Impact of intracranial blood-flow redistribution on stroke size during ischemia–reperfusion in 7-day-old rats

Bonnin, Philippe; Leger, Pierre‐Louis; Deroide, Nicolas; Fau, Sébastien; Baud, Olivier; Pocard, Marc; Charriaut‐Marlangue, Christiane; Renolleau, Sylvain

doi:10.1016/j.jneumeth.2011.02.030

Cited by 38 publications

(60 citation statements)

References 40 publications

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“…In contrast, the trend in higher perfusion rates in the contralateral hemisphere of ischemic rats was more widespread in the brain, except in the rostral parts where blood flow was abolished. This trend refers to reflow originating in the BT 16 and reaching vascular beds slightly more vasodilated after ischemia on the ipsilateral side, as detected here with ultrasound Doppler records.…”

Section: Discussionsupporting

confidence: 67%

“…Ischemia was induced in Wistar P7 rat pups (16 to 18 g; Janvier, Le Genest St-Isle, France) 15 and was adapted to isoflurane anesthesia. 16 Briefly, thermoregulated (37.0 ± 0.51C) and anesthetized pups (1% isoflurane in O 2 /N 2 O (1:3)) were exposed to left middle cerebral artery electrocoagulation (MCAo) combined with a transient (50 minutes), concomitant occlusion of both common carotid arteries (CCAs). Carotid blood-flow restoration was assessed by release of the carotid clips.…”

Section: Neonatal Ischemia-reperfusionmentioning

confidence: 99%

“…17 Ultrasound Imaging Thermoregulated rat pups (n ¼ 6) were subjected to ultrasound measurements under isoflurane (0.5% inhalation via a facemask in O 2 /N 2 O (1:3)) anesthesia using an echograph (Vivid 7, GE Medical Systems ultrasound, Horten, Norway) equipped with a 12-MHz linear transducer. 16 Heart rate and time-average mean blood-flow velocities (mBFVs) were measured in both the intracranial carotid arteries (ICAs) and the basilar trunk (BT) before surgery, during ischemia (at 40 minutes) and monitored from 1 to 15 minutes after removal of the CCAo. Heart rates were measured and reflected changes in cardiac output, as left ventricular stroke volume is quite invariable in newborns.…”

Section: Magnetic Resonance Imaging Acquisitionmentioning

confidence: 99%

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Dynamic Spatio-Temporal Imaging of Early Reflow in a Neonatal Rat Stroke Model

Leger

Bonnin

Lacombe

et al. 2012

J Cereb Blood Flow Metab

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The aim of the study was to better understand blood-flow changes in large arteries and microvessels during the first 15 minutes of reflow in a P7 rat model of arterial occlusion. Blood-flow changes were monitored by using ultrasound imaging with sequential Doppler recordings in internal carotid arteries (ICAs) and basilar trunk. Relative cerebral blood flow (rCBF) changes were obtained by using laser speckle Doppler monitoring. Tissue perfusion was measured with [ 14 C]-iodoantipyrine autoradiography. Cerebral energy metabolism was evaluated by mitochondrial oxygen consumption. Gradual increase in mean blood-flow velocities illustrated a gradual perfusion during early reflow in both ICAs. On ischemia, the middle cerebral artery (MCA) territory presented a residual perfusion, whereas the caudal territory remained normally perfused. On reflow, speckle images showed a caudorostral propagation of reperfusion through anastomotic connections, and a reduced perfusion in the MCA territory. Autoradiography highlighted the caudorostral gradient, and persistent perfusion in ventral and medial regions. These blood-flow changes were accompanied by mitochondrial respiration impairment in the ipsilateral cortex. Collectively, these data indicate the presence of a primary collateral pathway through the circle of Willis, providing an immediate diversion of blood flow toward ischemic regions, and secondary efficient cortical anastomoses in the immature rat brain.

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Section: Discussionsupporting

confidence: 67%

Section: Neonatal Ischemia-reperfusionmentioning

confidence: 99%

Section: Magnetic Resonance Imaging Acquisitionmentioning

confidence: 99%

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Dynamic Spatio-Temporal Imaging of Early Reflow in a Neonatal Rat Stroke Model

Leger

Bonnin

Lacombe

et al. 2012

J Cereb Blood Flow Metab

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“…These animals probably developed efficient cortical arterial anastomoses during ischemia as we previously demonstrated by using sonography. 6 MR imaging also allowed excluding no-reflow animals because the absence of recanalization was shown to block the development of further edema. 7 All animals exhibited a quite reproducible time course of ADC or T2 volume.…”

Section: Discussionmentioning

confidence: 99%

Do Early MRI Signals Predict Lesion Size in a Neonatal Stroke Rat Model?

