Search

Dynamic changes in tissue water diffusion and glucose metabolism occur during and after hypoxia in cerebral hypoxia-ischemia reflecting a bioenergetics disturbance in affected cells. Diffusion weighted magnetic resonance imaging (MRI) identifies regions that are damaged, potentially irreversibly, by hypoxia-ischemia. Alterations in glucose utilization in the affected tissue may be detectable by positron emission tomography (PET) imaging of 2-deoxy-2-(18F)fluoro-ᴅ-glucose ([18F]FDG) uptake. Due to the rapid and variable nature of injury in this animal model, acquisition of both modes of data must be performed simultaneously in order to meaningfully correlate PET and MRI data. In addition, inter-animal variability in the hypoxic-ischemic injury due to vascular differences limits the ability to analyze multi-modal data and observe changes to a group-wise approach if data is not acquired simultaneously in individual subjects. The method presented here allows one to acquire both diffusion-weighted MRI and [18F]FDG uptake data in the same animal before, during, and after the hypoxic challenge in order to interrogate immediate physiological changes.

Glia account for 90% of human brain cells and have a significant role in brain homeostasis. Thus, specific in vivo imaging markers of glial metabolism are potentially valuable. In the brain, 2-fluoroacetate is selectively taken up by glial cells and becomes metabolically trapped in the tricarboxylic acid cycle. Recent work in rodent brain injury models demonstrated elevated lesion uptake of 2-[(18)F]fluoroacetate ([(18)F]FACE), suggesting possible use for specifically imaging glial metabolism. To assess this hypothesis, we evaluated [(18)F]FACE kinetics in rodent models of cerebral hypoxia-ischemia at 3 and 24 hours post insult. Lesion uptake was significantly higher at 30 minutes post injection (P

• DEX attenuates brain damage in neonatal rats with cerebral hypoxia–ischemia; • DEX curbs hippocampal astrocyte pyroptosis in cerebral hypoxic-ischemic neonatal rats; • DEX attenuates brain injury in rats through upregulation of miR-148a-3p. • miR-148a-3p inhibits pyroptosis of rat hippocampal astrocytes; • miR-148a-3p inhibits the STAT/JMJD3 axis: Dexmedetomidine (DEX), a selective α2-adrenoceptor agonist, is an anesthetic and sedative agent and has been reported to confer neuroprotective effects after cerebral hypoxic ischemia (CHI). This study was undertaken to elucidate the mechanisms by which microRNA (miR)-148a-3p is involved in the neuroprotective effect of DEX on hypoxic-ischemic brain damage in neonatal rats. Neonatal rats were exposed to CHI conditions, a miR-148a-3p inhibitor, and DEX. Hippocampal astrocytes were isolated to construct an oxygen-glucose deprivation (OGD) model. qRT-PCR and western blot were utilized to inspect miR-148a-3p, STAT1, STAT3, JMJD3, cleaved-Caspase-1, ASC, NLRP3, GSDMD, and GSDMD-N expression in rats and astrocytes. TUNEL staining was employed to measure astrocyte apoptosis rate, immunofluorescence to inspect cleaved-Caspase-1 and ASC levels, and ELISA to determine IL-1β and IL-18 expression. The target genes of miR-148a-3p were predicted using online software and verified by a dual-luciferase reporter gene assay. A prominent increase in astrocyte apoptosis rate and the expression of pyroptosis- and inflammation-related factors were found in rats with CHI and OGD-treated astrocytes. DEX suppressed astrocyte apoptosis rate and decreased expression of pyroptosis- and inflammation-related factors. Knockdown of miR-148a-3p facilitated astrocyte pyroptosis, indicating that DEX exerted its protective effect by upregulating miR-148a-3p. miR-148a-3p negatively mediated STAT to inactivate JMJD3. Overexpression of STAT1 and STAT3 facilitated pyroptosis in astrocytes, which was negated by the overexpression of miR-148a-3p. DEX inhibited hippocampal astrocyte pyroptosis by upregulating miR-148a-3p to inactivate the STAT/JMJD3 axis, thereby alleviating cerebral damage in neonatal rats with CHI. [ABSTRACT FROM AUTHOR]

