The Role of Chemoprophylactic Agents in Modulating Platelet Aggregability After Traumatic Brain Injury

Morris, Mackenzie C.; Kassam, Farzaan; Bercz, Aron P.; Beckmann, Nadine; Schumacher, Fabian; Gulbins, Erich; Makley, Amy T.; Goodman, Michael D.

doi:10.1016/j.jss.2019.06.022

Cited by 12 publications

(11 citation statements)

References 38 publications

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“…For example, cerebral microcirculation disturbance can aggravate ischemia and hypoxia, decrease ATP synthesis, and destroy blood-brain barrier. In addition, the increase in monoamine neurotransmitters, glutamic acid, nitric oxide, bradykinin, endothelin, and arachidonic acid also participate in the occurrence and development of traumatic brain edema (Li et al, 2015;Kozlov et al, 2017;Treble-Barna et al, 2017;Armstead and Vavilala, 2019;Morris et al, 2019). No matter what the pathogenesis of TBI are, the brain tissue edema and nerve fiber damage will occur, which will cause the FA value to decrease and the MD value to increase in DTI (Hanks et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Low-Intensity Transcranial Ultrasound Stimulation in Moderate Traumatic Brain Injury Rats

Zheng

Yuan

et al. 2020

Front. Neurosci.

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Traumatic brain injury (TBI) is a kind of severe brain injury characterized with a high incidence rate and a high disability rate. Low-intensity transcranial ultrasound stimulation (LITUS) is a promising neuroprotective method for improving the functional prognosis of TBI. The fractional anisotropy (FA) value and mean diffusivity (MD) value can be sensitive to abnormal brain structure and function and can thus be used to evaluate the effect of LITUS on TBI. Our purpose was to evaluate the therapeutic effect of LITUS in a moderate TBI rat model with FA and MD values. For our method, we used 45 male Sprague Dawley rats (15 sham normal, 15 TBI, and 15 LITUS treatment rats). We used singleshot spin echo echo-planar imaging sequences at 3.0T to obtain the DTI parameters. Parameters of FA and MD on the treated side of the injury cortex were measured to evaluate the therapeutic effect of LITUS in a TBI rat model. For FA and MD values, groups were compared by using a two-way analysis of variance for repeated measures, and this was followed by Tukey's post hoc test. Differences were considered significant at P < 0.05. The results were that the FA value in the LITUS treatment group at 1 day after TBI was significantly higher than that in the control group (adjusted P = 0.0422) and significantly lower than that in the TBI group at 14, 21, and 35 days after TBI (adjusted P = 0.0015, 0.0064, and 0.0173, respectively). At the end of the scan time point, the differences between the two groups were not significant (adjusted P = 0.3242). The MD values in the LITUS treatment group were significantly higher in the early stage than that in the TBI group (adjusted P = 0.0167) and significantly lower at the following time points than in the TBI group. In conclusion, daily treatment with LITUS for 10 min effectively improved the brain damage in the Controlled Cortical Impact (CCI)-caused TBI model. FA and MD values can serve as evaluation indicators for the neuro-protective effect of LITUS.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Low-Intensity Transcranial Ultrasound Stimulation in Moderate Traumatic Brain Injury Rats

Zheng

Yuan

et al. 2020

Front. Neurosci.

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“…Mice underwent a controlled weight drop injury, as previously described, to induce a TBI of moderate severity, as defined by righting reflex response times 13–16 . In brief, mice were anesthetized with 2% inhaled isoflurane in 100% oxygen at 1 L/min for approximately 2 minutes.…”

Section: Methodsmentioning

confidence: 99%

“…After determining that an appropriate level of anesthesia was obtained, mice were placed in a prone position onto the TBI platform. The head was centered under a 400-g cylindrical rod that was dropped from 2.5 cm above the surface of the table to induce a global concussive blunt TBI 13–15 . All mice were observed until appropriate respiratory and neurologic recovery had been achieved.…”

