Effect of ischemic preconditioning on cerebral blood flow after subsequent lethal ischemia in gerbils

Nakamura, Hidenori; Katsumata, T; Nishiyama, Yutaka; Otori, Tatsuo; Katsura, Ken‐ichiro; Katayama, Yasuo

doi:10.1016/j.lfs.2005.08.008

Cited by 43 publications

(31 citation statements)

References 43 publications

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“…In contrast to the studies outlined in section II, data obtained with CSD preconditioning in rats and ischemic preconditioning in gerbils suggested that ischemic tolerance was associated with improved tissue perfusion during the subsequent test ischemia (269,297).…”

Section: Residual Cbf During the Test Ischemia: Is It Improved By Isccontrasting

confidence: 58%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

230

176

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Ischemic tolerance describes the adaptive biological response of cells and organs that is initiated by preconditioning (i.e., exposure to stressor of mild severity) and the associated period during which their resistance to ischemia is markedly increased. This topic is attracting much attention because preconditioning-induced ischemic tolerance is an effective experimental probe to understand how the brain protects itself. This review is focused on the molecular and related functional changes that are associated with, and may contribute to, brain ischemic tolerance. When the tolerant brain is subjected to ischemia, the resulting insult severity (i.e., residual blood flow, disruption of cellular transmembrane gradients) appears to be the same as in the naive brain, but the ensuing lesion is substantially reduced. This suggests that the adaptive changes in the tolerant brain may be primarily directed against postischemic and delayed processes that contribute to ischemic damage, but adaptive changes that are beneficial during the subsequent test insult cannot be ruled out. It has become clear that multiple effectors contribute to ischemic tolerance, including: 1) activation of fundamental cellular defense mechanisms such as antioxidant systems, heat shock proteins, and cell death/survival determinants; 2) responses at tissue level, especially reduced inflammatory responsiveness; and 3) a shift of the neuronal excitatory/inhibitory balance toward inhibition. Accordingly, an improved knowledge of preconditioning/ischemic tolerance should help us to identify neuroprotective strategies that are similar in nature to combination therapy, hence potentially capable of suppressing the multiple, parallel pathophysiological events that cause ischemic brain damage.

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Section: Residual Cbf During the Test Ischemia: Is It Improved By Isccontrasting

confidence: 58%

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Obrenovitch¹

2008

Physiological Reviews

230

176

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“…These investigations have established that ischemic tolerance is associated with genetic, biochemical, and neurophysiological changes in neurons and glia that render the brain more resistant to ischemia. However, it has also been observed that tolerance-inducing stimuli improve microvascular perfusion or cerebral blood flow (CBF) in the postischemic brain (Dawson et al, 1999;Furuya et al, 2005;Hoyte et al, 2006;Nakamura et al, 2006;Zhao and Nowak, 2006). Although these studies have suggested that preconditioning protects cerebral blood vessels from the vasoparalysis induced by cerebral ischemia, the effects of preconditioning on cerebrovascular function and the specific contribution of vascular factors to the protection have not been determined.…”

Section: Introductionmentioning

confidence: 99%

Neurovascular Protection by Ischemic Tolerance: Role of Nitric Oxide and Reactive Oxygen Species

Kunz¹,

Park²,

Abe³

et al. 2007

J. Neurosci.

131

117

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Cerebral ischemic preconditioning or tolerance is a powerful neuroprotective phenomenon by which a sublethal injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. We used lipopolysaccharide (LPS) as a preconditioning stimulus in a mouse model of middle cerebral artery occlusion (MCAO) to examine whether improvements in cerebrovascular function contribute to the protective effect. Administration of LPS 24 h before MCAO reduced the infarct by 68% and improved ischemic cerebral blood flow (CBF) by 114% in brain areas spared from infarction. In addition, LPS prevented the dysfunction in cerebrovascular regulation induced by MCAO, as demonstrated by normalization of the increase in CBF produced by neural activity, hypercapnia, or by the endotheliumdependent vasodilator acetylcholine. These beneficial effects of LPS were not observed in mice lacking inducible nitric oxide synthase (iNOS) or the nox2 subunit of the superoxide-producing enzyme NADPH oxidase. LPS increased reactive oxygen species and the peroxynitrite marker 3-nitrotyrosine in wild-type mice but not in nox2 nulls. The peroxynitrite decomposition catalyst 5,10,15, 20-tetrakis(4-sulfonatophenyl)porphyrinato iron (III) attenuated LPS-induced nitration and counteracted the beneficial effects of LPS on infarct volume, ischemic CBF, and vascular reactivity. Thus, LPS preserves neurovascular function and ameliorates CBF in regions of the ischemic territory at risk for infarction. This effect is mediated by peroxynitrite formed from iNOS-derived NO and nox2-derived superoxide. The data indicate that preservation of cerebrovascular function is an essential component of ischemic tolerance and suggest that combining neuroprotection and vasoprotection may be a valuable strategy for treating ischemic brain injury.

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“…The preconditioning paradigm has been previously confirmed to be effective at protecting neurons against ischemia in this ischemic model (27). The animals in the ischemia group and the IPC + ischemia groups were assigned recovery durations of 1, 2 and 5 days, as pyramidal neurons in the hippocampal CA1 region do not die until 3 days and begin to die 4 days after ischemia-reperfusion (5).…”

Section: Induction Of Transient Cerebral Ischemia In Animal Groupsmentioning

confidence: 99%

“…Further studies have been performed in other animal models, including global and focal cerebral ischemia (12,(31)(32)(33)(34)(35). The preconditioning time-period used in the present study was determined by that described in a previous report (27), which indicated that at least a 1 day interval between the sublethal 2 min ischemia and lethal 5 min ischemia is necessary for induction of the neuroprotection of the CA1 pyramidal cells. This protective mechanism has been termed 'ischemic tolerance,', however, the molecular mechanisms underlying ischemic tolerance remain to be fully elucidated.…”

Section: Time Following Ischemia-reperfusion ------------------------mentioning

confidence: 99%

Ischemic preconditioning maintains immunoreactivities of glucokinase and glucokinase regulatory protein in neurons of the gerbil hippocampal CA1 region following transient cerebral ischemia

et al. 2015

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Effect of ischemic preconditioning on cerebral blood flow after subsequent lethal ischemia in gerbils

Cited by 43 publications

References 43 publications

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

Neurovascular Protection by Ischemic Tolerance: Role of Nitric Oxide and Reactive Oxygen Species

Ischemic preconditioning maintains immunoreactivities of glucokinase and glucokinase regulatory protein in neurons of the gerbil hippocampal CA1 region following transient cerebral ischemia

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