Objective: This study aims to categorize infants treated with therapeutic hypothermia who presented with suspected subacute hypoxia-ischemia-that is, injury that likely occurred well before delivery and thus beyond the 6-hour window for therapeutic hypothermia-and to contrast the clinical characteristics with infants who suffered a known acute hypoxia-ischemia event.Design: A retrospective chart review was undertaken of infants treated with therapeutic hypothermia at our center during a 6-year period. Suspected subacute injury is defined as decreased fetal movement greater than 6 hours before delivery or severe depression at birth without need for cardiopulmonary resuscitation. Acute injury is defined as an acute perinatal event including placental abruption, ruptured uterus, or umbilical cord abnormalities. Abnormal outcome is defined as death, cognitive delay, or spastic quadriplegia at follow-up.Results: Infants with subacute (n = 7) versus acute injury (n = 26) were less likely to require cardiopulmonary resuscitation, were less acidotic at birth on cord gases with no significant difference in initial postnatal pH or base deficit, were more severely encephalopathic with severe amplitude electroencephalogram suppression, and demonstrated universal adverse outcome.Conclusions: These data demonstrate greater benefit of therapeutic hypothermia for those infants with acute versus subacute injury. Early initiation of therapeutic hypothermia relative to the presumed onset of hypoxia-ischemia is critical. Early severe encephalopathy in the absence of a known acute perinatal event should raise concern in some cases for a subacute insult where the effect of therapeutic hypothermia is unlikely to be of benefit. [ABSTRACT FROM AUTHOR]

Abstract: Background: Hippocampal injury is most often observed in conjunction with basal ganglia injury after hypoxia-ischemia in term newborns. Objective was to determine perinatal characteristics leading to selective hippocampal injury vs basal ganglia injury on diffusion-weighted imaging in term encephalopathic infants following intrapartum hypoxia-ischemia treated with selective head cooling and to correlate specific injury to subsequent neurodevelopmental outcome. Methods: Retrospective chart review of obstetric and/or perinatal risk factors and patient characteristics in term infants treated with selective head cooling. All infants met standard enrollment criteria for cooling. MRI was obtained at a median of 7 days of life. Abnormal outcome was defined as spastic quadriplegia, cognitive delay, both, or death. Results: Fifty-seven infants were included for analysis. Diffusion-weighted imaging findings included normal (n = 31), basal ganglia injury (n = 16), and selective hippocampal injury (n = 10). No differences in gestational age, birth weight, sex, or labor complications between groups. More infants in the basal ganglia vs hippocampal group required delivery room cardiopulmonary resuscitation (P = 0.05), exhibited persistent severe acidosis, severe amplitude electroencephalography suppression, and encephalopathy at birth (P < 0.05). Abnormal neurodevelopmental outcome or death was observed in 88% vs 10% of infants in the basal ganglia vs the hippocampal group, respectively (P = 0.0001). Conclusions: Infants with hippocampal injury on diffusion-weighted imaging recovered from an intrapartum asphyxial insult more rapidly as reflected by an earlier correction of acid-base status, were less likely to need cardiopulmonary resuscitation, and were less severely encephalopathic. These findings highlight the exquisite vulnerability of the hippocampus to acute hypoxia unaffected by selective head cooling, whereas the normal appearance of the basal ganglia in these infants suggests a neuroprotective effect of cooling. [Copyright &y& Elsevier]

Summary: Hypoxia–ischemia is an infrequent event which may occur prior to or during delivery, following a period of decreased placental and/or fetal blood flow. Following recovery, a reperfusion phase and secondary energy failure may occur 6–48 h subsequent to the initial insult. Therapeutic hypothermia may be offered to infants at risk for evolving encephalopathy if identified within the 6 h therapeutic window, and should be instituted as early as possible for eligible infants. Additionally, the clinician must pay close attention to supportive measures such as avoidance of hyperthermia, as well as comprehensive management of clinical or electrographic seizures, blood pressure, blood glucoses, and carbon dioxide levels. [Copyright &y& Elsevier]