Fau¹,

Po²,

Goyenvalle³

et al. 2012

AJNR Am J Neuroradiol

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SUMMARY:In this study, we compared lesion size by using V ADC and V T2 at 0, 2, 5, 24, and 48 hours and histologic lesions at 48 hours in a P7 rat stroke model. The best correlation between V HISTO and V ADC was at H0, and between V HISTO and V T2 , at H2-H5. Early MR imaging signals allowed excluding "no-lesion" and "no-reflow" animals to help standardize this neonatal stroke model and predict lesion size.ABBREVIATIONS: H0, H2, H5, H24, and H48 ϭ 15 minutes and 2, 5, 24, and 48 hours after reperfusion, respectively; P7 ϭ 7-day-old; RARE ϭ rapid acquisition

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“…7 NO is also involved in several critical processes in the developing brain; indeed, exposure to inhaled NO (iNO) during the first week of postnatal life has recently been shown to play a key role in myelination in the developing brain 8 and to significantly reduce the size of excitotoxic lesions in neonatal rat pups. 9 We recently demonstrated, by using 2-dimensional color-coded pulsed ultrasound imaging, that collateral recruitment or failure during ischemia, as revealed by changes in blood flow velocities in the basilar trunk (BT), determined the extent of the ischemic lesion in P7 rats 10 and was…”

mentioning

confidence: 99%

Inhaled Nitric Oxide Reduces Brain Damage by Collateral Recruitment in a Neonatal Stroke Model

Charriaut‐Marlangue

Bonnin

Gharib

et al. 2012

Stroke

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N eonatal hypoxia-ischemia is a common cause of neonatal brain injury and results in cerebral palsy, learning disabilities, and epilepsy.1 In addition to global cerebral ischemia arising from systemic asphyxia, recent data suggest a higher incidence of focal ischemia-reperfusion leading to stroke in near-term neonates.2 Tissue-type plasminogen activator is the only approved agent capable of improving reperfusion after ischemia in the adult brain. 3 However, no safe neuroprotective molecule is currently available to protect the immature brain.Among vasoactive molecules, nitric oxide (NO) is a small, highly diffusible and reactive molecule produced by the NO synthases and released from endothelial cells 4 and perivascular nitrergic neurons. 5,6 Endogenous NO is widely recognized as an important messenger and effector molecule for vascular tone and tolerance to damage as well as a mediator in a variety of acute and chronic inflammatory systems. 7 NO is also involved in several critical processes in the developing brain; indeed, exposure to inhaled NO (iNO) during the first week of postnatal life has recently been shown to play a key role in myelination in the developing brain 8 and to significantly reduce the size of excitotoxic lesions in neonatal rat pups. 9 We recently demonstrated, by using 2-dimensional color-coded pulsed ultrasound imaging, that collateral recruitment or failure during ischemia, as revealed by changes in blood flow velocities in the basilar trunk (BT), determined the extent of the ischemic lesion in P7 rats 10 and wasBackground and Purpose-We recently demonstrated that endogenous nitric oxide (NO) modulates collateral blood flow in a neonatal stroke model in rats. The inhalation of NO (iNO) has been found to be neuroprotective after ischemic brain damage in adults. Our objective was to examine whether iNO could modify cerebral blood flow during ischemiareperfusion and reduce lesions in the developing brain. Methods-In vivo variations in cortical NO concentrations occurring after 20-ppm iNO exposure were analyzed using the voltammetric method in P7 rat pups. Inhaled NO-mediated blood flow velocities were measured by ultrasound imaging with sequential Doppler recordings in both internal carotid arteries and the basilar trunk under basal conditions and in a neonatal model of ischemia-reperfusion. The hemodynamic effects of iNO (5 to 80 ppm) were correlated with brain injury 48 hours after reperfusion. Results-Inhaled NO (20 ppm) significantly increased NO concentrations in the P7 rat cortex and compensated for the blockade of endogenous NO synthesis under normal conditions. Inhaled NO (20 ppm) during ischemia increased blood flow velocities and significantly reduced lesion volumes by 43% and cellular damage. In contrast, both 80 ppm iNO given during ischemia and 5 or 20 ppm iNO given 30 minutes after reperfusion were detrimental. Blood flow increases in the BT mirror the efficiency of collateral support through the circle of Willis and the opening of cortical arterial anastomoses among anter...

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Impact of intracranial blood-flow redistribution on stroke size during ischemia–reperfusion in 7-day-old rats

Cited by 38 publications

References 40 publications

Dynamic Spatio-Temporal Imaging of Early Reflow in a Neonatal Rat Stroke Model

Dynamic Spatio-Temporal Imaging of Early Reflow in a Neonatal Rat Stroke Model

Do Early MRI Signals Predict Lesion Size in a Neonatal Stroke Rat Model?

Inhaled Nitric Oxide Reduces Brain Damage by Collateral Recruitment in a Neonatal Stroke Model

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