Journal articles: 'Transient Ischemia'

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Briones, Tess L., and Barbara Therrien. "Behavioral Effects of Transient Cerebral Ischemia." Biological Research For Nursing 1, no. 4 (April 2000): 276–86. http://dx.doi.org/10.1177/109980040000100404.

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CA1 neurons in the hippocampus, a brain structure involved in learning and memory, are selectively vulnerable to ischemic effects. In this study, the authors examined if duration of ischemia is directly related to extent of CA1 damage and degree of spatial learning deficit. Adult female Wistar rats received either 5-min or 10-min ischemia or sham surgery. Following recovery, rats were tested in the Morris water maze. Histological analysis showed moderate cell loss in CA1 (31%) and CA3 (12%) and minimal cell loss in CA2 (4%) with 5-min ischemia. Increased cell loss was seen in CA1 (68%), CA2 (16%), and CA3 (23%) with 10-min ischemia. Behavioral testing revealed that animals with 10-min ischemia have greater spatial learning deficits and they remain impaired across the test days compared to the 5-min ischemic group. Furthermore, degree of CA1 cell loss accounted for approximately 45% of the variance in spatial learning deficits in the ischemic group. The authors conclude that cell loss is largely confined to CA1 region in rats who received 5 and 10 min of ischemia and that increased ischemic duration results in persistent learning deficits in female rats; also, the degree of behavioral impairment is related to extent of CA1 cell loss.

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Hong, Kyung Pyo, Soon Ok Park, Jung Sik Park, Chong Yun Rim, Young Bahk Koh, and Young Lee. "Transient Myocardial Ischemia in Ischemic Heart Disease." Korean Circulation Journal 18, no. 1 (1988): 31. http://dx.doi.org/10.4070/kcj.1988.18.1.31.

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Matias-Guiu, J., A. Davalos, and A. Codina. "Transient global ischemia." Stroke 16, no. 1 (January 1985): 132–33. http://dx.doi.org/10.1161/str.16.1.132b.

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Nedergaard, Maiken, and Anker Jon Hansen. "Characterization of Cortical Depolarizations Evoked in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (July 1993): 568–74. http://dx.doi.org/10.1038/jcbfm.1993.74.

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Cortical tissue surrounding acute ischemic infarcts undergoes repetitive spontaneous depolarizations. It is unknown whether these events are episodes of spreading depression (SD) elicited by the elevated interstitial K+ ([K+]e) in the ischemic core or whether they are evoked by transient decreases of the local blood flow. Electrophysiologically, depolarization caused by SD or by ischemia (ID) can be distinguished by their characteristic patterns of [K+]e rise: During SD, [K+]e rises abruptly, while in ID, this fast rate of increase is preceded by a slow rate lasting minutes. To characterize the depolarizations, we occluded the right middle cerebral artery (MCA) in rats and inserted two K+-sensitive microelectrodes into the cortex surrounding the evolving infarct. Repeated increases in [K+]e arose spontaneously following MCA occlusion. [K+]e increased during these transients from a resting level of 3–6 to 60 m M. One-third of these transient increases in [K+]e were biphasic, consisting of a slow initial increase to 10–12 m M, which lasted for minutes, followed by an abrupt increase, a pattern characteristic of ID. The remaining two-thirds exhibited a steep monotonic increase in [K+]e (>10 s), characteristic of SD. The duration of the transients was a function of the pattern of [K+]e increase: ID-like transients lasted an average 10.7 ±5.1 min, whereas the duration of SD-like transients was 5.7 ± 3.4 min. Both types of K+ transients occurred in an apparently random fashion in individual animals. A K+ transient was never observed solely at one electrode. In 40% of the cases, the K+ transients occurred simultaneously at the two electrode sites, and in the remaining a temporal separation of 20–420 s was observed. Our data suggest that the majority of the spontaneous depolarizations evoked by focal ischemia are SD-like phenomena probably evoked by the high values of [K+]e or glutamate in the ischemic focus, while the rest are elicited by independent foci of low blood flow within the ischemic border areas.

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Prabhakaran, Shyam. "Reversible brain ischemia: lessons from transient ischemic attack." Current Opinion in Neurology 20, no. 1 (February 2007): 65–70. http://dx.doi.org/10.1097/wco.0b013e328013f445.

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Nishijima, Yasuo, Kuniyasu Niizuma, Miki Fujimura, Yosuke Akamatsu, Hiroaki Shimizu, and Teiji Tominaga. "Consistent delayed unilateral neuronal death after modified transient focal cerebral ischemia in mice that mimics neuronal injury after transient global cerebral ischemia." Journal of Neurosurgery 123, no. 1 (July 2015): 243–53. http://dx.doi.org/10.3171/2014.9.jns14778.

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OBJECT Numerous studies have attempted to reveal the pathophysiology of ischemic neuronal injury using a representative transient global cerebral ischemia (tGCI) model in rodents; however, most of them have used gerbil or rat models. Recent advances in transgene and gene-knockout technology have enabled the precise molecular mechanisms of ischemic brain injury to be investigated. Because the predominant species for the study of genetic mutations is the mouse, a representative mouse model of tGCI is of particular importance. However, simple mouse models of tGCI are less reproducible; therefore, a more complex process or longer duration of ischemia, which causes a high mortality rate, has been used in previous tGCI models in mice. In this study, the authors aimed to overcome these problems and attempted to produce consistent unilateral delayed hippocampal CA1 neuronal death in mice. METHODS C57BL/6 mice were subjected to short-term unilateral cerebral ischemia using a 4-mm silicone-coated intraluminal suture to obstruct the origin of the posterior cerebral artery (PCA), and regional cerebral blood flow (rCBF) of the PCA territory was measured using laser speckle flowmetry. The mice were randomly assigned to groups of different ischemic durations and histologically evaluated at different time points after ischemia. The survival rate and neurological score of the group that experienced 15 minutes of ischemia were also evaluated. RESULTS Consistent neuronal death was observed in the medial CA1 subregion 4 days after 15 minutes of ischemia in the group of mice with a reduction in rCBF of < 65% in the PCA territory during ischemia. Morphologically degenerated cells were mostly positive for terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling and cleaved caspase 3 staining 4 days after ischemia. The survival rates of the mice 24 hours (n = 24), 4 days (n = 15), and 7 days (n = 7) after being subjected to 15 minutes of ischemia were 95.8%, 100%, and 100%, respectively, and the mice had slight motor deficits. CONCLUSIONS The authors established a model of delayed unilateral hippocampal neuronal death in C57BL/6 mice by inducing ischemia in the PCA territory using an intraluminal suture method and established inclusion criteria for PCAterritory rCBF monitored by laser speckle flowmetry. This model may be useful for investigating the precise molecular mechanisms of ischemic brain injury.

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Yang, Wei, Huaxin Sheng, David S. Warner, and Wulf Paschen. "Transient Global Cerebral Ischemia Induces a Massive Increase in Protein Sumoylation." Journal of Cerebral Blood Flow & Metabolism 28, no. 2 (June 13, 2007): 269–79. http://dx.doi.org/10.1038/sj.jcbfm.9600523.

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A new group of proteins, small ubiquitin-like modifier (SUMO) proteins, has recently been identified and protein sumoylation has been shown to play a major role in various signal transduction pathways. Here, we report that transient global cerebral ischemia induces a marked increase in protein sumoylation. Mice were subjected to 10 mins severe forebrain ischemia followed by 3 or 6 h of reperfusion. Transient cerebral ischemia induced a massive increase in protein sumoylation by SUMO2/3 both in the hippocampus and cerebral cortex. SUMO2/3 conjugation was associated with a decrease in levels of free SUMO2/3. After ischemia, protein levels of the SUMO-conjugating enzyme Ubc9 were transiently decreased in the cortex but not in the hippocampus. We also exposed HT22 cells to arsenite, a respiratory poison that impairs cytoplasmic function and induces oxidative stress. Arsenite exposure induced a marked rise in protein sumoylation, implying that impairment of cytoplasmic function and oxidative stress may be involved in the massive post-ischemic activation of SUMO conjugation described here. Sumoylation of transcription factors has been shown to block their activation, with some exceptions such as the heat-shock factor and the hypoxia-responsive factor, where sumoylation blocks their degradation, and the nuclear factor-κB (NF-κB) essential modulator where sumoylation leads to an activation of NF-κB. Because protein sumoylation is known to be involved in the regulation of various biologic processes, the massive post-ischemic increase in protein sumoylation may play a critical role in defining the final outcome of neurons exposed to transient ischemia.

