Brain Protection (brain + protection)

Distribution by Scientific Domains
Medical Sciences80%

Selected Abstracts

Immediate Clinical Outcome after Prolonged Periods of Brain Protection: Retrospective Comparison of Hypothermic Circulatory Arrest, Retrograde, and Antegrade Perfusion

JOURNAL OF CARDIAC SURGERY, Issue 5 2009
Anil Z. Apaydin M.D.
Methods: Between 1993 and 2006, 339 patients underwent proximal aortic operations using a period of cerebral protection. Among these, 161 patients (mean age of 55 ± 12 years) who required cerebral protection longer than 25 minutes were included in the analysis. Ascending aorta with or without root was replaced in all patients. In addition, total arch replacement was performed in 36 patients. All patients were cooled to rectal temperature of 16 °C. Hypothermic circulatory arrest without adjunctive perfusion was used in 48 patients. Retrograde or antegrade cerebral perfusion was added in 94 and 19 patients, respectively. The mean duration of total cerebral protection was 42 ± 17 minutes. Results: Overall mortality was 15.5% (25/161) and did not differ among the perfusion groups. There was no difference in the incidence of overall neurological events, temporary neurological dysfunction, or major stroke among the groups. Multivariate analysis revealed that transfusion of >3 units of blood (p < 0.03) was an incremental risk factor for mortality. History of hypertension (p < 0.03), coexisting systemic diseases (p < 0.005), and transfusion of >3 units of blood (p < 0.04) were predictors of temporary neurological dysfunction. Conclusion: In proximal aortic operations requiring prolonged periods of cerebral protection, the mortality and neurological morbidity are not determined by the type of cerebral protection method only. Factors like hypertension and diabetes may play a role in the development of temporary neurological dysfunction. [source]

Brain Protection During Pediatric Cardiopulmonary Bypass

ARTIFICIAL ORGANS, Issue 4 2010
Xiaowei W. Su
Abstract Improvements in peri- and postoperative surgical techniques have greatly improved outcomes for pediatric patients undergoing cardiopulmonary bypass (CPB) in the treatment of congenital heart defects (CHDs). With decreased mortality rates, the incidence of adverse neurological outcomes, comprising cognitive and speech impairments, motor deficits, and behavioral abnormalities, has increased in those patients surviving bypass. A number of mechanisms, including ischemia, reperfusion injury, hypothermia, inflammation, and hemodilution, contribute to brain insult, which is further confounded by unique challenges presented in the pediatric population. However, a number of brain monitoring and preventative techniques have been developed or are being currently evaluated in the practice of pediatric CPB. Monitoring techniques include electroencephalography, near-infrared as well as visible light spectroscopy, transcranial Doppler ultrasound, and emboli detection and classification quantitation. Preventative measures include hypothermic perfusion techniques such as deep hypothermic circulatory arrest, low-flow CPB, blood gas management, and pharmacologic prophylaxes, among others. The present review summarizes the principles of brain insult, neurodevelopmental abnormalities, monitoring techniques, methods of prevention, as well as preexisting morbidities and risk factors in pediatric CPB, with a focus on brain protection. Clinical and translational research is presented with the aim of determining methods that may optimize neurological outcomes post CPB and guiding further study. [source]

Neurovascular and neuronal protection by E64d after focal cerebral ischemia in rats

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2006
Tamiji Tsubokawa
Abstract Calpains and cathepsins are two families of proteases that play an important role in ischemic cell death. In this study, we investigated the effect of E64d, a ,-calpain and cathepsin B inhibitor, in the prevention of neuronal and endothelial apoptotic cell death after focal cerebral ischemia in rats. Rats underwent 2 hr of transient focal ischemia from middle cerebral artery occlusion (MCAO) and were sacrificed 24 hr later. E64d (5 mg/ kg intraperitoneally) was administered 30 min before MCAO. Assessment included neurological function, infarction volume, brain water content, blood,brain barrier permeability, histology, and immunohistochemistry. The E64d-treated rats had significant brain protection against ischemic damage. We observed a reduction of infarction volume, brain edema, and improved neurological scores in E64d-treated rats compared with the nontreated control. Furthermore, there was a remarkable reduction in both proteases and caspase-3 activation and apoptotic changes in both neurons and endothelial cells in E64d-treated rats. These results suggest that E64d protects the brain against ischemic/reperfusion injury by attenuating neuronal and endothelial apoptosis. © 2006 Wiley-Liss, Inc. [source]

Brain Protection During Pediatric Cardiopulmonary Bypass

ARTIFICIAL ORGANS, Issue 4 2010
Xiaowei W. Su
Abstract Improvements in peri- and postoperative surgical techniques have greatly improved outcomes for pediatric patients undergoing cardiopulmonary bypass (CPB) in the treatment of congenital heart defects (CHDs). With decreased mortality rates, the incidence of adverse neurological outcomes, comprising cognitive and speech impairments, motor deficits, and behavioral abnormalities, has increased in those patients surviving bypass. A number of mechanisms, including ischemia, reperfusion injury, hypothermia, inflammation, and hemodilution, contribute to brain insult, which is further confounded by unique challenges presented in the pediatric population. However, a number of brain monitoring and preventative techniques have been developed or are being currently evaluated in the practice of pediatric CPB. Monitoring techniques include electroencephalography, near-infrared as well as visible light spectroscopy, transcranial Doppler ultrasound, and emboli detection and classification quantitation. Preventative measures include hypothermic perfusion techniques such as deep hypothermic circulatory arrest, low-flow CPB, blood gas management, and pharmacologic prophylaxes, among others. The present review summarizes the principles of brain insult, neurodevelopmental abnormalities, monitoring techniques, methods of prevention, as well as preexisting morbidities and risk factors in pediatric CPB, with a focus on brain protection. Clinical and translational research is presented with the aim of determining methods that may optimize neurological outcomes post CPB and guiding further study. [source]

Effects of sepsis on mast cells in rat dura mater: influence of L -NAME and VIP

BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2001
F Tore
The influence of lipopolysaccharide (LPS)-induced sepsis on the various mast cell phenotypes of rat dura mater were examined both by immunohistochemical and biochemical methods. Three different populations of mast cells were identified in control rats: connective tissue type mast cells (CTMC) which contain rat mast cell protease1 (RMCP1), histamine, serotonin and heparin, mucosal type mast cells (MMC) which contain RMCP2, histamine and serotonin, and intermediate type which contains both RMCP1 and RMCP2 and probably various proportions of amines and heparin. LPS (25 mg kg,1 i.p.) caused changes in the proportions of the various types of mast cells. The number of MMC and intermediate type mast cells significantly increased and the number of mast cells immunopositive for both heparin and serotonin significantly decreased. Biochemical analysis showed that the histamine concentration of dura increased while its serotonin concentration decreased. While vasoactive intestinal peptide (VIP) (25 ng kg,1 i.p.) appears to potentiate LPS effects on dura mater mast cells, non-selective inhibition of nitric oxide (NO) synthase by Ng -nitro- L -arginine methyl ester (L -NAME) (30 mg kg,1 i.p.) did not influence sepsis-induced mast cell changes. These findings suggest that mast cells of dura mater may play a role in brain protection during sepsis. British Journal of Pharmacology (2001) 134, 1367,1374; doi:10.1038/sj.bjp.0704412 [source]