Cerebral hypothermia is one of the first neuroprotective strategies that can improve outcome of experimental and human perinatal cerebral hypoxia-ischemia. Now, international guidelines for hypoxic-ischemic encephalopathy in term neonates recommend hypothermia. At several places, hypothermia could block the cascade of neurochemical events that mediate brain damage insult in term infants. Extended cooling must be initiated 6 h after injury, after obtaining accurate data about perinatal asphyxia and the severity of hypoxic-ischemic encephalopathy. At 18 months of life, hypothermia reduces the risk of death or disability in infants with moderate or severe hypoxic-ischemic encephalopathy. However, longer-term data have not been available to assess whether the benefits of hypothermia persist after 2 years of age. Extensions of indication are debated for late preterm infants or newborns admitted in intensive care unit after 6 hours of life, and clinical studies are actually performed on these subjects. However, if prognosis at 18 months is improved, more than 40% of treated newborns will have an unfavorable evolution. Other neuroprotective strategies as erythropoietin, melatonin, and xenon or magnesium sulfate are actually evaluated. Results of these last studies would be interesting in the future, because these strategies could be associated with hypothermia. [ABSTRACT FROM AUTHOR]

Background: Oxygen supplementation is still part of international resuscitation protocols for premature children. Mechanisms for tissue damage by hypoxia/ischemia in the extreme premature involve inflammation. Aim and method: To study cerebral inflammation after hypoxia/ischemia and oxygen treatment in the premature, we measured NF-κB activity in 5-day-old transgenic reporter mice in response to experimental hypoxia/ischemia. Results were correlated to cerebral histological evaluation and plasma cytokine levels. A treatment strategy with the antioxidant tempol was tested. Results: One day after hypoxia/ischemia NF-κB activation was increased compared to controls [mean difference: 10.6±4.6% (P=0.03)]. Exposure to 100% oxygen after hypoxia/ischemia further increased NF-κB activation compared to hypoxia/ischemia alone [mean difference: 15.0±5.5% (P=0.01)]. Histological changes in the brain were positively correlated with NF-κB activity (P<0.001), but we found no significant difference in tissue damage between resuscitation with air and resuscitation with pure oxygen. Administration of tempol reduced NF-κB activation [mean difference: 14.6±5.0% (P=0.01)] and the plasma level of cytokines; however, the histological damage score was not affected. Conclusion: Cerebral inflammatory response after hypoxia/ischemia in a mouse model with immature brain development corresponding to human prematurity prior to 32 weeks' gestation was influenced by administration of oxygen. Tempol treatment attenuated inflammation but did not reduce the extent of histological cerebral damage. [ABSTRACT FROM AUTHOR]

Aim: Our aim was to show the effect of one-lung ventilation (OLV) on cerebral blood flow (CBF) by measuring carotid blood flow. This technique has been the subject of experimental and clinical studies. Materials and methods: Carotid doppler flows were measured at 4 different times. Peak systolic velocity (PSV) and end diastolic velocity (EDV) were measured and pulsatility index (PI) and resistive index (RI) calculated. Results: There were no significant changes in PSV, PI, RI, or flow volume in the normal or diseased sides at repeated measures (P > 0.05).There was no significant difference between the flow velocities, PIs, RIs, or flow volumes measured in the supine and decubitus positions during OLV. In addition, there was no significant difference between the flow parameters of the upper and lower carotids measured in the lateral decubitus position before and after OLV. There was no correlation between any of the flow parameters and duration of OLV. Conclusion: OLV poses no additional risk in terms of CBF. However, further studies, supported by biochemical parameters and involving wider patient groups, are now needed. [ABSTRACT FROM AUTHOR]