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Ok, Engin, Zeki Yilmaz, Erhan Akgün, Erdoğan M. Sözüer, Yaşar Yeşilkaya, and Figen Öztürk. "Development of Collaterals in Intermittent and Permanent Ischemia of the Liver." HPB Surgery 10, no. 1 (January 1, 1996): 35–40. http://dx.doi.org/10.1155/1996/94108.

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The ischemia caused by hepatic dearterialization as therapy for hepatic malignancies is transient because of the rapid formation of collaterals. In order to prevent this transient repeated ischemia has been suggested.An experimental study was planned to compare the collateral occurrence in persistent ischemia and transient repeated ischeamia of the liver. Fourteen dogs (seven persistent ischemia, seven transient repeated ischemia) were used in this study. Hepatic dearterialization were performed in both groups. In the first group (persistent ischemia), the hepatic artery was ligated proximal to the gastroduodenal artery. In the second group (transient repeated ischemia), the hepatic artery was occluded externally in the same region as the first group by means of a device modified from 8 guage Foley catheter and after occlusion for one hour it was reopened. Occlusions were repeated twice in a day. Five dogs in the first group and six dogs in the second group completed a three weeks ischemia period and angiography were then performed in all. The dogs were sacrificed after the angiography and examined for possible abscess formation, arterial thrombosis, peritoneal adhesions and liver necrosis. After angiography, the two groups were also examined for collateral occurrence. Only one collateral occurred in the transient repeated ischemia group, but in the persistent ischemia group, collaterals occurred in all dogs. This difference between two groups is statistically significant (Fischer Absolute Chi Square Test, p=0.013).Transient repeated ischemia is superior to persistent ischemia because of fewer collaterals, but in practise, total dearterialization of the liver is impossible.

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Pang, Jinming, Toshifumi Itano, Kazunori Sumitani, Tetsuro Negi, and Osamu Miyamoto. "Electroacupuncture Attenuates Both Glutamate Release and Hyperemia After Transient Ischemia in Gerbils." American Journal of Chinese Medicine 31, no. 02 (January 2003): 295–303. http://dx.doi.org/10.1142/s0192415x03000977.

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Although many studies have indicated that electroacupuncture (EA) provides a neuroprotective effect against ischemic brain damage, the protective mechanism is not fully understood. Glutamate release and hippocampal blood flow in ischemia with EA were investigated to elucidate the neuroprotective mechanism of EA. Transient 5-minute ischemia was induced in gerbils. EA (7 Hz, 6 mA, for 30 minutes) delivered to the points called Fengfu (GV16) and Shendao (GV11) was administered pre-, intra- or post-ischemia. The procedure rescued hippocampal neurons from ischemic insult and significantly attenuated both ischemia-induced glutamate release and transient increase of cerebral blood flow (CBF) during reperfusion (hyperemia). Hyperemia as well as excessive glutamate after ischemia are regarded as important factors in brain damage as they lead to reperfusion injury. These results suggest that EA protects neurons by suppressing both glutamate release and reperfusion injury after ischemia.

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Lin, Baowan, Myron D. Ginsberg, Raul Busto, and Lin Li. "Hyperglycemic Transient Ischemia Induces Massive Neutrophil Deposition in Brain." Stroke 32, suppl_1 (January 2001): 353. http://dx.doi.org/10.1161/str.32.suppl_1.353-c.

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P80 Acute hyperglycemia worsens neurological signs and accentuates neuropathology after ischemia, but the mechanisms are poorly understood. In this study, we tested whether polymorphonuclear leukocytes (neutrophils) might be contributory. Anesthetized, physiologically monitored Wistar rats underwent global forebrain ischemia for 12.5 min by bilateral carotid artery occlusions plus hypotension (45 mm Hg). To induce hyperglycemia, rats received 2.5 ml of 25% dextrose i.p. 30 min prior to ischemia. Normoglycemic rats received saline. Plasma glucose levels were 340±66 and 133 ±21 mg/dl, respectively (mean±SD). Animals were sacrificed at either 24 h or 3 days by perfusion-fixation with FAM. Brain sections were reacted for the immunohistochemical visualization of myeloperoxidase (MPO), a specific and quantitative marker of neutrophil activity in the brain. In sham rats and in normoglycemic-ischemic animals, almost no MPO-positive cells were identified. In marked contrast, brains of hyperglycemic-ischemic rats studied at 24 h contained dramatic accumulations of MPO-positive cells within pial and parenchymal blood vessels as well as within cortical and subcortical parenchyma. MPO-positivity was most robust in areas of severe injury (on H&E sections), but MPO cells were also observed in areas without overt injury. Intravascular MPO-positive cells commonly obstructed the vascular lumen. Following 3-d survival, MPO-positivity of hyperglycemic-ischemic brains had significantly decreased. In hyperglycemic brains studied at 24 h, median numbers of MPO-positive cells were increased by 130-fold in cortex and 110-fold in striatum above values in normoglycemic-ischemic rats. In summary, this study shows that preischemic hyperglycemia triggers the early and dramatic deposition of polymorphonuclear leukocytes in the postischemic brain, with neutrophil adherence to cerebral blood vessels and their migration into brain parenchyma following brief forebrain ischemia. These events may contribute to the enhanced tissue destruction, extension of infarction, and BBB disruption observed in hyperglycemic ischemia. Supported by NIH Grant NS05820.

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De Simoni, M. G., C. Storini, M. Barba, L. Catapano, A. M. Arabia, E. Rossi, and L. Bergamaschini. "Neuroprotection by Complement (C1) Inhibitor in Mouse Transient Brain Ischemia." Journal of Cerebral Blood Flow & Metabolism 23, no. 2 (February 2003): 232–39. http://dx.doi.org/10.1097/01.wcb.0000046146.31247.a1.

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The authors investigated the effect of the C1 inhibitor (C1-INH), the only known inhibitor of complement C1, in a murine model of transient focal ischemia. Ischemia was induced by intraluminal occlusion of the middle cerebral artery. After 2 hours, reperfusion was produced by removing the nylon monofilament occluding the artery. The effect of 15 U C1-INH (intravenously) was evaluated in terms of general and focal neurologic deficits, ischemic volume, neutral red staining (to identify the brain areas subject to ischemic damage), and glial fibrillary acidic protein immunoreactivity (to show astrocytic response). Forty-eight hours after ischemia, C1-INH significantly improved general and focal deficits by 36% and 54%, respectively, and significantly reduced infarct volume (CI-INH, 6.69% ± 2.93%; saline, 24.24% ± 8.24%) of total brain. Neutral red staining further showed the strong protective effect of C1-INH in cortex, hippocampus, and striatum. Astrocyte activation induced by ischemia was not affected by C1-INH. These findings show that C1-INH displayed a potent neuroprotective action by effectively reducing ischemia—reperfusion injury.

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Saxena, Pankaj, Arul Bala, Kym Campbell, Bruno Meloni, Yves d'Udekem, and Igor E. Konstantinov. "Does remote ischemic preconditioning prevent delayed hippocampal neuronal death following transient global cerebral ischemia in rats?" Perfusion 24, no. 3 (May 2009): 207–11. http://dx.doi.org/10.1177/0267659109346902.

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Objective: To determine if remote ischemic preconditioning (RIPC) induced by transient limb ischemia is protective against delayed hippocampal neuronal death in rats undergoing transient global cerebral ischemia (GCI). Method: Animals were randomized into 3 groups: Group I (Control, n = 5) underwent sham procedure, namely, general anesthesia x 2, without cerebral ischemia; Group II (RIPC + GCI, n = 5) was subjected to RIPC, induced by transient left hind limb ischemia under general anesthesia prior to GCI; Group III (GCI only, n = 5) underwent sham procedure under general anesthesia prior to GCI. Twenty-four hours after the RIPC or sham procedure, a transient GCI was induced for 8 minutes in Groups II and III by means of bilateral common carotid artery occlusion and hypotension. Hippocampal CA1 neurons were histologically examined at 7 days after ischemia. Results: There was no significant difference between the RIPC group and the ischemia only group. The number of neurons in the RIPC group were 0.90 (95% CI 0.20, 4.08) times the number in the ischemia group (p=0.89). The number of neurons in the RIPC group were 0.03 (95% CI 0.01, 0.10) times the number in the Control group (p=0.0001). Conclusion: Second window of the RIPC does not prevent hippocampal CA1 neuronal death at 7 days after transient global cerebral ischemia.

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Zhang, Yuchun, Ping Deng, Yan Li, and Zao C. Xu. "Enhancement of Excitatory Synaptic Transmission in Spiny Neurons After Transient Forebrain Ischemia." Journal of Neurophysiology 95, no. 3 (March 2006): 1537–44. http://dx.doi.org/10.1152/jn.01166.2005.

