Home About us Contact
|
Home About us Contact | ||
|
|
||
Common Carotid Artery Occlusion (common + carotid_artery_occlusion)
Kinds of Common Carotid Artery Occlusion Selected AbstractsSevoflurane-induced post-conditioning has no beneficial effects on neuroprotection after incomplete cerebral ischemia in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2010H.-M. LEE Background: The aim of this study was to investigate whether sevoflurane-induced post-conditioning has a neuroprotective effect against incomplete cerebral ischemia in rats. Methods: After cerebral ischemia by right common carotid artery occlusion in combination with hemorrhagic hypotension (35 mmHg) for 30 min, 1.0 minimum alveolar concentration of sevoflurane was administered for 15 min (Post-C 15, n=8), 30 min (Post-C 30, n=8), or 60 min (Post-C 60, n=8) in rats. Sevoflurane was not administered in control (n=8) and sham control rats (n=8). Neurologic evaluations were performed at 24, 48, and 72 h after ischemia. Degrees of neuronal damage in ischemic hippocampal CA1 and the cortex were assessed by counting eosinophilic neurons, and detection of DNA fragmentation was performed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Results: Neurologic deficit scores in the Post-C 60 group were higher than in the control group at 48 and 72 h post-ischemia (P<0.05). No differences were observed in the percentages of eosinophilic neurons among the control (CA1: 37.3 ± 25.4, cortex: 26.0 ± 8.9), Post-C 15 (CA1: 54.0 ± 21.4, cortex: 30.8 ± 19.9), or Post-C 30 (CA1: 68.4 ± 17.5, cortex: 38.0 ± 11.0) groups in ischemic CA1 and cortices. However, in the Post-C 60 group, the percentages of eosinophilic neurons were higher than in the control group in CA1 and cortices (P<0.05). The percentages of TUNEL-positive cell were similar in the control group and the post-conditioned groups. Conclusion: These findings show that sevoflurane administration after ischemia does not provide neuroprotection in rats subjected to incomplete cerebral ischemia. [source] Effects of sevoflurane on cognitive deficit, motor function, and histopathology after cerebral ischemia in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009E. EBERSPÄCHER Background: The volatile anesthetic sevoflurane exhibits neuroprotective properties when assessed for motor function and histopathology after cerebral ischemia in rats. Damage of hippocampal neurons after ischemia relates to a number of cognitive deficits that are not revealed by testing animals for motor function. Therefore, the present study evaluates cognitive and behavioral function as well as hippocampal damage in rats subjected to cerebral ischemia under sevoflurane compared with fentanyl/nitrous oxide (N2O)/O2 anesthesia. Methods: Thirty-four rats were trained for 10 days using a hole-board test to detect changes in cognitive and behavioral function. Rats were randomly assigned to the following groups: (A) sham/fentanyl/N2O/O2 (n=7); (B) ischemia/fentanyl/N2O/O2 (n=10); (C) sham/2.0 vol% sevoflurane in O2/air (n=7); and (D) ischemia/2.0 vol% sevoflurane in O2/air (n=10). Cerebral ischemia was produced by unilateral common carotid artery occlusion combined with hemorrhagic hypotension (mean arterial blood pressure 40 mmHg for 45 min). Temperature, arterial blood gases, and pH were maintained constant. Cerebral blood flow was measured using laser-Doppler flowmetry. After surgery, cognitive and behavioral function was re-evaluated for 10 days. On day 11, the brains were removed for histopathologic evaluation (hematoxylin/eosin-staining). Results: Cognitive testing revealed deficits in declarative and working memory in ischemic rats anesthetized with fentanyl/N2O. Rats anesthetized with sevoflurane during ischemia showed a significantly better outcome. Hippocampal damage was significantly worse with fentanyl/N2O. Conclusion: The present data add to previous investigations showing that sevoflurane prevents a deficit in cognitive function and histopathological damage induced by cerebral ischemia in rats. [source] Dose-dependent effect of S(+) ketamine on post-ischemic endogenous neurogenesis in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2009U. WINKELHEIDE Background: Ketamine is a non-competitive antagonist at N -methyl- d -aspartate (NMDA) receptors and reduces neuronal injury after cerebral ischemia by blocking the excitotoxic effects of glutamate. However, cerebral regeneration by means of endogenous neurogenesis may be impaired with blockade of NMDA receptors. The effects of S(+) ketamine on post-ischemic neurogenesis are unknown and investigated in this study. Methods: Thirty-two male Sprague,Dawley rats were randomly assigned to the following treatment groups with intravenous S(+) ketamine anesthesia: S(+) ketamine 0.75 mg/kg/min with or without cerebral ischemia and S(+) ketamine 1.0 mg/kg/min with or without cerebral ischemia. Eight non-anesthetized, non-ischemic animals were investigated as naïve controls. Forebrain ischemia was induced by bilateral common carotid artery occlusion in combination with hemorrhagic hypotension. 