The aim of the present work was to perform clinical and neurophysiological assessment of the rates of neuromental development during the first year of life in preterm neonates with cerebral ischemia grade II-III, allowing for the effects of treatment with Cytoflavin and resuscitation measures. A total of 120 children with gestational ages of 28-36 weeks and body weights of 1060-3150 g were studied. The study group included 61 children whose complex treatment included Cytoflavin at a dose of 2 ml/kg/day i.v. for five days. The control group consisted of 59 patients who received basal treatment without Cytoflavin. Follow-up to a corrected age (CA) of one year included assessment of overall condition and neurological status (using a quantitative assessment of postural muscle tone on the INFANIB scale, psychomotor development on the BSID-II scale, and the functional state of the CNS by computerized electroencephalography by monitoring of physiological sleep). The results demonstrated faster normalization of all study measures of development in children receiving Cytoflavin in their complex treatment as compared with the control group. [ABSTRACT FROM AUTHOR]

Abstract: Cerebral ischemia initiates various injurious processes including neuroinflammatory responses such as activation of microglia and increases in cytokine and nitric oxide release. Evidence primarily from in vitro studies, indicates that neuroinflammatory effects can be either beneficial or harmful, possibly related to stimulus strength. We investigated using in vivo models, the effect of a mild or substantial cerebral hypoxia–ischemia on: cerebral microglial/macrophage activation (ED1), pro-inflammatory cytokines (tumor necrosis factor-alpha), nitrosative stress (nitrotyrosine) and permanent brain damage. A mild insult produced a transient (1–2 days post) increase in activated microglia/macrophages within subcortical white and not gray matter but transiently increased cytokine or nitrotyrosine expression in cortex and not white matter. There was also prolonged scattered cell death in cortex and white matter over weeks along with loss of myelin/axons and cortical atrophy at 4 weeks post-insult. In contrast, a substantial insult produced white and gray matter necrosis, cyst formation and atrophy, along with increases in tumor necrosis factor and nitrotyrosine staining within both white and gray matter starting at 1–2 days post-insult. Microglial/macrophage staining was increased starting at 1-week post a substantial insult and remained elevated for weeks thereafter. Thus, a transient neuroinflammatory response occurs following a mild insult whereas prolonged scattered cell death occurs for weeks, particularly in white matter. Insult severity also affects the progression of the neuroinflammatory response, which is prolonged after a substantial insult. Effective therapy will need to be customized for insult severity and timing; and, monitoring the injury processes with imaging or biomarkers may help guide treatment. [Copyright &y& Elsevier]

Abstract: Cerebral hypoxic–ischemic injury represents a serious health problem and is the third leading cause of mortality in developed countries. Early diagnosis of hypoxic–ischemic injury to the brain is inevitable for timely and efficient treatment. However, routinely applied cranial ultrasonography or computed tomography is often not sensitive enough to detect cerebral hypoxic–ischemic injury in its early stages. Therefore searching for a more effective diagnostic tool has been an intensive process in many laboratories within the last decades. Nowadays, magnetic resonance imaging (MRI) and spectroscopy (MRS) are the most promising non-invasive and non-destructive tools working in-real-time. These magnetic resonance-based techniques are progressively utilized in neurological and neonatology departments to confirm or refute cerebral hypoxic–ischemic injury in adults and neonates. The purpose of the present paper was therefore (i) to provide a brief overview on mechanisms of hypoxic–ischemic injury to the brain and (ii) to summarize main findings of both clinical reports and experimental studies, performed on various animal models of brain hypoxia–ischemia, with a particular focus on the monitoring of the evolving cerebral hypoxic–ischemic injury by means of in vivo MRI and MRS. [Copyright &y& Elsevier]

