5 research outputs found

    Ischemic Postconditioning Fails to Protect against Neonatal Cerebral Stroke

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    <div><p>The lack of efficient neuroprotective strategies for neonatal stroke could be ascribed to pathogenic ischemic processes differentiating adults and neonates. We explored this hypothesis using a rat model of neonatal ischemia induced by permanent occlusion of the left distal middle cerebral artery combined with 50 min of occlusion of both common carotid arteries (CCA). Postconditioning was performed by repetitive brief release and occlusion (30 s, 1 and/or 5 min) of CCA after 50 min of CCA occlusion. Alternative reperfusion was generated by controlled release of the bilateral CCA occlusion. Blood-flow velocities in the left internal carotid artery were measured using color-coded pulsed Doppler ultrasound imaging. Cortical perfusion was measured using laser Doppler. Cerebrovascular vasoreactivity was evaluated after inhalation with the hypercapnic gas or inhaled nitric oxide (NO). Whatever the type of serial mechanical interruptions of blood flow at reperfusion, postconditioning did not reduce infarct volume after 72 hours. A gradual perfusion was found during early re-flow both in the left internal carotid artery and in the cortical penumbra. The absence of acute hyperemia during early CCA re-flow, and the lack of NO-dependent vasoreactivity in P7 rat brain could in part explain the inefficiency of ischemic postconditioning after ischemia-reperfusion.</p> </div

    Protocols for cerebral ischemia without and with postconditioning.

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    <p>Animals were divided into three groups. All animals were subjected to MCA electrocoagulation, and bilateral CCA were transiently (50 min) occluded 2 min later. Re-flow was initiated by CCA occlusion release in controls (nβ€Š=β€Š17 in the first set, nβ€Š=β€Š11 in the second set and nβ€Š=β€Š11 in the third set of experiments). Postconditioning with 3 cycles (occlusion/reperfusion) of 30 s (nβ€Š=β€Š11), 1 (nβ€Š=β€Š18) or 5 (nβ€Š=β€Š12) min was performed on both or only left CCA within 15 s after the initial CCA reperfusion. Alternative reperfusion was initiated by first occlusion release of the left (L/R, nβ€Š=β€Š11) or of the right (R/L, nβ€Š=β€Š12) CCA followed by occlusion release of the other CCA.</p

    Laser Doppler monitoring during reperfusion.

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    <p><b>A</b>: Representative brain from a pup killed at 48 hours after ischemia showing a pale delineated lesion (white dotted line) and 3 regions of interest (ROI), and representative cresyl violet-stained section showing a cortical infarct and 2 ROI for rCBF measurements in the penumbra with the laser probe. <b>B</b>: Changes in rCBF (mean of 3 ROI Β± S.D) in 6 animals subjected to ischemia-reperfusion. Upon MCA occlusion, the rCBF dropped to 55Β±8% of baseline, and additional bilateral CCA occlusion further decreased rCBF to 18Β±5%. After CCA release, a gradual reperfusion was observed from 30Β±11% at 1 min to 44Β±9% 20 min after. *p<0.05, ** p<0.01 <i>vs</i> basal.</p

    Postconditioning did not reduce infarct size. Infarct size was measured 3 days after ischemia.

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    <p><b>A</b>: Infarct size measured in animals subjected to postconditioning with 3 cycles of occlusion/reperfusion of 1 and 5 min on both CCA. <b>B</b>: Infarct size measured in animals subjected to postconditioning with 3 cycles of occlusion/reperfusion of 30 s on the left CCA. <b>C</b>: Infarct size measured in animals subjected to alternative reperfusion. The median (horizontal bar) and the mean (cross) were indicated. No significant difference was detected in the different groups.</p

    Changes in arterial cerebral blood flow in animals subjected to neonatal ischemia.

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    <p><b>A</b>: spectral analyses of blood-flow velocity waveforms acquired with pulsed Doppler in the left ICA before ischemia (basal, left) and at 3 min after re-flow (right). <b>B</b>: Time course of mBFV in the left ICA and in the basilar trunk (BT) during reperfusion. Mean BFVs were plotted before ischemia, during ischemia (at 40 min) and during the first 15 min of the reperfusion. Note that mBFVs in the left ICA at the reperfusion did not reach the level of its mean value in basal condition. In the BT, mBFVs were increased during ischemia (*p<0.05 <i>vs</i> basal) and returned to basal values at the reperfusion. <b>C–D</b>: Time course of mBFV in the left ICA during reperfusion in animals subjected to neonatal ischemia and/or postconditioning. <b>C</b>: Mean BFVs were plotted before ischemia (basal), during ischemia (at 40 min) and during the first 15 min of the reperfusion after release on both CCA (ischemic controls, red line, nβ€Š=β€Š5), and after 1/1 min postC (3 cycles, green line, nβ€Š=β€Š6). <b>D</b>: Mean BFVs were plotted before ischemia (basal), during ischemia (at 40 min) and during the first 15 min of the reperfusion after release on both CCA (ischemic controls, red line, nβ€Š=β€Š6), after release occlusion on left CCA then right CCA 5 min later (green line, nβ€Š=β€Š5), and after release on the right then left CCA 5 min later (blue line, nβ€Š=β€Š5). Data are expressed as meanΒ±SD.</p
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