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Spiny neurons in the neostriatum are highly vulnerable to ischemia. Enhancement of excitatory synaptic transmissions has been implicated in ischemia-induced excitotoxic neuronal death. Here we report that evoked excitatory postsynaptic currents in spiny neurons were potentiated after transient forebrain ischemia. The ischemia-induced potentiation in synaptic efficacy was associated with an enhancement of presynaptic release as demonstrated by an increase in the frequency of miniature excitatory postsynaptic currents (mEPSCs) and a decrease in the paired-pulse ratio. The amplitude of inward currents evoked by exogenous application of glutamate did not show significant changes after ischemia, suggesting that postsynaptic mechanism is not involved. The ischemia-induced increase in mEPSCs frequency was not affected by blockade of voltage-gated calcium channels, but it was eliminated in the absence of extracellular calcium. Bath application of ATP P2X receptor antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS) significantly reduced mEPSC frequency in ischemic neurons but had no effects on the control ones. Furthermore, the inhibitory effect of PPADS on ischemic neurons was abolished in Ca2+-free external solution. These results indicate that excitatory synaptic transmissions in spiny neurons are potentiated after ischemia via presynaptic mechanisms. Activation of P2X receptors and the consequent Ca2+ influx might contribute to the ischemia-induced facilitation of glutamate release.

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Liu, C., S. Chen, F. Kamme, and B. R. Hu. "Ischemic preconditioning prevents protein aggregation after transient cerebral ischemia." Neuroscience 134, no. 1 (January 2005): 69–80. http://dx.doi.org/10.1016/j.neuroscience.2005.03.036.

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Kharbanda, R. K., U. M. Mortensen, P. A. White, S. B. Kristiansen, M. R. Schmidt, J. A. Hoschtitzky, M. Vogel, K. Sorensen, A. N. Redington, and R. MacAllister. "Transient Limb Ischemia Induces Remote Ischemic Preconditioning In Vivo." Circulation 106, no. 23 (December 3, 2002): 2881–83. http://dx.doi.org/10.1161/01.cir.0000043806.51912.9b.

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Handayani, Ety Sari, Rina Susilowati, Ismail Setyopranoto, and Ginus Partadiredja. "Transient Bilateral Common Carotid Artery Occlusion (tBCCAO) of Rats as a Model of Global Cerebral Ischemia." Bangladesh Journal of Medical Science 18, no. 3 (May 30, 2019): 491–500. http://dx.doi.org/10.3329/bjms.v18i3.41616.

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Background: Transient bilateral common carotid artery occlusion (tBCCAO) has been performed in rats as a model of global ischemia. However, the technique varied between laboratories and produced difficulties in the comparison of results. Variations such as rat strain, age, ischemic and reperfusion duration could affect the results. This review aims to provide a general overview of the variation of animal strains, duration of tBCCAO, reported cerebral ischemic area produced by tBCCAO, use of TTC staining for measurement of volume of brain ischemia and functional neurological tests. Method: The data of this review were obtained from abstracts in PubMed database and Google Scholars and were not limited by publication time. Keywords used to search the abstracts were (BCCAO OR “bilateral common carotid artery occlusion” OR “stroke” OR “cerebral ischemia” OR “brain ischemia”) AND (rat OR rats). The research method of each study was identified from the collected abstracts. The abstracts were chosen for further study on the basis that they met the inclusion criteria which were English language articles; original research article; animal model used were adolescent, adult, and elderly rats; ischemic finding in rats’ cerebrum by BCCAO technique was presented; ischemic size were assessed and the result was described; studies that had control group; and studies that induced transient global ischemic to the rats’ cerebrum. Data that were extracted to the datasheet were references; animal model strain; ischemic duration; reperfusion duration; ischemic area; 2,3,5 Triphenyltetrazolium Chloride (TTC) staining; Cavalieri method; and rats’ neurological functional tests. Results and Conclusions: There were differences in the ischemic area between Wistar and Sprague-Dawley rats after transient BCCAO. There were differences in the TTC staining solution concentration that was used to identify ischemic area of the brain following transient BCCAO. There was a very limited number of studies using Cavalieri method for the quantification of ischemic volume of rats’ brain after transient BCCAO. Neurological functional tests in animal models post transient BCCAO did not include sensory and memory functions tests. Bangladesh Journal of Medical Science Vol.18(3) 2019 p.491-500

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Zhan, Xinhua, Bradley P. Ander, Glen Jickling, Renée Turner, Boryana Stamova, Huichun Xu, Dazhi Liu, Ryan R. Davis, and Frank R. Sharp. "Brief Focal Cerebral Ischemia That Simulates Transient Ischemic Attacks in Humans Regulates Gene Expression in Rat Peripheral Blood." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (September 9, 2009): 110–18. http://dx.doi.org/10.1038/jcbfm.2009.189.

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Blood gene expression profiles of very brief (5 and 10 mins) focal ischemia that simulates transient ischemic attacks in humans were compared with ischemic stroke (120 mins focal ischemia), sham, and naïve controls. The number of significantly regulated genes after 5 and 10 mins of cerebral ischemia was 39 and 160, respectively (fold change ⩾∣1.5∣ and P<0.05). There were 103 genes common to brief focal ischemia and ischemic stroke. Ingenuity pathway analysis showed that genes regulated in the 5 mins group were mainly involved in small molecule biochemistry. Genes regulated in the 10 mins group were involved in cell death, development, growth, and proliferation. Such genes were also regulated in the ischemic stroke group. Genes common to ischemia were involved in the inflammatory response, immune response, and cell death—indicating that these pathways are a feature of focal ischemia, regardless of the duration. These results provide evidence that brief focal ischemia differentially regulates gene expression in the peripheral blood in a manner that could distinguish brief focal ischemia from ischemic stroke and controls in rats. We postulate that this will also occur in humans.

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Antonawich, Francis J., Stanislaw Krajewski, John C. Reed, and James N. Davis. "Bcl-x1 Bax Interaction after Transient Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 18, no. 8 (August 1998): 882–86. http://dx.doi.org/10.1097/00004647-199808000-00008.

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Five minutes of bilateral common carotid artery occlusion in the Mongolian gerbil results in a selective, delayed death of CA1 pyramidal neurons. Although Bcl-2 appears to protect a variety of cells from cell death, the precise role of this apoptosis-regulating protein is complicated. We used immunoblots to estimate levels of Bcl-2, Bcl-xl, and Bax at various times after carotid occlusion. Rather than Bcl-2, Bcl-xl appears to be the predominant neuroprotective form of this family of proto-oncogenes in the gerbil hippocampus. After transient ischemia, Bcl-2 and Bcl-xl protein levels remained the same. However, Bax levels were dramatically increased at 6 hours after ischemia, compared with sham-operated animals, and were still elevated at 72 hours after ischemia. To monitor dimerization interactions among theses apoptosis-regulating molecules, immunoprecipitation studies were conducted. These studies demonstrated that Bcl-xl association with Bax increases after ischemia. Therefore, Bax may disrupt the more favorable Bcl-xl (Bcl-2) interactions necessary for normal neuronal functioning and thus promote transient ischemic death.

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Yanaka, Kiyoyuki, Paul J. Camarata, Stephen R. Spellman, James B. McCarthy, Leo T. Furcht, Walter C. Low, and Roberto C. Heros. "Synthetic fibronectin peptides and ischemic brain injury after transient middle cerebral artery occlusion in rats." Journal of Neurosurgery 85, no. 1 (July 1996): 125–30. http://dx.doi.org/10.3171/jns.1996.85.1.0125.

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✓ Leukocytes play an important role in the development of ischemia—reperfusion injury. This study was conducted to ascertain whether synthetic peptides corresponding to the cell- and heparin-binding sequences of fibronectin that disturb leukocyte adhesion molecules were effective in neuronal protection after transient focal cerebral ischemia in rats. The authors evaluated the efficacy of peptides on infarction size, leukocyte infiltration in the ischemic tissue, and neurological outcome in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. Twenty-one animals were divided into three groups: transient ischemia without treatment (Group I), transient ischemia with administration of vehicle (Group II), and transient ischemia with administration of fibronectin peptides (Group III). The mean myeloperoxidase activity (U/g wet wt) in the ischemic area was as follows: Group I, 0.19% ± 0.05; Group II, 0.21% ± 0.03; and Group III, 0.08% ± 0.02. The mean size of the infarction as a percentage of the total hemispheric volume was as follows: Group I, 38.35% ± 1.34%; Group II, 39.21% ± 2.42%; and Group III, 25.81% ± 4.87%. Group III showed a significant decrease in myeloperoxidase activity in the lesion and the infarction size was smaller when compared to Groups I and II (p < 0.05). The neurological grade in Group III was significantly better than in Groups I and II at 48 hours after reperfusion (p < 0.01). This study is the first to explore the therapeutic potential of synthetic fibronectin peptides in brain protection after transient focal ischemia, and the results also serve as a basis for studies of important cellular and molecular events that contribute to tissue damage.