Abstract: To determine whether intranasal administration (iN) of recombinant human insulin-like growth factor-1 (rhIGF-1) provides neuroprotection to the neonatal rat brain following cerebral hypoxia-ischemia (HI), two doses of rhIGF-1 (50 μg at a 1 h interval) were infused into the right naris of postnatal day 7 (P7) rat pups with or without a prior HI insult (right common carotid artery ligation, followed by an exposure to 8% oxygen for 2 h). Our result showed that rhIGF-1 administered via iN was successfully delivered into the brain 30 min after the second dose. In the following studies rhIGF-1 was administered to P7 rat pups at 0, 1 or 2 h after HI at the dose described above. Pups in the control group received cerebral HI and vehicle treatment. Pups that underwent sham operation and vehicle treatment served as the sham group. Brain pathological changes were evaluated 2 and 15 days after HI. Our results showed that rhIGF-1 treatment up to 1 h after cerebral HI effectively reduced brain injury as compared to that in the vehicle-treated rats. Moreover, rhIGF-1 treatment improved neurobehavioral performance (tested on P5–P21) in juvenile rats subjected to HI. Our results further showed that rhIGF-1 inhibited apoptotic cell death, possibly through activating the Akt signal transduction pathway. rhIGF-1 enhanced proliferation of neuronal and oligodendroglial progenitors after cerebral HI as well. These data suggest that iN administration of IGF-1 has the potential to be used for clinical treatment. [Copyright &y& Elsevier]

Abstract: Xanthine oxidase (XO), an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid, is thought to contribute to hypoxic–ischemic brain injury by generating oxygen-free radicals during reperfusion. This is based largely on the observation that inhibition of XO reduces brain damage, but the precise mechanism by which the enzyme contributes to cerebral ischemic injury has not been specifically evaluated. We examined the role of XO in generating oxygen-free radicals that cause brain injury, hypothesizing that if XO generated a significant amount of free radicals during hypoxia–ischemia and reperfusion, providing additional substrate at the time of injury should increase brain damage. Anesthetized rabbits were first subjected to 8 min of cerebral hypoxia by breathing 3% oxygen and then to 8 min of ischemia by raising intracranial pressure equal to mean arterial pressure with an artificial CSF. In order to promote oxygen-free radical generation, hypoxanthine (n =9) or xanthine (n =9), XO substrates, or the vehicle (n =8) was infused intravenously beginning 30 min before and continuing until 30 min after the insult. Animals were sacrificed after 4 h of reperfusion. Neither hypoxanthine nor xanthine infusion increased brain damage. However, administration of hypoxanthine significantly improved somatosensory evoked potential recovery and preserved neurofilament 68 kDa protein, a neuronal structural protein. This study does not support free radical generation by XO as a major cause of damage in cerebral hypoxia–ischemia. Infusion of hypoxanthine reduced cerebral injury suggesting that another mechanism may explain why inhibition of XO reduces brain damage. [Copyright &y& Elsevier]

Abstract: Our previous study has demonstrated that α-phenyl-tert-butyl-nitrone (PBN) provided neuroprotection to the neonatal white matter following cerebral hypoxia-ischemia (HI). Free radical scavenging was involved in the neuroprotection of PBN. To investigate if other mechanisms contribute to the neuroprotection of PBN, postnatal day 4 SD rats were subjected to bilateral common carotid artery ligation, followed by 8% oxygen exposure for 20min. A single dose of PBN (100mg/kg, i.p.) was given prior to the hypoxic exposure. Expression of inflammatory cytokines: interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS) and tumor necrosis factor-α (TNF-α) was determined by RT-PCR, ELISA and immunohistochemistry. Activation of transcriptional factor nuclear factor-kappa B (NF-κB) was measured by ELISA. PBN significantly inhibited HI-induced up-regulation of IL-1β, TNF-α and iNOS mRNA expression at 4h following HI. PBN treatment also reduced the brain concentration of IL-1β significantly and decreased the number of IL-1β- or iNOS-expressing cells in the white matter area at 12h following HI. Moreover, PBN suppressed the HI-induced NF-κB activation at 1h after HI. The overall results indicate that besides free radical scavenging, anti-inflammation might partly contribute to the neuroprotection afforded by PBN on neonatal white matter following cerebral HI. [Copyright &y& Elsevier]

