Effects of naloxone on systemic and cerebral responses to experimental concussive brain injury in cats

1983 ◽  
Vol 58 (5) ◽  
pp. 720-728 ◽  
Author(s):  
Ronald L. Hayes ◽  
Brian J. Galinat ◽  
Pramod Kulkarne ◽  
Donald P. Becker
Keyword(s):  
Brain Injury ◽  
Cerebral Perfusion ◽  
Control Group ◽  
Severely Injured ◽  
Blood Gas ◽  
Narcotic Antagonist ◽  
Endogenous Opiates ◽  
Content Type ◽  
Naloxone Hydrochloride ◽  
Cardiovascular Variables

✓ This study examined the effects of bolus injections of naloxone hydrochloride, a specific narcotic antagonist, on systemic cardiovascular function, intracranial and cerebral perfusion pressures, blood gas status, and cortical encephalograms (EEG's) in 38 cats after two different grades of experimental brain injury. Naloxone had no prolonged effects on uninjured control animals. However, as compared to a saline-injected control group, naloxone significantly reversed the hypotension and reduction in pulse pressure seen after higher grades of injury. These changes persisted for at least 60 minutes after injection and were accompanied by increased intracranial and perfusion pressures. More severely injured hypotensive cats injected with naloxone also had higher values of arterial pO2 and pH, lower pCO2, as well as higher EEG amplitudes. In less severely injured normotensive cats, naloxone produced greater effects on cardiovascular variables and intracranial pressure when injected 15 minutes rather than 45 minutes after injury. These data suggest that endogenous opiates may contribute to some instances of hypotension seen after concussive brain injury. Levels of endogenous opiates may also increase transiently even with lesser degrees of injury not associated with hypotension. The possible clinical application of narcotic antagonists to the treatment of head injury is discussed.

Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Roberto Imberti ◽  
Guido Bellinzona ◽  
Martin Langer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Cerebral Perfusion ◽  
Content Type ◽  
Secondary Damage ◽  
Tissue Po2 ◽  
Two Parameters ◽  
Fine Print

Object. The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). Methods. Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27–32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score ≤ 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation — posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. Conclusions. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.

Experimental brain injury: successful therapy with the weak base, tromethamine

1984 ◽  
Vol 60 (5) ◽  
pp. 961-971 ◽  
Author(s):  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Brain Injury ◽  
Control Group ◽  
Weak Base ◽  
Post Injury ◽  
Content Type ◽  
Ringer’S Solution ◽  
Fluid Percussion Injury ◽  
Lactated Ringer's Solution ◽  
Injury Control ◽  
Fine Print

✓ The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p < 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p < 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.

Dimethyl sulfoxide in experimental brain injury, with comparison to mannitol

1980 ◽  
Vol 53 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Frederick D. Brown ◽  
Lydia M. Johns ◽  
Sean Mullan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Brain Injury ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Missile Injury ◽  
Fine Print

✓ The effects of dimethyl sulfoxide therapy were studied in rhesus monkeys following a standardized occipitofrontal missile injury. This therapy resulted in substantially higher blood pressure, cerebral perfusion pressure, blood flow, and oxidative metabolism than those of a group of monkeys that had been treated similarly with mannitol, and than those of an untreated group.

scholarly journals Effect of naloxone hydrochloride on β-EP, CD4+, CD8+, IL2, MMP-9 and S100-B levels in peripheral blood after traumatic brain injury in rats

2021 ◽  
Vol 18 (4) ◽  
pp. 735-740
Author(s):  
Feng Du ◽  
Dedong Zhang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Normal Saline ◽  
Peripheral Blood ◽  
Control Group ◽  
Control Value ◽  
Naloxone Hydrochloride ◽  
Time Changes ◽  
Time Point

Purpose: To study the influence of naloxone hydrochloride on traumatic brain injury (TBI). Methods: Three groups of rats were used: normal control, TBI, and TBI + naloxone hydrochloride groups (12 rats/group). In the control group, only the osseous foramen was opened. Rats in TBI group were intraperitoneally injected with normal saline, while the naloxone group received naloxone hydrochloride injection at the same time. Changes in peripheral blood β-EP, CD4+, CD8+, IL-2, and S100-B levels; and brain tissue MMP-9 were assessed. Results: The levels of β-EP in the TBI- and naloxone-treated rats were higher than control values, while levels of CD4+ in TBI and naloxone groups were significantly lower than those of control group (p < 0.01). At every time point, CD8+ level in naloxone group was significantly lower than that in TBI group (p < 0.01). Compared with control group, the levels of IL-2 in the TBI and naloxone groups were significantly lower. Higher levels of S100-B were seen in TBI- and naloxone-treated rats, relative to control value. In the naloxone group, MMP-9 expression was downregulated, when compared to the expression TBI rats (p < 0.05). Conclusion: Naloxone hydrochloride reduces β-EP, alleviates inflammation, protects nerve cells and reduces brain injury in TBI rats. There is, thus, a potential to develop naloxone for the management of brain injury

Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study

1998 ◽  
Vol 89 (6) ◽  
pp. 971-982 ◽  
Author(s):  
Paul Vespa ◽  
Mayumi Prins ◽  
Elizabeth Ronne-Engstrom ◽  
Michael Caron ◽  
Ehud Shalmon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Microdialysis ◽  
Extracellular Glutamate ◽  
Content Type ◽  
The Mean ◽  
Fine Print