Section: Methodsmentioning

confidence: 99%

“…Mice underwent a controlled weight drop injury, as previously described, to induce a TBI of moderate severity, as defined by righting reflex response times. [13][14][15][16] In brief, mice were anesthetized with 2% inhaled isoflurane in 100% oxygen at 1 L/min for approximately 2 minutes. After determining that an appropriate level of anesthesia was obtained, mice were placed in a prone position onto the TBI platform.…”

Section: Animal and Tbi Injury Modelmentioning

confidence: 99%

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Effects of antifibrinolytics on systemic and cerebral inflammation after traumatic brain injury

Wallen

Singer

Baucom

et al. 2022

J Trauma Acute Care Surg

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“…Our previously described weight drop model was used to induce a moderate TBI. [24][25][26] Briefly, mice were anesthetized with 2% inhaled isoflurane in 100% oxygen at 1 L/min for approximately 2 minutes. After an appropriate level of anesthesia was obtained, mice were placed in the prone position on a platform.…”

Section: Animal and Injury Modelmentioning

confidence: 99%

Postinjury treatments to make early tactical aeromedical evacuation practical for the brain after TBI

Singer

Wallen²,

Morris³

et al. 2021

J Trauma Acute Care Surg

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BACKGROUND:Traumatic brain injury (TBI) is common in civilians and military personnel. No potential therapeutics have been evaluated to prevent secondary injury induced by the hypobaric hypoxia (HH) environment integral to postinjury aeromedical evacuation (AE).We examined the role of allopurinol, propranolol, adenosine/lidocaine/magnesium (ALM), or amitriptyline administration prior to simulated flight following murine TBI. METHODS:Mice underwent TBI and were given allopurinol, propranolol, amitriptyline, or ALM prior to simulated AE or normobaric normoxia (NN) control. Heart rate (HR), respiratory rate, and oxygen saturation (SpO 2 ) were recorded throughout simulated AE. Mice were sacrificed at 24 hours, 7 days, or 30 days. Serum and cerebral cytokines were assessed by enzyme-linked immunosorbent assay. Motor function testing was performed with Rotarod ambulation. Immunohistochemistry was conducted to examine phosphorylated tau (p-tau) accumulation in the hippocampus at 30 days. RESULTS:While all treatments improved oxygen saturation, propranolol, amitriptyline, and allopurinol improved AE-induced tachycardia. At 24 hours, both propranolol and amitriptyline reduced tumor necrosis factor alpha levels while allopurinol and ALM reduced tumor necrosis factor alpha levels only in NN mice. Propranolol, amitriptyline, and ALM demonstrated lower serum monocyte chemoattractant protein-1 7 days after AE. Both amitriptyline and allopurinol improved Rotarod times for AE mice while only allopurinol improved Rotarod times for NN mice. Propranolol was able to reduce p-tau accumulation under both HH and NN conditions while ALM only reduced p-tau in hypobaric hypoxic conditions. CONCLUSION:Propranolol lowered post-TBI HR with reduced proinflammatory effects, including p-tau reduction. Amitriptyline-induced lower post-TBI HR and improved functional outcomes without affecting inflammatory response. Allopurinol did not affect vital signs but improved late post-TBI systemic inflammation and functional outcomes. Adenosine/lidocaine/magnesium provided no short-term improvements but reduced p-tau accumulation at 30 days in the HH cohort. Allopurinol may be the best of the four treatments to help prevent short-term functional deficits while propranolol may address long-term effects.

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The Role of Chemoprophylactic Agents in Modulating Platelet Aggregability After Traumatic Brain Injury

Cited by 12 publications

References 38 publications

Neuroprotective Effect of Low-Intensity Transcranial Ultrasound Stimulation in Moderate Traumatic Brain Injury Rats

Neuroprotective Effect of Low-Intensity Transcranial Ultrasound Stimulation in Moderate Traumatic Brain Injury Rats

Effects of antifibrinolytics on systemic and cerebral inflammation after traumatic brain injury

Postinjury treatments to make early tactical aeromedical evacuation practical for the brain after TBI

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