The present study examines the effect of dexamethasone treatment on the intensity of changes in T2-weighted and diffusion-weighted (DW) magnetic resonance images occurring in infant rats during and after cerebral hypoxia-ischemia. The right carotid artery was occluded under isoflurane anesthesia in 7-day-old rats and images were acquired in sedated animals using a Bruker 9.4 T magnetic resonance (MR) system. Imaging changes were markedly different in rats pretreated with dexamethasone phosphate (0.1 mg/kg, i.p.) 24 h before hypoxia than in controls. In control animals, areas of hyperintensity ipsilateral to the occlusion occurred during hypoxia-ischemia in both the DW- and T2-weighted images with some recovery of the changes in early posthypoxia. In contrast, in dexamethasone-treated animals, areas of increased hyperintensity in the MR images did not occur. Thus, dexamethasone treatment prevents MR imaging changes during ischemia, suggesting that the cytotoxic edema associated with energy depletion and/or ionic disturbances during ischemia are also prevented by dexamethasone treatment. [ABSTRACT FROM AUTHOR]

The primary cause of neurologic impairment in newborn infants is hypoxic-ischemic injury. Studies of the mechanisms involved in the damaging effects of hypoxia-ischemia and reperfusion in brain tissue indicate significant contributions from reactive oxygen species, with the loss of homeostatic control of intracellular iron an important determinant of oxidant-mediated damage. We investigated the effects of cerebral hypoxiaischemia and reperfusion on the redistribution of nonheme iron in newborn piglets. Anesthetized newborn piglets were subjected to reductions in cerebral blood flow by phlebotomy and cervical cuff compression. Control animals were sham-operated. Subcellular fractions were isolated from brain tissue homogenates by differential centrifugation, and nonheme iron contents of these fractions were measured with ferene-S. Iron contents in the homogenates were not altered. However, iron contents of the microsomal fractions of animals subjected to 30 minutes of hypoxia-ischemia increased from 0.517±0.053 to 0.930±0.061 nmol/mg protein (p<0.01); 120 minutes of reperfusion caused no further changes. This translocation of iron may be linked to oxidative alterations of brain proteins, which we investigated by detection of dinitrophenylhydrazine-derivitized protein carbonyls, which are characteristic of iron-catalyzed oxidation reactions. [ABSTRACT FROM AUTHOR]

• OIP5-AS1 is down-regulated in IR patients, tMCAO/R rat models, and OGD/R treated microglia. • OIP5-AS1 depresses inflammation and oxidative stress in tMCAO/R and OGD/R. • OIP5-AS1 exerts it role through the miR-186-5p/CTRP3 axis. Inflammation and oxidative stress is closely associated with the development of ischemic brain stroke. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long non-coding RNA (lncRNA), has been suggested to play an important role in the development of many types of human cancers. However, the functional involvement of OIP5-AS1 in ischemic stroke is still unknown. Quantitative real-time polymerase chain reaction and /or western blot were conducted to determine the expression profiles of OIP5-AS1, C1q/TNF-related protein 3 (CTRP3) and miR-186-5p in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and microglial cells treated with oxygen glucose deprivation/re-oxygenation (OGD/R). Upon selective regulation of OIP5-AS1 and miR-186-5p, the inflammation and oxidative stress responses in microglia/macrophage as well as neurologic functions in MCAO/R rats were detected. Furthermore, the interactions between OIP5-AS1 and miR-186-5p, miR-186-5p and CTRP3 were investigated by RNA immunoprecipitation (RIP) assay, luciferase report assay and bioinformation anaylsis. We observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis. Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p. [ABSTRACT FROM AUTHOR]

