Development and Application of a Novel Pressure System for Evaluating Trauma Severities Using a Physiological Approach After Traumatic Brain Injury in Rats.

OBJECTIVE: The fluid percussion injury (FPI) model is a surgical method for mimicking traumatic brain injury (TBI) models as it automatically and accurately measures peak impact pressure. Nevertheless, its elevated costs have led numerous researchers to develop more inexpensive alternative methods. Therefore, we used a copy of the classic FPI device to develop a novel method to evaluate the pressure pulse and determine injury severity with even more precision during the surgical procedure to induce an injury. METHODS: The electronic components, algorithms, and hardware assembly were initially studied. Adult male Wistar rats received 2 different impact forces, and our novel system measured the pressure pulse in atmospheres to verify the differences between mild and moderate severity and the physiological alterations. RESULTS: The newly developed system was capable of detecting differences between mild and moderate severity, and severity parameters (e.g., apnea and unconsciousness) were more significant in animals with more moderate FPI than those with mild FPI. Additionally, electrocardiographic signals were modified 1 day after TBI, and mild and moderate FPI decreased R-wave peak to R-wave peak intervals (increased heart rate) and high frequency (HF) index as well as increased low frequency (LF) and low frequency/high frequency ratio indices. All electrocardiographic parameters evaluated were more expressive in the more moderate FPI than in the mild one, corroborating clinical heart impairments after TBI. CONCLUSIONS: The method developed to evaluate pressure pulse in an FPI model proved capable of precisely determining different degrees of injury.

Capsaicin-sensitive fibers mediate periorbital allodynia and activation of inflammatory cells after traumatic brain injury in rats: Involvement of TRPV1 channels in post-traumatic headache.

Post-traumatic headache (PTH) is a condition that frequently affects individuals after traumatic brain injury (TBI). Inflammation is one of the major causes of this disability. However, little is known about the trigger for, and endurance of, this painful process. Thus, the involvement of fibers containing the transient receptor potential vanilloid 1 (TRPV1) channels on the PTH and inflammation after TBI through neonatal treatment with capsaicin are investigated. Fluid percussion injury (FPI) in adult male Wistar rats caused periorbital allodynia in one, three and seven days after injury, and the neonatal treatment reversed the painful sensation in seven days. The lack of TRPV1 channels reduced the activation of macrophages and glial cells induced by TBI in the trigeminal system, which were characterized by glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecule-1 (IBA-1) immune content in the ipsilateral trigeminal ganglion, brainstem, and perilesional cortex. Immunofluorescence analyses of the ipsilateral Sp5C nucleus demonstrated a hypertrophic astrocytes profile after TBI which was reduced with treatment. Moreover, effects of succinate sumatriptan (SUMA - 1 mg/kg), TRPV1 selective antagonist capsazepine (CPZ - 2 mg/kg), and TRP non-selective antagonist ruthenium red (RR - 3 mg/kg) were evaluated. Although all mentioned drugs reduced the painful sensation, SUMA and CPZ demonstrated a stronger effect compared to the RR treatment, reinforcing the involvement of TRPV1 channels in periorbital allodynia after TBI. Hence, this report suggests that TRPV1-containing fibers and TRPV1 channels are able to induce inflammation of the trigeminal system and maintain the painful sensation after TBI.