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Fujimura, Miki, Yuiko Morita-Fujimura, Kensuke Murakami, Makoto Kawase, and Pak H. Chan. "Cytosolic Redistribution of Cytochrome C after Transient Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 18, no. 11 (November 1998): 1239–47. http://dx.doi.org/10.1097/00004647-199811000-00010.

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Recent in vitro cell-free studies have shown that cytochrome c release from mitochondria is a critical step in the apoptotic process. The present study examined the expression of cytochrome c protein after transient focal cerebral ischemia in rats, in which apoptosis was assumed to contribute to the expansion of the ischemic lesion. In situ labeling of DNA breaks in frozen sections after 90 minutes of middle cerebral artery (MCA) occlusion showed a significant number of striatal and cortical neurons, which were maximized at 24 hours after ischemia, exhibiting chromatin condensation, nuclear segmentation, and apoptotic bodies. Cytosolic localization of cytochrome c was detected immunohistochemically in the ischemic area as early as 4 hours after 90 minutes of MCA occlusion. Western blot analysis of the cytosolic fraction revealed a strong single 15-kDa band, characteristic of cytochrome c, only in the samples from the ischemic hemisphere. Western blot analysis of the mitochondrial fraction showed a significant amount of mitochondrial cytochrome c in nonischemic brain, which was decreased in ischemic brain 24 hours after ischemia. These results provide the first evidence that cytochrome c is being released from mitochondria to the cytosol after transient focal ischemia. Although further evaluation is necessary to elucidate its correlation with DNA fragmentation, our results suggest the possibility that cytochrome c release may play a role in DNA-damaged neuronal cell death after transient focal cerebral ischemia in rats.

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Seyfarth, Melchior, Gert Richardt, Anna Mizsnyak, Thomas Kurz, and Albert Schömig. "Transient Ischemia Reduces Norepinephrine Release During Sustained Ischemia." Circulation Research 78, no. 4 (April 1996): 573–80. http://dx.doi.org/10.1161/01.res.78.4.573.

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Li, Zhen, Shengzhong Cui, Zhuo Zhang, Rong Zhou, Yingbin Ge, Masahiro Sokabe, and Ling Chen. "DHEA-Neuroprotection and -Neurotoxicity after Transient Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 29, no. 2 (October 15, 2008): 287–96. http://dx.doi.org/10.1038/jcbfm.2008.118.

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Dehydroepiandrosterone (DHEA) has been implicated not only to prevent N-methyl-d-aspartate (NMDA)-induced neurotoxicity but also to enhance Ca2+ influx through NMDA receptor (NMDAr). However, these DHEA effects, which would produce inconsistent outcomes about neuronal damages, are not well studied in ischemia-induced cerebral damages. Herein, we report that a single administration of DHEA (20 mg/kg) during 3 to 48 h after transient global cerebral ischemia in rats exerted neuroprotective effects such as reduction of ischemia-induced neuronal death in the hippocampal CA1 and improvement of ischemia-induced deficits in spatial learning. By contrast, at 1 h before or after ischemia, the administration of DHEA exacerbated the ischemia-induced neuronal death and learning impairment. This DHEA neurotoxicity appeared to be caused by DHEA itself, but not through its metabolite testosterone, and was inhibited by a pretreatment with the NMDAr blocker MK801 or the sigma-1 (σ1) receptor antagonist NE100. However, the DHEA neuroprotection was blocked by NE100. These results show that DHEA not only provides robust ischemic neuroprotection with a long therapeutic opportunity but also exerts neurotoxicity when administered during ischemia and early reperfusion, which points to the importance of administration timing of DHEA in the clinical treatment of brain damages by the transient brain ischemia including stroke.

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Parker, Kevin Kit, James A. Lavelle, L. Katherine Taylor, Zifa Wang, and David E. Hansen. "Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion." Journal of Applied Physiology 97, no. 1 (July 2004): 377–83. http://dx.doi.org/10.1152/japplphysiol.01235.2001.

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Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteration of the action potential waveform, and stretch-induced arrhythmia (SIA). We demonstrate that regional ventricular ischemia due to coronary artery occlusion increases arrhythmogenic effects of transient diastolic stretch, whereas globally ischemic hearts showed no such increase. We tested our hypothesis that, during phase Ia ischemia, regionally ischemic hearts may be more susceptible to triggered arrhythmogenesis due to transient diastolic stretch. During the first 20 min of regional ischemia, the probability of eliciting a ventricular SIA ( PSIA) by transient diastolic stretch increased significantly. However, after 30 min, PSIA decreased to a value comparable with baseline measurements, as expected during phase Ib, where most ventricular arrhythmias are of reentrant mechanisms. We also suggest that mechanoelectrical coupling may contribute to the nonreentrant mechanisms underlying reperfusion-induced arrhythmia. When coronary artery occlusion was relieved after 30 min of ischemia, we observed an increase in PSIA and the maintenance of this elevated level throughout 20 min of reperfusion. We conclude that mechanoelectrical coupling may underlie triggered arrhythmogenesis during phase 1a ischemia and reperfusion.

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Fujimura, Miki, Yuiko Morita-Fujimura, Makoto Kawase, and Pak H. Chan. "Early Decrease of Apurinic/Apyrimidinic Endonuclease Expression after Transient Focal Cerebral Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 19, no. 5 (May 1999): 495–501. http://dx.doi.org/10.1097/00004647-199905000-00003.

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The authors examined the protein expression of apurinic/apyrimidinic endonuclease (APE/Ref-1), a multifunctional protein in the DNA base excision repair pathway, before and after transient focal ischemia in mice. Immunohistochemistry showed the nuclear expression of APE/Ref-1 in the entire region of the control brains. Nuclear immunoreactivity was decreased as early as 5 minutes after 60 minutes of ischemia in the ischemic core, which was followed by a significant reduction of APE/Ref-1-positive cells in the entire middle cerebral artery territory, Western blot analysis of the sample from the nonischemic brain showed a characteristic 37-kDa band, which was reduced after ischemia. A significant amount of DNA fragmentation was observed at 24 hours, but not at 4 hours, after ischemia. The authors' data provide the first evidence that APE/Ref-1 rapidly decreases after transient focal ischemia, and that this reduction precedes the peak of DNA fragmentation in the brain regions that are destined to show necrosis and apoptosis. Although further examination is necessary to elucidate the direct relationship between the APE/Ref-1 decrease and ischemic necrosis and apoptosis, our results suggest the possibility that rapid decrease of APE/Ref-1 and the failure of the DNA repair mechanism may contribute to necrosis or apoptosis after transient focal ischemia.

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Ahn, Ji Hyeon, Bich Na Shin, Joon Ha Park, Tae-Kyeong Lee, Young Eun Park, Jae-Chul Lee, Go Eun Yang, et al. "Pre- and Post-Treatment with Novel Antiepileptic Drug Oxcarbazepine Exerts Neuroprotective Effect in the Hippocampus in a Gerbil Model of Transient Global Cerebral Ischemia." Brain Sciences 9, no. 10 (October 17, 2019): 279. http://dx.doi.org/10.3390/brainsci9100279.

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Oxcarbazepine, an antiepileptic drug, has been reported to modulate voltage-dependent sodium channels, and it is commonly used in epilepsy treatment. In this study, we investigated the neuroprotective effect of oxcarbazepine in the hippocampus after transient ischemia in gerbils. Gerbils randomly received oxcarbazepine 100 or 200 mg/kg before and after transient ischemia. We examined its neuroprotective effect in the cornu ammonis 1 subfield of the gerbil hippocampus at 5 days after transient ischemia by using cresyl violet staining, neuronal nuclei immunohistochemistry and Fluoro-Jade B histofluorescence staining for neuroprotection, and by using glial fibrillary protein and ionized calcium-binding adapter molecule 1 immunohistochemistry for reaction of astrocytes and microglia, respectively. Pre- and post-treatment with 200 mg/kg of oxcarbazepine, but not 100 mg/kg of oxcarbazepine, protected pyramidal neurons of the cornu ammonis 1 subfield from transient ischemic damage. In addition, pre- and post-treatment with oxcarbazepine (200 mg/kg) significantly ameliorated astrocytes and microglia activation in the ischemic cornu ammonis 1 subfield. In brief, our current results indicate that post-treatment as well as pre-treatment with 200 mg/kg of oxcarbazepine can protect neurons from ischemic insults via attenuation of the glia reaction.

