mass, were evaluated with cardiac echo; the morphology of cardiomyocytes was examined by hematoxylin and eosin (HE) and Masson trichrome staining; and the biomarkers of cardiac injury troponin I and B-type natriuretic peptide (BNP) were also examined. Results Compared to sham-operated controls, the TBI groups had higher ICP, lower CPP, and higher brain neuronal apoptosis and infarction contusion volume. The impact of TBI on heart function showed hyperdynamic response trends in IVSd, LVIDd, EDV, EF, FS, and LVd mass within 30 min after TBI; however, EF and FS exhibited eventual decreasing trends. Simultaneously, the values of the biomarkers troponin I and BNP were within normal limits, and HE and Mass trichrome staining revealed no significant differences between the sham-operated control group and the TBI group. Conclusions Our results suggest that TBI due to 2.4 atm fluid percussion injury in healthy experimental rats may cause significant damage to the brain and affect the heart function as investigated by cardiac echo but not as investigated by HE and Masson trichrome stainings or troponin I and BNP evaluation.