5-bromo-2-deoxyuridine (BrdU) was injected intraperitoneally for seven consecutive post-operative days. BrdU-positive neurons in the dentate gyrus and histopathological damage of the hippocampus were analyzed after 28 days. Results: The number of new neurons was not affected by S(+) ketamine in the absence of cerebral ischemia. The ischemia-induced increase in neurogenesis was reduced by high-dose S(+) ketamine. Cell death of ischemic animals did not vary between low- and high-dose S(+) ketamine. Conclusion: While low concentrations of S(+) ketamine allow an ischemia-induced increase in the number of new neurons, high S(+) ketamine concentrations block the post-ischemic increase in newly generated neurons. This effect is irrespective of the extent of other histopathological damage and in line with studies showing that NMDA receptor antagonists like MK-801 inhibit neurogenesis after cerebral ischemia. [source] Increases in tumor necrosis factor-, following transient global cerebral ischemia do not contribute to neuron death in mouse hippocampusJOURNAL OF NEUROCHEMISTRY, Issue 6 2005Yuki Murakami Abstract The actions of tumor necrosis factor-, (TNF-,) produced by resident brain cells and bone marrow-derived cells in brain following a transient global ischemia were evaluated. In wild-type mice (C57Bl/6J) following 20 min ischemia with bilateral common carotid artery occlusion (BCCAo), TNF-, mRNA expression levels in the hippocampus were significantly increased at 3 h and 36 h and exhibited a biphasic expression pattern. There were no hippocampal TNF-, mRNA expression levels at early time points in either wild-type mice bone marrow transplanted (BMT)-chimeric-TNF-, gene-deficient (T/W) or TNF-, gene-deficient mice BMT-TNF-, gene-deficient mice (T/T), although TNF-, mRNA levels were detectable in T/W BMT mice at 36 h. Histopathological findings showed no intergroup differences between wild-type and TNF-, gene-deficient mice at 4 and 7 days after transient ischemia. In addition, nuclear factor-,B (NF-,B) was activated within 12 h after global cerebral ischemia, but electrophoretic mobility shift assays (EMSA) showed no intergroup differences between wild type and TNF-, gene-deficient mice. In summary, early hippocampal TNF-, mRNA expression may not be related to bone marrow-derived cells, and secondary TNF-, expression as early as 36 h after ischemia probably resulted mainly from endogenous brain cells and possibly a few bone marrow-derived cells. Although we cannot exclude the possibility of the TNF-, contribution to the physiologic changes of hippocampus after transient global ischemia, these results indicate that TNF-, does not influence the morphological changes of the hippocampal neurons under our study condition. [source] Pretreatment with the ciclosporin derivative NIM811 reduces delayed neuronal death in the hippocampus after transient forebrain ischaemiaJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2010Masaaki Hokari Dr Abstract Objectives There have been several previous studies showing that ciclosporin, a ligand for cyclophilin D (CypD), reduces mitochondrial permeability transition (mPT) and ameliorates delayed neuronal death. NIM811 is a non-immunosuppressive ciclosporin derivative that also inhibits mPT, but has significantly less cytotoxicity than ciclosporin. Actually, in animal experiments, several investigators have reported that NIM811 ameliorates central nervous system disorders, such as traumatic brain injury, transient focal cerebral ischaemia and spinal cord injury. Therefore, we evaluated whether the ciclosporin derivative, NIM811 reduces mPT and ameliorates delayed neuronal death in the hippocampal CA1 sectors in mice when subjected to transient forebrain ischaemia. Methods Male C57BL/6 mice were treated with 50 mg/kg ciclosporin, 10, 50 or 100 mg/kg NIM811 or phosphate-buffered saline. At 30 min post-injection, all mice were subjected to 20 min bilateral common carotid artery occlusion (BCCAO). To estimate delayed neuronal