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Gao, T. M., E. M. Howard, and Z. C. Xu. "Transient Neurophysiological Changes in CA3 Neurons and Dentate Granule Cells After Severe Forebrain Ischemia In Vivo." Journal of Neurophysiology 80, no. 6 (December 1, 1998): 2860–69. http://dx.doi.org/10.1152/jn.1998.80.6.2860.

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Gao, T. M., E. M. Howard, and Z. C. Xu. Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo. J. Neurophysiol. 80: 2860–2869, 1998. The spontaneous activities, evoked synaptic responses, and membrane properties of CA3 pyramidal neurons and dentate granule cells in rat hippocampus were compared before ischemia and ≤7 days after reperfusion with intracellular recording and staining techniques in vivo. A four-vessel occlusion method was used to induce ∼14 min of ischemic depolarization. No significant change in spontaneous firing rate was observed in both cell types after reperfusion. The amplitude and slope of excitatory postsynaptic potentials (EPSPs) in CA3 neurons decreased to 50% of control values during the first 12 h reperfusion and returned to preischemic levels 24 h after reperfusion. The amplitude and slope of EPSPs in granule cells slightly decreased 24–36 h after reperfusion. The amplitude of inhibitory postsynaptic potentials in CA3 neurons transiently increased 24 h after reperfusion, whereas that in granule cells showed a transient decrease 24–36 h after reperfusion. The duration of spike width of CA3 and granule cells became longer than that of control values during the first 12 h reperfusion. The spike threshold of both cell types significantly increased 24–36 h after reperfusion, whereas the frequency of repetitive firing evoked by depolarizing current pulse was decreased during this period. No significant change in rheobase and input resistance was observed in CA3 neurons. A transient increase in rheobase and a transient decrease in input resistance were detected in granule cells 24–36 h after reperfusion. The amplitude of fast afterhyperpolarization in both cell types increased for 2 days after ischemia and returned to normal values 7 days after reperfusion. The results from this study indicate that the neuronal excitability and synaptic transmission in CA3 and granule cells are transiently suppressed after severe forebrain ischemia. The depression of synaptic transmission and neuronal excitability may provide protection for neurons after ischemic insult.

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Booker, Kathy J., Karyn Holm, Barbara J. Drew, Dorothy M. Lanuza, Frank D. Hicks, Tim Carrigan, Michelle Wright, and John Moran. "Frequency and Outcomes of Transient Myocardial Ischemia in Critically Ill Adults Admitted for Noncardiac Conditions." American Journal of Critical Care 12, no. 6 (November 1, 2003): 508–17. http://dx.doi.org/10.4037/ajcc2003.12.6.508.

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• Background Critically ill adults admitted for noncardiac conditions are at risk for acute myocardial ischemia.• Objectives To detect myocardial ischemia and injury in patients admitted for noncardiac conditions and to examine the relationship of myocardial ischemia, injury, and acuity to cardiac events.• Methods Transient myocardial ischemia, acuity, elevations in serum troponin I, and in-hospital cardiac events were examined in 76 consecutive patients. Transient myocardial ischemia, determined by using continuous electrocardiography, was defined as a 1-mm (0.1-mV) change in ST level from baseline to event in 1 or more leads lasting 1 or more minutes. Acuity was determined by scores on Acute Physiology and Chronic Health Evaluation II.• Results A total of 37 ischemic events were detected in 8 patients (10.5%); 32 (86%) were ST-segment depressions, and 35 (96%) were silent. Twelve patients (15.8%) had elevated levels of troponin I. Transient myocardial ischemia, elevated troponin I levels, and advanced age were significant predictors of cardiac complications (R2 = 0.387, F = 15.2, P < .001). Acuity correlated only modestly with increased length of stay in the intensive care unit (r = 0.26, P = .02) and elevated troponin I levels (r = 0.25, P = .03). Patients with transient myocardial ischemia had significantly higher rates of elevations in troponin I (P < .001) and cardiac events (P < .001) than did patients without.• Conclusions Transient myocardial ischemia and advanced age are predictors of cardiac events and may indicate patients at risk for cardiac events.

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Shimizu, Shigetoshi, Tetsuya Nagayama, Kun Lin Jin, Li Zhu, J. Eric Loeffert, Simon C. Watkins, Steven H. Graham, and Roger P. Simon. "bcl-2 Antisense Treatment Prevents Induction of Tolerance to Focal Ischemia in the Rat Brain." Journal of Cerebral Blood Flow & Metabolism 21, no. 3 (March 2001): 233–43. http://dx.doi.org/10.1097/00004647-200103000-00007.

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In the rat, 60 minutes of transient ischemia to the middle cerebral artery results in infarction of the caudate putamen. Ischemic preconditioning with 20 minutes of transient focal ischemia produced tolerance (attenuated infarction volume) to 60 minutes of subsequent focal ischemia administered three days, five days, or seven days later. Western blots from tolerant caudate putamen demonstrated increased bcl-2 expression, maximum at 3 days and persisting through 7 days. Immunocytochemical examination found that bcl-2 was expressed in cells with both neuronal and nonneuronal morphology in striatum after preconditioning ischemia. bcl-2 antisense oligodeoxynucleotides (ODNs), bcl-2 sense ODNs, or artificial cerebrospinal fluid (CSF, vehicle) was infused into the lateral ventricle for the 72 hours between the 20-minute ischemic preconditioning and the 60-minute period of ischemia. Antisense ODN treatment reduced expression of bcl-2 in the striatum and blocked the induction of tolerance by preconditioning ischemia. Sense and CSF treatments had no effect on either bcl-2 expression or tolerance. In this model of induced tolerance to focal ischemia, bcl-2 appears to be a major determinant.

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Takizawa, Shunya, Matthew J. Hogan, Alastair M. Buchan, and Antoine M. Hakim. "In vivo Binding of [3H]Nimodipine in Rat Brain after Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 14, no. 3 (May 1994): 397–405. http://dx.doi.org/10.1038/jcbfm.1994.51.

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We report the regional variation in relative in vivo binding of the l-type voltage sensitive calcium channel (VSCC) antagonist [3H]nimodipine to brain following transient forebrain ischemia in the rat. At 30-min of reperfusion after 20 min of forebrain ischemia, [3H]nimodipine binding was significantly increased in striatum, CA3 and CA4, and dentate relative to binding in sham-operated rats, suggesting that VSCCs were responding to ischemic depolarization. Two h following ischemia, binding in all brain structures returned to normal levels indicating repolarization of cell membranes. At 24 h of recirculation, increased [3H]nimodipine binding was again observed in striatum and dentate. Binding remained elevated in the striatum and dentate, and increased binding became evident in the CA1 region of the hippocampus after 48 h of reperfusion. With the exception of the dentate gyrus, the second rise in [3H]nimodipine binding anticipated or coincided with the observed regional ischemic cell changes. These observations in global cerebral ischemia support previous work indicating that in vivo binding of [3H]nimodipine to the l-type VSCC may be an early and sensitive indicator of impending ischemic injury. Such measurements may be of use in identifying vulnerable brain regions and defining a therapeutic window of opportunity in models of cerebral ischemia.

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Zhao, Heng, Midori A. Yenari, Danye Cheng, Robert M. Sapolsky, and Gary K. Steinberg. "Biphasic Cytochrome c Release After Transient Global Ischemia and its Inhibition by Hypothermia." Journal of Cerebral Blood Flow & Metabolism 25, no. 9 (March 23, 2005): 1119–29. http://dx.doi.org/10.1038/sj.jcbfm.9600111.

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Hypothermia is effective in preventing ischemic damage. A caspase-dependent apoptotic pathway is involved in ischemic damage, but how hypothermia inhibits this pathway after global cerebral ischemia has not been well explored. It was determined whether hypothermia protects the brain by altering cytochrome c release and caspase activity. Cerebral ischemia was produced by two-vessel occlusion plus hypotension for 10 mins. Body temperature in hypothermic animals was reduced to 33°C before ischemia onset and maintained for 3 h after reperfusion. Western blots of subcellular fractions revealed biphasic cytosolic cytochrome c release, with an initial peak at about 5 h after ischemia, which decreased at 12 to 24 h, and a second, larger peak at 48 h. Caspase-3 and −9 activity increased at 12 and 24 h. A caspase inhibitor, Z-DEVD-FMK, administered 5 and 24 h after ischemia onset, protected hippocampal CA1 neurons from injury and blocked the second cytochrome c peak, suggesting that caspases mediate this second phase. Hypothermia (33°C), which prevented CA1 injury, did not inhibit cytochrome c release at 5 h, but reduced cytochrome c release at 48 h. Caspase-3 and −9 activity was markedly attenuated by hypothermia at 12 and 24 h. Thus, biphasic cytochrome c release occurs after transient global ischemia and mild hypothermia protects against ischemic damage by blocking the second phase of cytochrome c release, possibly by blocking caspase activity.

