Edema, cation content, and ATPase activity after middle cerebral artery occlusion in rats.

Yang, Guo‐Yuan; Chen, S F; Kinouchi, Hiroyuki; Chan, Pak H.; Weinstein, Philip

doi:10.1161/01.str.23.9.1331

Cited by 88 publications

(41 citation statements)

References 29 publications

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“…Spontaneously ventilating adult male SV-129 mice (n ϭ 173; 19-23 g; Taconic Farms) were initially anesthetized with 1.0% and maintained on 0.4-0.8% halothane in 70% N 2 O and 30% O 2 using a Fluotec 3 vaporizer (Colonial Medical, Amherst, NH). The left MCA was occluded with an 8-0 nylon monofilament (Ethicon, Somerville, NJ) coated with a mixture of silicone resin (Xantopren; Bayer Dental, Osaka) and a hardener (Elastomer Activator; Bayer Dental) as described (37,38). The procedure lasted 15 min, and the anesthesia was discontinued.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

Hara

Friedlander

Gagliardini

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

798

481

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Section: Methodsmentioning

confidence: 99%

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

Hara

Friedlander

Gagliardini

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

798

481

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“…The findings that various agents can decrease cerebral infarct size after 2 h of middle cerebral artery occlusion (MCAO) with 22-h reperfusion (Ellsworth et al, 2003;Endres et al, 1998a) suggest that such ischemia-induced brain injury can still be reversed. Cerebral edema is also present 24 h after 2 h of MCAO (Yang et al, 1992). Moreover, transient MCAO with reperfusion is proposed to more closely mimic the clinical situation (Hunter et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Deletion of Aldose Reductase Leads to Protection against Cerebral Ischemic Injury

Cheung

Hung

et al. 2007

J Cereb Blood Flow Metab

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Previously, we reported that transgenic mice overexpressing endothelin-1 in astrocytes showed more severe neurological deficits and increased infarct after transient focal ischemia. In those studies, we also observed increased level of aldose reductase (AR), the first and rate-limiting enzyme of the polyol pathway, which has been implicated in osmotic and oxidative stress. To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase (SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Most interestingly, AR À/À brains showed lowered expression of transferrin and transferrin receptor with less iron deposition and nitrotyrosine accumulation. The protection against oxidative stress in AR À/À brain was also associated with less poly(adenosine diphosphate-ribose) polymerase (PARP) and caspase-3 activation. Pharmacological inhibition of AR by Fidarestat also protected animals against cerebral ischemic injury. These findings are the first to show that AR contributes to iron-and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury.

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“…2,10,18,19) Our previous study showed that SM-20220 prevented the infarction in a rat transient MCA occlusion model 10,11) ; however, the relationship between the timing of drug administration and its beneficial effects was not clear. In the present study, we investigated the dependence of the effect of SM-20220 on infarct size on the dose and on the timing of drug administration.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] This phenomenon is thought to play a key role in ischemic damage. 5) The Na ϩ /H ϩ exchanger (NHE) is a mammalian plasma membrane glycoprotein that mediates the exchange of intracellular H ϩ for extracellular Na ϩ with a 1 : 1 stoichiometry and thus influences the regulation of cell volume and pHi.…”

mentioning

confidence: 99%

Relationship between the Neuroprotective Effect of Na<SUP>+</SUP>/H<SUP>+</SUP> Exchanger Inhibitor SM-20220 and the Timing of Its Administration in a Transient Middle Cerebral Artery Occlusion Model of Rats

Horikawa¹,

Kuribayashi²,

Matsui³

et al. 2001

Biological & Pharmaceutical Bulletin

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The aim of this study was to determine the relationship between the neuroprotective effect of SM-20220 (N-(aminoiminomethyl)-1-methyl-1H-indole-2-carboxamide methanesulfonate) and the timing of its administration in an experimental stroke model. Two hours of occlusion followed by 22 h of perfusion of the left middle cerebral artery (MCA) was performed by inserting a nylon thread into the MCA to occlude it, and pulling the thread to initiate reperfusion. Intravenous infusion of SM-20220 for 1 h reduced the infarct volume at doses of 0.2-0.8 mg/kg in a dose-dependent manner without causing changes in the systemic arterial blood pressure or blood gases, when SM-20220 administration was started 1 h after the onset of occlusion. Administration of SM-20220 at a dose of 0.4 mg/kg also reduced the edema formation induced by ischemia. In contrast, SM-20220 failed to reduce the infarction, even at 1.6 mg/kg, when administration was started 2 h after the onset of occlusion. Thus, the therapeutic time window of SM-20220 for this transient MCA occlusion model is 1 h. Daily administration of SM-20220 (0.4 mg/kg) for the 7 d following 1.5 h of middle cerebral artery occlusion reduced the infarct volume with statistical significance ( pϽ0.05), showing that SM-20220 did not merely delay but prevented ischemic damage. Key words Naϩ /H ϩ exchanger; brain ischemia; infarction; SM-20220; edema; therapeutic time window centage of the area of the left hemisphere for each coronal section. The infarct volume was calculated by integration of the infarct areas and the areas of the left hemisphere that were determined for the five coronal sections. Measurement of Arterial Blood Pressure, Gases, and pH In some animals, a femoral artery was cannulated to directly and continuously measure the systemic arterial blood pressure with a pressure transducer (P10EZ, Nihon Kohden, Osaka, Japan) attached to a blood-pressure amplifier (AP-641G, Nihon Kohden) and to sample blood for the analysis of blood gases and pH using I-STAT (Fuso Chemicals, Osaka, Japan). Measurement of Cerebral Water ContentTo measure the brain water content, rats were decapitated 4 h after the onset of reperfusion and the left hemisphere of the occluded MCA territory was cut into 4-mm-thick slices (1 mm anterior-3 mm posterior to the bregma).10) The water content was determined by the dry-weight method. 13)Experimental Protocol The experimental protocol is shown in Fig. 1. SM-20220 was dissolved in 8% polyethylene glycol 400 (w/v) to 0.4 mg/ml and diluted with the same solution to 0.04, 0.08, 0.16, and 0.32 mg/ml. The diluted SM-20220 or just the solution as vehicle was given as an intravenous infusion (5 ml/kg/h) for 1 h using an infusion pump (model 100, KD Scientific, U.S.A.).For the first experiment, the administration of SM-20220 or vehicle was started 1 h after the onset of occlusion, and physiological variables were measured before surgery, before drug administration, and 30 min after the onset of reperfusion; the infarct size was measured 22 h after the onset.For the sec...

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Edema, cation content, and ATPase activity after middle cerebral artery occlusion in rats.

Cited by 88 publications

References 29 publications

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

Deletion of Aldose Reductase Leads to Protection against Cerebral Ischemic Injury

Relationship between the Neuroprotective Effect of Na<SUP>+</SUP>/H<SUP>+</SUP> Exchanger Inhibitor SM-20220 and the Timing of Its Administration in a Transient Middle Cerebral Artery Occlusion Model of Rats

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