death, the sections were prepared for HE staining and terminal deoxynucleotidyl transferase-mediated dUTP end-labelling (TUNEL) staining at 72 h after 20 min BCCAO. Furthermore, using 5,5,,6,6,-tetrachloro-1,1,,3,3,-tetraethylbenzimidazolocarbocyanine iodide (JC-1) staining technique, we evaluated whether NIM811 (1, 10, 100 or 1000 ,m) inhibited mPT in the neurons exposed to 100 ,m glutamate. Results Both delayed neuronal injury and apoptosis in the hippocampal CA1 sectors were significantly ameliorated at 72 h after transient forebrain ischaemia in the mice treated with 100 mg/kg NIM811 or 50 mg/kg ciclosporin. The treatments with 100 ,m and 1000 ,m NIM811 significantly inhibited the reduction of mitochondrial membrane potential in the neurons exposed to 100 ,m glutamate. Conclusions These findings strongly suggest that NIM811 inhibits mPT and ameliorates delayed neuronal death in mice subjected to transient forebrain ischaemia. [source] A Post-ischaemic Single Administration of Galanthamine, a Cholinesterase Inhibitor, Improves Learning Ability in RatsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2000A. I. ILIEV Transient forebrain ischaemia is widely observed in clinical practice. We have examined the effect of a single administration of the Cholinesterase inhibitor galanthamine (2 mgkg,1, i.p.) 25 min after reperfusion in male Sprague-Dawley rats (180 ± 20 g) after a 20-min common carotid artery occlusion. Twenty-four-hours post-ischaemia there was no difference in motor co-ordination or muscle tonus of the rats treated with or without galanthamine as assessed by the rota-rod test. Learning ability was examined using the shuttle-box test, evaluating the latency time and the number of errors for six days in succession. The performance of the ischaemic saline-injected rats was significantly impaired on days 4, 5, 6 (latency time) compared with the non-ischaemic rats and with the ischaemic animals administered galanthamine (P< 0.05). Similar results were obtained when counting the number of errors (failure to cross the cage during conditioned or unconditioned stimulus). The monitoring of body temperature during the first 12-h post-ischaemia did not show any significant difference between the groups. The data showed a beneficial effect of galanthamine on the recovery of learning ability when administered once only post-ischaemia. This suggests a direct effect on the early pathologic mechanisms of CNS damage. Cholinesterase inhibitors may prove useful in the early clinical treatment of ischaemic conditions. [source] Long-term effects of hypothermia on neuronal cell death and the concentration of apoptotic proteins after incomplete cerebral ischemia and reperfusion in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2005E. Eberspächer Background:, The present study investigates the long-term effects of postischemic hypothermia on neuronal cell damage and concentration changes of apoptotic proteins after cerebral ischemia. Methods: Sixty-four Sprague-Dawley rats were anesthetized, intubated and ventilated with 2.0 Vol% isoflurane and 70% N2O/O2. After preparation the animals were randomly assigned to the following groups: group 1 (n = 32, fentanyl-N2O/normothermia 37.5°C), and group 2 (n = 32, fentanyl-N2O/hypothermia 34.0°C. Ischemia (45 min) was induced by common carotid artery occlusion plus hemorrhagic hypotension (MAP = 40 mmHg). Arterial blood gases and pH were maintained constant. After 1, 3, 7, or 28 days (each n = 8) the brains were removed, frozen and cut. Neuronal damage was assessed by analyzing Bax, Bcl-2, p53, and Mdm-2 proteins, activated caspases-3-positive and eosinophilic cells. A third group (n = 8) of untreated animals served as naive controls. Results:, In hypothermic animals, Bax concentration was decreased by 50,70% over time compared to normothermia. On days 1 and 3, Bcl-2 was increased by 50% with hypothermia. The amount of activated caspase-3-positive cells in the ischemic hemisphere was 0.5% in the hypothermic and 1,2% in the normothermic animals. Of the hippocampal cells, 10,25% were eosinophilic in both groups over time. Conclusion:, The present data show that hypothermia prevents an ischemia-induced increase of the pro-apoptotic protein Bax for as long as 28 days and increases the concentration of the antiapoptotic protein Bcl-2 up to 3 days compared to normothermic animals. Therefore, after cerebral ischemia, hypothermia has the sustained neuroprotective potential to shift apoptosis-related proteins towards neuronal cell survival. [source] Heterogeneous