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Yagita, Yoshiki, Kazuo Kitagawa, Toshiho Ohtsuki, Shigeru Tanaka, Masatsugu Hori, and Masayasu Matsumoto. "Induction of the HSP110/105 Family in the Rat Hippocampus in Cerebral Ischemia and Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 21, no. 7 (July 2001): 811–19. http://dx.doi.org/10.1097/00004647-200107000-00006.

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Recently, the authors isolated a novel gene of the HSP110 family, ischemia responsive protein 94 kDa (irp94), and demonstrated the expression of this gene after transient forebrain ischemia. In the current study, the authors investigated the expression profiles of all HSP110 family members including hsp110/105 and osp94/apg-1, after transient forebrain ischemia using rat four-vessel occlusion model. Among three members of the HSP110 family, induction of hsp110/105 was the most prominent after ischemia. hsp110/105 mRNA expression was clearly enhanced from 4 to 24 hours after a 6-minute or longer ischemic period. First, hsp110/105 mRNA expression was induced in the dentate gyrus, and later in the pyramidal layer. HSP110/105 protein expression also was enhanced by a 6-minute or longer period of ischemia. Profiles of HSP110/105 expression after ischemia were similar to those of inducible HSP70. After transient forebrain ischemia for 10 minutes, HSP110/105 protein was induced in the dentate gyrus and the CA3 pyramidal layer, but not in the CA1 pyramidal neurons. However, 6 minutes of ischemia induced the HSP110/105 protein, as well as the HSP70 protein, in the CA1 region. CA1 pyramidal neurons expressing HSP110/105 acquired tolerance against subsequent severe ischemia. In conclusion, HSP110/105 showed the most prominent induction after ischemia among the three HSP110 gene family members. Colocalization of HSP110/105 and HSP70 in the CA1 neurons that acquired tolerance suggested that induced HSP110/105 might contribute to ischemic tolerance together with HSP70.

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Liu, Shimin, Honglian Shi, Wenlan Liu, Takamitsu Furuichi, Graham S. Timmins, and Ke Jian Liu. "Interstitial pO2 in Ischemic Penumbra and Core are Differentially Affected following Transient Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 24, no. 3 (March 2004): 343–49. http://dx.doi.org/10.1097/01.wcb.0000110047.43905.01.

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Stroke causes heterogeneous changes in tissue oxygenation, with a region of decreased blood flow, the penumbra, surrounding a severely damaged ischemic core. Treatment of acute ischemic stroke aims to save this penumbra before its irreversible damage by continued ischemia. However, effective treatment remains elusive due to incomplete understanding of processes leading to penumbral death. While oxygenation is central in ischemic neuronal death, it is unclear exactly what actual changes occur in interstitial oxygen tension (pO2) in ischemic regions during stroke, particularly the penumbra. Using the unique capability of in vivo electron paramagnetic resonance (EPR) oximetry to measure localized interstitial pO2, we measured both absolute values, and temporal changes of pO2 in ischemic penumbra and core during ischemia and reperfusion in a rat model. Ischemia rapidly decreased interstitial pO2 to 32% ± 7.6% and 4% ± 0.6% of pre-ischemic values in penumbra and core, respectively 1 hour after ischemia. Importantly, whilst reperfusion restored core pO2 close to its pre-ischemic value, penumbral pO2 only partially recovered. Hyperoxic treatment significantly increased penumbral pO2 during ischemia, but not in the core, and also increased penumbral pO2 during reperfusion. These divergent, important changes in pO2 in penumbra and core were explained by combined differences in cellular oxygen consumption rates and microcirculation conditions. We therefore demonstrate that interstitial pO2 in penumbra and core is differentially affected during ischemia and reperfusion, providing new insights to the pathophysiology of stroke. The results support normobaric hyperoxia as a potential early intervention to save penumbral tissue in acute ischemic stroke.

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Kitagawa, Kazuo, Masayasu Matsumoto, Takuma Mabuchi, Yoshiki Yagita, Toshiho Ohtsuki, Masatsugu Hori, and Takehiko Yanagihara. "Deficiency of Intercellular Adhesion Molecule 1 Attenuates Microcirculatory Disturbance and Infarction Size in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 18, no. 12 (December 1998): 1336–45. http://dx.doi.org/10.1097/00004647-199812000-00008.

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Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against ICAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using ICAM-1–knockout mice. Ischemic lesions were significantly mitigated in knockout mice after permanent and transient focal ischemia, even though the number of granulocytes in the infarcted tissue was almost the same between knockout and wild-type mice. Depletion of granulocytes further decreased the size of ischemic lesions after transient focal ischemia in ICAM-1–knockout mice. Microcirculation was reduced after focal ischemia, but it was better preserved in the cerebral cortex of knockout mice than that of wild-type mice. The present study demonstrated that ICAM-1 played a role in microcirculatory failure and subsequent development and expansion of infarction after focal cerebral ischemia. However, it is highly unlikely that ICAM-1 played a key role in accumulation of granulocytes after focal cerebral ischemia.

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Yoshioka, Hideyuki, Masataka Katsu, Hiroyuki Sakata, Nobuya Okami, Takuma Wakai, Hiroyuki Kinouchi, and Pak H. Chan. "The Role of Parl and HtrA2 in Striatal Neuronal Injury After Transient Global Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 11 (August 7, 2013): 1658–65. http://dx.doi.org/10.1038/jcbfm.2013.139.

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The presenilin-associated rhomboid-like (PARL) protein and high temperature requirement factor A2 (HtrA2) are key regulators of mitochondrial integrity and play pivotal roles in apoptosis. However, their roles after cerebral ischemia have not been thoroughly elucidated. To clarify these roles, mice were subjected to transient global cerebral ischemia, and striatal neuronal injury was assessed. Western blot and coimmunoprecipitation analyses revealed that PARL and processed HtrA2 localized to mitochondria, and that PARL was bound to HtrA2 in sham animals. Expression of PARL and processed HtrA2 in mitochondria significantly decreased 6 to 72 hours after ischemia, and the binding of PARL to HtrA2 disappeared after ischemia. In contrast, expression of processed HtrA2 increased 24 hours after ischemia in the cytosol, where HtrA2 was bound to X chromosome-linked inhibitor-of-apoptosis protein (XIAP). Administration of PARL small interfering RNA inhibited HtrA2 processing and worsened ischemic neuronal injury. Our results show that downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability. In addition, processed HtrA2 released into the cytosol after ischemia contributes to neuronal injury via inhibition of XIAP.

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Vinogradova, I. V., and D. O. Ivanov. "TRANSIENT MYOCARDIAL ISCHEMIA IN NEWBORN." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 4 (August 28, 2013): 343–47. http://dx.doi.org/10.18705/1607-419x-2013-19-4-343-347.

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Objective. To study the transient myocardial ischemia in newborn of different gestational age survived after severe perinatal pathology.Design and methods. A total of 110 newborn were examined. One group included newborns weighed 2000–2500 g at birth, group 2 was formed by children with extremely low birth weight (ELBW). In both groups the frequency of transient myocardial ischemia was assessed. Results and conclusion. As a result, the comparative study showed that transient myocardial ischemia is more common in infants with ELBW. It is associated with the worsening of the underlying disease and increased mortality in the group of newborns with ELBW.

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Stark, S. R. "Transient dyskinesia and cerebral ischemia." Neurology 35, no. 3 (March 1, 1985): 445. http://dx.doi.org/10.1212/wnl.35.3.445.

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Margolin, D. I. "Transient dyskinesia and cerebral ischemia." Neurology 35, no. 3 (March 1, 1985): 445. http://dx.doi.org/10.1212/wnl.35.3.445-a.

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Sasaki, Tsutomu, Kazuo Kitagawa, Kanato Yamagata, Takako Takemiya, Shigeru Tanaka, Emi Omura-Matsuoka, Shiro Sugiura, Masayasu Matsumoto, and Masatsugu Hori. "Amelioration of Hippocampal Neuronal Damage after Transient Forebrain Ischemia in Cyclooxygenase-2—Deficient Mice*." Journal of Cerebral Blood Flow & Metabolism 24, no. 1 (January 2004): 107–13. http://dx.doi.org/10.1097/01.wcb.0000100065.36077.4a.