Hypoxic-ischemic encephalopathy (HIE) remains to be a major cause of morbidity, mortality and severe neurodevelopmental disability in term neonates. Moderate whole body hypothermia is an established, effective neuroprotective therapy to reduce mortality and long-term disability associated with HIE, however, research for adjunct therapies is still warranted to complement the effect of hypothermia. In the last decade, molecular hydrogen emerged as a simple, available, inexpensive substance with advantageous pharmacokinetics to ameliorate hypoxic-ischemic cellular damage. The present review examines the preclinical studies employing hydrogen to combat the deleterious consequences of hypoxic-ischemic insults in rodent and piglet HIE models. Hydrogen exerted unequivocal neuroprotective actions shown by preserved neurovascular function, neuronal viability, and neurocognitive functions in virtually all model species and hypoxic-ischemic insult types tested. Administration of hydrogen started in most studies after the hypoxic-ischemic insult enhancing the translational value of the findings. Among the explored mechanisms of hydrogen-induced neuroprotection, antioxidant, anti- apoptotic and anti-inflammatory effects appeared to be dominant. Unfortunately, the additive neuroprotective effect of hydrogen and therapeutic hypothermia has not yet been demonstrated, thus such studies are warranted to promote the clinical testing of molecular hydrogen as an adjunct neuroprotective treatment of HIE., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To explore the basic values of regional cerebral oxygen saturation (rSO 2 ) among different age groups., Methods: One hundred twenty patients who were scheduled for elective surgery aged 0 to 80 years (American Society of Anesthesiologists [ASA] physical status I or II) or neonates just after birth via cesarean section were enrolled and divided into the following six groups: infant (0 month and ≤12 months), toddler (>1 and ≤3 years old), preschool (>3 and ≤6 years old), school age (>6 and ≤18 years old), adult (>18 and ≤65 years old), and elderly (>65 and ≤80 years old) groups. There were 20 patients in each group., Results: The basic values of rSO 2 in infant, toddler, preschool, school age, adults, and elderly groups were 70.41% ± 4.66%, 72.43% ± 3.81%, 70.77% ± 3.27%, 70.62% ± 2.20%, 69.76% ± 6.02%, and 62.69% ± 3.14%, respectively. The basic value in the elderly group was lower compared with other five groups. There was no significant difference among infant, toddler, preschool age, school age, and adult groups., Conclusions: The basic value of rSO 2 in elderly patients is lower. Age is an important factor that affects the underlying value of rSO 2 .

Objective: To observe the effect of electroacupuncture (EA) on changes of learning-memory ability, psychomotor coordination and anxiety-like behavior of cerebral hypoxic-ischemia (CHI) young rats, so as to explore its protective effect on neurons under hypoxic-ischemic conditions., Methods: SD rats (aged 7 days) were randomly divided into sham operation (sham, n =12), model ( n =11), and EA groups ( n =12). In addition, 6 young rats in each group were used for observing the number of dendritic spines after Golgi staining. The CHI model was established by ligation of the left common carotid artery combined with hypoxia in a closed transparent vessel. EA was applied to "Baihui" (GV 20)and "Dazhui" (GV 14) for 20 min, once every other day, for 28 days. The rats' behavior changes were assessed by using rotarod performance (for psychomotor coordination), elevated plus maze (anxiety-like behavior) tests and Morris water maze (learning-memory ability) tests, separately., Results: After modeling, the average escape latency and average escape distance of location navigation test within 70 seconds were significantly increased ( P <0.05), and the average times and average duration of safe-platform quadrant crossing of spacial probing test were markedly reduced relevant to the sham group ( P <0.05). After EA treatment, CHI-induced increases of escape latency and escape distance, and the decreased times and duration of platform quadrant crossing were significantly reversed ( P <0.05). No significant differences were found among the three groups in the falling latency of rotarod performance test, and in the time of opening and closing arms of elevated plus maze tests ( P >0.05). The density of dendritic spines was significantly lo-wer in the model group than in the sham group (P <0.05), and notably higher in the EA group than in the model group ( P <0.05)., Conclusion: EA can improve the learning-memory ability of CHI young rats, which may be related to its effect in protecting the dendritic spines of CA 1 region of hippocampus from injury.