hyperactivity and distribution of ischemic lesions after focal cerebral ischemia in Mongolian gerbilsNEUROPATHOLOGY, Issue 4 2006Noriko Katsumata Various types of poststroke hyperactivity exist in humans, but studies of each mechanism using animal models are scarce. We aimed to analyze the heterogeneity of postischemic hyperlocomotion and to identify the ischemic lesions responsible for postischemic hyperlocomotion in rodent models of focal ischemia. Mongolian gerbils underwent right common carotid artery occlusion (CCAO) for 10 or 20 min. At 24 h, 2 days, and 7 days postischemia, we performed quantitative and qualitative locomotor analysis and correlated these results with the extent of ischemic lesions. Intermittent explosive hyperlocomotion was induced transiently in a 10-min CCAO group at 24 h after ischemia and continual unexplosive hyperlocomotion persisted for 7 days in the 20-min CCAO animals. Selective neuronal death, confined to the hippocampal cornu ammonis 1 (CA1), was observed in the 10-min CCAO group and widespread cortical and basal ganglia infarction was observed in the 20-min CCAO group. Amyloid precursor protein was transiently observed in the hippocampus at 24 h postischemia in the 10-min CCAO animals, while it was widely distributed over the ischemic regions throughout the 7 days postischemia in the 20-min CCAO animals. Incidence maps and correlation analysis revealed hippocampal neuronal death of the CA1 sector and widespread hemispheric infarction, including the cortex, as the region responsible for the 10-min and 20-min CCAO-induced hyperactivity, respectively. Two distinct types of locomotor hyperactivity were observed that varied with regard to the distribution of the ischemic lesion, that is, hippocampal neuronal death and widespread infarction involving the cortex. These two types of locomotor hyperactivity appear to be models of the different types of poststroke hyperactivity seen in stroke patients. [source] Irradiation attenuates neurogenesis and exacerbates ischemia-induced deficitsANNALS OF NEUROLOGY, Issue 3 2004Jacob Raber PhD Increased neurogenesis after cerebral ischemia suggests that functional recovery after stroke may be attributed, in part, to neural regeneration. In this study, we investigated the role of neurogenesis in the behavioral performance of gerbils after cerebral global ischemia. We used ionizing radiation to decrease neural regeneration, and 2 weeks later cerebral global ischemia was induced by bilateral common carotid artery occlusion. One month after the occlusion, the animals were behaviorally tested. Irradiation alone reduced neurogenesis but did not change vascular or dendritic morphology at the time of behavioral testing. Neither did irradiation, ischemia, or combined treatment impair rotor-rod performance or alter open-field activity. Gerbils subjected to both irradiation and ischemia demonstrated impaired performance in the water-maze task, compared with those that received only ischemia, radiation, or no treatment. These impairments after cerebral global ischemia under conditions of reduced neurogenesis support a role for the production of new cells in mediating functional recovery. [source] Stroke Induces Histamine Accumulation and Mast Cell Degranulation in the Neonatal Rat BrainBRAIN PATHOLOGY, Issue 1 2008V. Biran Inflammatory processes are a major cause of hypoxic-ischemic brain damage. The present study focuses on both the cerebral histamine system and mast cells in a model of transient focal ischemia induced by permanent left middle cerebral artery, and homolateral transient common carotid artery occlusion (50 minutes) in the P7 newborn rat. Immunohistochemical analysis revealed that ischemia induces histamine (HA) accumulation in the core of the infarct 6,12 h post-ischemia, and in the penumbra at 24,48 h, although in situ hybridization failed to detect any histidine decarboxylase gene transcripts in these regions. Immunohistochemical co-localization of HA with the MAP2 marker revealed that HA accumulates in neuronal cells before they degenerate, and is accompanied by a very significant increase in the number of mast cells at 12 h and 48 h of reperfusion. In mast cells, histamine immunoreactivity is detected at 2, 6 and 12 h after ischemia, whereas it disappears at 24 h, when a concomitant degranulation of mast cells is observed. Taken together, these data suggest that the recruitment of cerebral mast cells releasing histamine may contribute to ischemia-induced neuronal death in the immature brain. [source] | ||||||||||