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Several studies have suggested that cyclooxygenase-2 (COX-2) plays a role in ischemic neuronal death. Genetic disruption of COX-2 has been shown to reduce susceptibility to focal ischemic injury and N-methyl-D-aspartate-mediated neurotoxicity. The purpose of this study was to examine the effects of COX-2 deficiency on neuronal vulnerability after transient forebrain ischemia. Marked upregulation of COX-2 immunostaining in neurons was observed at the early stage and prominent COX-2 staining persisted in the CA1 medial sector and CA2 sector over 3 days after ischemia. The immunohistologic pattern of COX-2 staining in these sectors gradually condensed to a perinuclear location. The degree of hippocampal neuronal injury produced by global ischemia in COX-2–deficient mice was less than that in wild-type mice, coincident with attenuation of DNA fragmentation in the hippocampus. Also, treatment with a selective COX-2 inhibitor, nimesulide, after ischemia decreased hippocampal neuronal damages. These results of genetic disruption and chemical inhibition of cyclooxygenase-2 show that inhibition of COX-2 ameliorates selective neuronal death after transient forebrain ischemia in mice.

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Pang, Ting, Yang Zhao, Nan-Rong Zhang, San-Qing Jin, and San-Qiang Pan. "Transient Limb Ischemia Alters Serum Protein Expression in Healthy Volunteers: Complement C3 and Vitronectin May Be Involved in Organ Protection Induced by Remote Ischemic Preconditioning." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/859056.

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The protective mechanism underlying remote ischemic preconditioning (RIPC) is unclear. This study aims to verify whether the protein expression profile in the serum could be altered by RIPC and to detect potential protein mediators. Transient limb ischemia consisting of three cycles of 5-min ischemia followed by 5-min reperfusion was performed on sixty healthy volunteers. Serum samples were collected at 30 min before transient limb ischemia and at 1 hour (h), 3 h, 8 h, 24 h, and 48 h after completion of three cycles. Changes in the serum protein profile were analyzed by two-dimensional gel electrophoresis and proteins were identified by MALDI-TOF/TOF mass spectrometry. Fourteen differentially expressed proteins were identified and, respectively, involved in immune system, lipid binding and metabolism, apoptosis, and blood coagulation. Complement C3, vitronectin, and apolipoprotein A-I were further confirmed by western blotting, and the results showed that their contents decreased significantly after transient limb ischemia. It is concluded that transient limb ischemia alters the serum protein expression profile in human being, and that reduction of serum contents of complement C3 and vitronectin may represent an important part of the mechanism whereby RIPC confers its protection.

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Benndorf, K., S. Thierfelder, B. Doepner, C. Gebhardt, and H. Hirche. "Role of Cardiac KATP Channels During Anoxia and Ischemia." Physiology 12, no. 2 (April 1, 1997): 78–83. http://dx.doi.org/10.1152/physiologyonline.1997.12.2.78.

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In isolated heart cells, maintained anoxia causes a transient opening of KATP channels. In the ischemic myocardium, this extra K+ conductance results in a decreased contractility and may be arrhythmogenic. Recent studies provide further evidence that the transient activity of KATP channels during anoxia is correlated with the time course of extracellular K+ accumulation during ischemia.

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Berger, H. J., A. Taratuska, T. W. Smith, and J. A. Halperin. "Activated complement directly modifies the performance of isolated heart muscle cells from guinea pig and rat." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H267—H272. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h267.

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The complement system has been implicated in the pathogenesis of cardiovascular disorders including ischemia and atherosclerosis. Selective deposition of C5b-9, the membrane attack complex of complement, has been histochemically documented in human myocardium early after reperfusion of ischemic areas and in infarcted zones. However, functional sequelae of the C5b-9 complex binding to myocardial cells have not been identified. Insertion of C5b-9 complexes into the membrane of other cell types can generate transient changes in membrane permeability in the absence of cell lysis. We demonstrate in beating isolated adult guinea pig and rat cardiac myocytes that human derived C5b-9 can transiently augment in a dose-dependent manner both basal cytosolic calcium concentration and calcium transients, resulting in a temporary increase in contractility. If similar changes occur in human heart cells in vivo, they could significantly affect myocardial performance and contribute to functional abnormalities seen in ischemia and other pathological conditions associated with complement activation.

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Mitsufuji, Nobuto, Hiroshi Yoshioka, Sozo Okano, Tetsuo Nishiki, and Tadashi Sawada. "A New Model of Transient Cerebral Ischemia in Neonatal Rats." Journal of Cerebral Blood Flow & Metabolism 16, no. 2 (March 1996): 237–43. http://dx.doi.org/10.1097/00004647-199603000-00008.

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A new model of transient cerebral ischemia in 10-day-old rats is described. Under microscopic guidance, the right external and internal carotid arteries were electrically coagulated. A solid 0.47 mm diameter nylon thread was inserted into the right common carotid artery toward the ascending aorta up to 10–12 mm from the upper edge of the sternomastoid muscle (preischemic rats). A 60-min cerebral ischemia was induced by clamping the left external and internal carotid arteries (ischemic rats), followed by 3-h recirculation. 31P magnetic resonance (MRS) spectroscopic studies revealed that severe intracellular acidosis occurred and ATP disappeared completely for at least the last 20 min of ischemia. Cerebral blood flow (CBF), measured by the hydrogen clearance technique, decreased to ∼11% of the preischemic level in the frontal cortex soon after the induction of ischemia. On resuscitation, ATP recovered completely and the preischemic intracellular pH level was restored within 180 min. CBF had recovered to ∼30% of the preischemic level at 5 min after resuscitation. The CBF recovery was not complete even at 180 min after resuscitation. With this model, the effects of pure ischemia without hypoxia on the neonatal brain and the process of recovery from transient ischemia can be studied.

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Liu, Chinli, Shaoyi Chen, and Bingren Hu. "Ischemic preconditioning prevents translational complex aggregation after transient cerebral ischemia." Journal of Cerebral Blood Flow & Metabolism 25, no. 1_suppl (August 2005): S284. http://dx.doi.org/10.1038/sj.jcbfm.9591524.0284.

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Kaplan, Peter W. "Focal Seizures Resembling Transient Ischemic Attacks due to Subclinical Ischemia." Cerebrovascular Diseases 3, no. 4 (1993): 241–43. http://dx.doi.org/10.1159/000108708.

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Wang, Yang, Shao-wei Jiang, Xuan Liu, Lei Niu, Xiao-li Ge, Jin-cheng Zhang, Hai-rong Wang, Ai-hua Fei, Cheng-jin Gao, and Shu-ming Pan. "Degradation of TRPML1 in Neurons Reduces Neuron Survival in Transient Global Cerebral Ischemia." Oxidative Medicine and Cellular Longevity 2018 (December 18, 2018): 1–11. http://dx.doi.org/10.1155/2018/4612727.

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Postcardiac arrest syndrome yields poor neurological outcomes, but the mechanisms underlying this condition remain poorly understood. Autophagy plays an important role in neuronal apoptosis induced by ischemia. However, whether autophagy is involved in neuron apoptosis induced by cardiac arrest has been less studied. This study found that TRPML1 participates in cerebral ischemic reperfusion injury. Primary neurons were isolated and treated with mucolipin synthetic agonist 1 (ML-SA1), as well as infected with the recombinant lentivirus TRPML1 overexpression vector in vitro. ML-SA1 was delivered intracerebroventricularly in transient global ischemia model. Protein expression levels were determined by western blot. Neurological deficit score and the infarct volume were analyzed for the detection of neuronal damage. We found that TRPML1 was significantly downregulated in vivo and in vitro ischemic reperfusion model. We also observed that TRPML1 overexpression or treatment with the ML-SA1 attenuated neuronal death in primary neurons and ameliorated neurological dysfunction in vivo. Our findings suggested that autophagy and apoptosis were activated after transient global ischemia. Administration of ML-SA1 before transient global ischemia ameliorated neurological dysfunction possibly through the promotion of autophagy and the inhibition of apoptosis.

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Combs, David J., Robert J. Dempsey, David Donaldson, and Mark S. Kindy. "Hyperglycemia Suppresses c-Fos mRNA Expression following Transient Cerebral Ischemia in Gerbils." Journal of Cerebral Blood Flow & Metabolism 12, no. 1 (January 1992): 169–72. http://dx.doi.org/10.1038/jcbfm.1992.21.

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The c- fos proto-oncogene is activated by transient cerebral ischemia. This activation may signify a specific genetic response to ischemia affecting tolerance to ischemia and ultimate cell survival. Hyperglycemia, which enhances brain injury from transient ischemia, was studied for its effects on this gene system in gerbils by measuring c- fos mRNA 2 h after 20 min of bilateral carotid artery occlusion. Brain c- fos mRNA was increased by ischemia (11.7 ± 5.0, p ≤ 0.05, fold increase) compared to nonischemic controls (1.0 ± 1.3). Pretreatment with 1 g/kg of glucose partially reduced postischemic c- fos mRNA (6.3 ± 1.6, p ≤ 0.05) while 4 g/kg of glucose completely suppressed postischemic c- fos expression (0.7 ± 0.3, p ≤ 0.05). These data indicate that hyperglycemia suppresses normal postischemic gene expression and suggest the possibility that such suppression is a predictor or even a contributor to hyperglycemia-enhanced ischemic brain damage.