Object. To determine the extent and duration of change in extracellular glutamate levels after human traumatic brain injury (TBI), 17 severely brain injured adults underwent implantation of a cerebral microdialysis probe and systematic sampling was conducted for 1 to 9 days postinjury. Methods. A total of 772 hourly microdialysis samples were obtained in 17 patients (median Glasgow Coma Scale score 5 ± 2.5, mean age 39.4 ± 20.4 years). The mean (± standard deviation) glutamate levels in the dialysate were evaluated for 9 days, during which the mean peak concentration reached 25.4 ± 13.7 (µM on postinjury Day 3. In each patient transient elevations in glutamate were seen each day. However, these elevations were most commonly seen on Day 3. In all patients there was a mean of 4.5 ± 2.5 transient elevations in glutamate lasting a mean duration of 4.4 ± 4.9 hours. These increases were seen in conjunction with seizure activity. However, in many seizure-free patients the increase in extracellular glutamate occurred when cerebral perfusion pressure was less than 70 mm Hg (p < 0.001). Given the potential injury-induced uncoupling of cerebral blood flow and metabolism after TBI, these increases in extracellular glutamate may reflect a degree of enhanced cellular crisis, which in severe head injury in humans appears to last up to 9 days. Conclusions. Extracellular neurochemical measurements of excitatory amino acids may provide a marker for secondary insults that can compound human TBI.

Effect of Continuous Display of Cerebral Perfusion Pressure on Outcomes in Patients With Traumatic Brain Injury

2006 ◽  
Vol 15 (6) ◽  
pp. 600-609 ◽  
Author(s):  
Catherine J. Kirkness ◽  
Robert L. Burr ◽  
Kevin C. Cain ◽  
David W. Newell ◽  
Pamela H. Mitchell
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Intervention Group ◽  
Control Group ◽  
End Points ◽  
Arterial Blood ◽  
Injured Patients

• Background Clinical bedside monitoring systems do not provide prominent displays of data on cerebral perfusion pressure (CPP). Immediate visual feedback would allow more rapid intervention to prevent or minimize suboptimal pressures. • Objective To evaluate the effect of a highly visible CPP display on immediate and long-term functional outcome in patients with traumatic brain injury. • Methods A total of 157 patients with traumatic brain injury at a level 1 trauma center who had invasive arterial blood pressure and intracranial pressure monitoring were randomized to beds with or without an additional, prominent continuous CPP display. Primary end points were scores on the Extended Glasgow Outcome Scale (GOSE) and Functional Status Examination (FSE) 6 months after injury. Secondary end points were GOSE scores at discharge and 3 months after injury and FSE score 3 months after injury. • Results Although GOSE and FSE scores at 6 months were better in the group with the highly visible CPP display, the differences were not significant. Slope of recovery for GOSE and FSE over all follow-up time points did not differ significantly between groups. However, the intervention’s positive effect on odds of survival at hospital discharge was strong and significant. Within a subgroup of more severely injured patients, the intervention group was much less likely than the control group to have CPP deviations. • Conclusions The presence of a highly visible display of CPP was associated with significantly better odds of survival and overall condition at discharge.

scholarly journals Remotely delivered environmental enrichment intervention for traumatic brain injury: Study protocol for a randomised controlled trial

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e039767
Author(s):  
Zorry Belchev ◽  
Mary Ellene Boulos ◽  
Julia Rybkina ◽  
Kadeen Johns ◽  
Eliyas Jeffay ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Active Control ◽  
Environmental Enrichment ◽  
Spatial Navigation ◽  
Controlled Trial ◽  
Control Group ◽  
Hippocampal Atrophy ◽  
Active Control Group ◽  
Navigation Group

IntroductionIndividuals with moderate-severe traumatic brain injury (m-sTBI) experience progressive brain and behavioural declines in the chronic stages of injury. Longitudinal studies found that a majority of patients with m-sTBI exhibit significant hippocampal atrophy from 5 to 12 months post-injury, associated with decreased cognitive environmental enrichment (EE). Encouragingly, engaging in EE has been shown to lead to neural improvements, suggesting it is a promising avenue for offsetting hippocampal neurodegeneration in m-sTBI. Allocentric spatial navigation (ie, flexible, bird’s eye view approach), is a good candidate for EE in m-sTBI because it is associated with hippocampal activation and reduced ageing-related volume loss. Efficacy of EE requires intensive daily training, prohibitive within most current health delivery systems. The present protocol is a novel, remotely delivered and self-administered intervention designed to harness principles from EE and allocentric spatial navigation to offset hippocampal atrophy and potentially improve hippocampal functions such as navigation and memory for patients with m-sTBI.Methods and analysisEighty-four participants with chronic m-sTBI are being recruited from an urban rehabilitation hospital and randomised into a 16-week intervention (5 hours/week; total: 80 hours) of either targeted spatial navigation or an active control group. The spatial navigation group engages in structured exploration of different cities using Google Street View that includes daily navigation challenges. The active control group watches and answers subjective questions about educational videos. Following a brief orientation, participants remotely self-administer the intervention on their home computer. In addition to feasibility and compliance measures, clinical and experimental cognitive measures as well as MRI scan data are collected pre-intervention and post-intervention to determine behavioural and neural efficacy.Ethics and disseminationEthics approval has been obtained from ethics boards at the University Health Network and University of Toronto. Findings will be presented at academic conferences and submitted to peer-reviewed journals.Trial registration numberVersion 3, ClinicalTrials.gov Registry (NCT04331392).

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