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Nishimura, Hiroyuki, Tomohiro Matsuyama, Kyoko Obata, Yatsuka Nakajima, Hideto Kitano, Minoru Sugita, and Masaya Okamoto. "Changes in Mint1, a Novel Synaptic Protein, After Transient Global Ischemia in Mouse Hippocampus." Journal of Cerebral Blood Flow & Metabolism 20, no. 10 (October 2000): 1437–45. http://dx.doi.org/10.1097/00004647-200010000-00005.

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Mints (munc18-interacting proteins) are novel multimodular adapter proteins in membrane transport and organization. Mint1, a neuronal isoform, is involved in synaptic vesicle exocytosis. Its potential effects on development of ischemic damage to neurons have not yet been evaluated. The authors examined changes in mint1 and other synaptic proteins by immunohistochemistry after transient global ischemia in mouse hippocampus. In sham-ischemic mice, immunoreactivity for mint1 was rich in fibers projecting from the entorhinal cortex to the hippocampus and in the mossy fibers linking the granule cells of the dentate gyrus to CA3 pyramidal neurons. Munc18-1, a binding partner of mint1, was distributed uniformly throughout the hippocampus, and synaptophysin 2, a synaptic vesicle protein, was localized mainly in mossy fibers. After transient global ischemia, mint1 immunoreactivity in mossy fibers was dramatically decreased at 1 day of reperfusion but actually showed enhancement at 3 days. However, munc18-1 and synaptophysin 2 were substantially expressed in the same region throughout the reperfusion period. These findings suggest that mint1 participates in neuronal transmission along the excitatory pathway linking the entorhinal cortex to CA3 in the hippocampus. Because mint1 was transiently decreased in the mossy fiber projection after ischemia, functional impairment of neuronal transmission in the projection from the dentate gyrus to CA3 pyramidal neurons might be involved in delayed neuronal death.

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Meng, Wei, Xiaoying Wang, Minoru Asahi, Tsuneo Kano, Kazuko Asahi, Robert H. Ackerman, and Eng H. Lo. "Effects of Tissue Type Plasminogen Activator in Embolic versus Mechanical Models of Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 19, no. 12 (December 1999): 1316–21. http://dx.doi.org/10.1097/00004647-199912000-00004.

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Tissue type plasminogen activator (tPA) can be effective therapy for embolic stroke by restoring cerebral perfusion. However, a recent experimental study showed that tPA increased infarct size in a mouse model of transient focal ischemia, suggesting a possible adverse effect of tPA on ischemic tissue per se. In this report, the effects of tPA in two rat models of cerebral ischemia were compared. In experiment 1, rats were subjected to focal ischemia via injection of autologous clots into the middle cerebral artery territory. Two hours after clot injection, rats were treated with 10 mg/kg tPA or normal saline. Perfusion-sensitive computed tomography scanning showed that tPA restored cerebral perfusion in this thromboembolic model. Treatment with tPA significantly reduced ischemic lesion volumes measured at 24 hours by >60%. In experiment 2, three groups of rats were subjected to focal ischemia via a mechanical approach in which a silicon-coated filament was used intraluminally to occlude the origin of the middle cerebral artery. In two groups, the filament was withdrawn after 2 hours to allow for reperfusion, and then rats were randomly treated with 10 mg/kg tPA or normal saline. In the third group, rats were not treated and the filament was not withdrawn so that permanent focal ischemia was present. In this experiment, tPA did not significantly alter lesion volumes after 2 hours of transient focal ischemia. In contrast, permanent ischemia significantly increased lesion volumes by 55% compared with transient ischemia. These results indicate that in these rat models of focal cerebral ischemia, tPA did not have detectable negative effects. Other potentially negative effects of tPA may be dependent on choice of animal species and model systems.

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Gorshkova, O. P., V. N. Shuvaeva, M. V. Lensman, and A. I. Artem'eva. "The influence of short-time cerebral ischemia on pial vessels adrenoreactivity in rats." Regional blood circulation and microcirculation 15, no. 2 (June 30, 2016): 73–79. http://dx.doi.org/10.24884/1682-6655-2016-15-2-73-79.

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Introduction and purpose. It is known that ischemia influences on endothelial reactions, changes metabolic and myogenic mechanisms of cerebral blood flow regulation. But the role of local neurogenic mechanisms of regulation in change of cerebral vessels reactions after ischemia is finally not found out. The aim of the current study was to examine the pial vessels reactivity in response to a brain surface irrigation by norepinephrine solution in rats, subjected to transient global cerebral ischemia, at 2, 7, 14 and 21 days after ischemia. Materials and methods. Transient global cerebral ischemia was induced in anesthetized Wistar rats by clamping of both common carotid arteries for 12 min with simultaneous controlled hypotension to 45±3 mm Hg, followed by blood reinfusion and recovering from anesthesia. Four different groups of rats were re-anesthetized at 2, 7, 14 or 21 days after ischemia and subjected to microvascular studies using in-vivo video microscopy method. The diameter changes of pial arteries and veins in response to norepinephrine were measured. Results and discussion. It was established that cerebral ischemia led to increase number of the constrictions to norepinephrine mainly at the vessels to relating to group of small pial arteries and arterioles and pial veins of the 3-rd generation. Reactivity changes were observed in all time points studied. This changes probably is connected with caused by ischemia the increase in reactivity and sensitivity of pial vessels adrenoceptors. The greatest changes are noted in 14 days after ischemia. The use of non-selective α-adrenergic antagonist - nicergoline at ischemic and intact rats, led to increase number of the constrictions to norepinephrine. But at ischemic rats decrease was more considerable. And number of dilation reactions to norepinephrine at ischemic rats was also above. It can indicate to increase of adrenoceptors reactivity and sensitivity. Conclusions. Thus, transient global cerebral ischemia cause marked and long lasting (3 weeks) increase in pial vessels reactivity in response to norepinephrine, that is probably connected with increase of adrenoceptors reactivity and sensitivity.

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Kuhmonen, Johanna, Jaroslav Pokorny, Riitta Miettinen, Antti Haapalinna, Jukka Jolkkonen, Paavo Sr Riekkinen, and Juhani Sivenius. "Neuroprotective Effects of Dexmedetomidine in the Gerbil Hippocampus after Transient Global Ischemia." Anesthesiology 87, no. 2 (August 1, 1997): 371–77. http://dx.doi.org/10.1097/00000542-199708000-00025.

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Background Cerebral ischemia induces a massive release of norepinephrine associated with neuronal death in the brain. It has been demonstrated that alpha2-adrenoceptor agonists decrease the release and turnover of noradrenaline, and this might prove advantageous in counteracting the neurodegeneration in ischemic brain. Therefore, in the present study, the authors tested whether dexmedetomidine, a selective alpha2-receptor agonist, has neuroprotective effects in a gerbil transient global ischemia model. Methods Ischemia was induced by bilateral carotid occlusion for 5 min in diethylether-anesthetized normothermic gerbils. Dexmedetomidine was administered subcutaneously in four different treatment paradigms (6-8 animals/group): 3 or 30 microg/kg 30 min before and thereafter at 3, 12, 24, and 48 h after the occlusion, or 3 or 30 microg/kg at 3, 12, 24, and 48 h after the occlusion. Control animals were subjected to forebrain ischemia but received only saline injections. One week after occlusion, animals were transcardially perfused for histochemistry. Neuronal death in the CA1 and CA3 regions of the hippocampus and in the hilus of the dentate gyrus was evaluated in silver-stained 60-microm coronal sections. Results Compared with saline-treated ischemic animals, dexmedetomidine at a dose of 3 microg/kg given before and continued after the induction of ischemia reduced the number of damaged neurons in the CA3 area (2 +/- 3 vs. 17 +/- 20 degenerated neurons/mm2; P < 0.05). Also in the dentate hilus, the number of damaged neurons was reduced by dexmedetomidine (3 microg/kg) given before and continued after ischemia (5 +/- 7 vs. 56 +/- 42 degenerated neurons/mm2; P < 0.01). Conclusions The present data demonstrate that dexmedetomidine effectively prevents delayed neuronal death in CA3 area and in the dentate hilus in gerbil hippocampus when the management is started before the onset of ischemia and continued for 48 h after reperfusion. Inhibition of ischemia-induced norepinephrine release may be associated with neuroprotection by dexmedetomidine.

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Journal articles on the topic 'Transient Ischemia'

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