Cerebral blood flow response to a hypoxic-ischemic insult differs in neonatal and juvenile rats

Qiao, Min; Latta, Peter; Foniok, Tadeusz; Buist, Richard; Meng, Shu; Tomanek, Bogusław; Tuor, Ursula I.

doi:10.1007/s10334-004-0058-4

Cited by 18 publications

(21 citation statements)

References 34 publications

(52 reference statements)

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“…Previously, we measured CBF changes in cortex within 24 h following a moderately severe hypoxic-ischemic insult in neonatal rats and demonstrated a return of CBF in parietal cortex toward normal by 24 h after hypoxia-ischemia (25). In contrast, in the present study, CBF in the ipsilateral white matter tended to be reduced at 1 h after hypoxia-ischemia, decreasing further at 24 and 48 h after hypoxia-ischemia.…”

Section: Mri Of Ischemic White Matter Injurycontrasting

confidence: 77%

Evolution of Magnetic Resonance Imaging Changes Associated with Cerebral Hypoxia-Ischemia and a Relatively Selective White Matter Injury in Neonatal Rats

et al. 2006

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ABSTRACT:We hypothesized that a combination of quantitative magnetic resonance imaging (MRI) sequences would detect a differential evolution of hypoxic-ischemic changes in white matter compared with gray matter in a recently developed model of unilateral mild cerebral hypoxia-ischemia in the 7-d-old rat. Using this model, which involved unilateral carotid artery occlusion and exposure to hypoxia for 45-50 min, maps of apparent diffusion coefficients of water (ADC), T 1 , T 2 , and cerebral blood flow (CBF) were acquired either before hypoxia-ischemia or at 1, 24, or 48 h and at 7 d post-hypoxia-ischemia followed by brain processing for histology. At 1 h post-hypoxia-ischemia, MRI changes in white matter ipsilateral to the hypoxia-ischemia were not as pronounced as those in gray matter. However, increases in T 1 , T 2 and ADC and decreases in CBF within white matter enhanced over time, with changes being maximal at 48 h post-hypoxia-ischemia, whereas changes in the cortical gray matter normalized over this time. By 7 d post-hypoxia-ischemia, there were no differences in ADC, T 1 , T 2 , or CBF between hemispheres despite there being histologic changes in white matter within the hypoxic-ischemic hemisphere including increased glial proliferation and reactivity, reduced myelin basic protein, and increased cell death. The results demonstrate that increases in ADC and T 2 observed subacutely in the days following hypoxia-ischemia are associated with rather selective white matter damage and suggest that diffuse white matter hyperintensities and increased ADC reported in infants are transient MRI changes post-hypoxia-ischemia. I mprovements in neonatal medicine have been accompanied by an increase in the survival of small premature infants, with substantial numbers having adverse neurologic sequelae related to cerebral white matter injury (1-3). Although the pathogenesis may be uncertain, such brain injury can be a result of hypoxic-ischemic damage to the white matter consisting of focal cystic lesions deep in the periventricular white matter or a more diffuse noncystic white matter injury. Diagnosis of such white matter injury at an early acute stage is necessary for developing optimal clinical management and treatment strategies.Despite MRI techniques gaining acceptance for their evaluation of cerebral hypoxic-ischemic injury in neonates, information on the acute hypoxic-ischemic MRI changes and their evolution in immature white matter compared with gray matter remains limited (3-8). In general, MRI studies have shown that diffusion weighted imaging (DWI) is able to detect acute changes in the cerebral white matter of preterm infants where these changes are often not demonstrated on conventional MRI, i.e. T 1 or T 2 (5,9). In addition, more recent studies in term infants with hypoxic-ischemic encephalopathy show that the ADC of water is decreased in severely damaged white matter within the first week after birth and then tends to increase after the first week (7,8,10).Our recent study in neonatal rats has demonstrate...

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Section: Mri Of Ischemic White Matter Injurycontrasting

confidence: 77%

Evolution of Magnetic Resonance Imaging Changes Associated with Cerebral Hypoxia-Ischemia and a Relatively Selective White Matter Injury in Neonatal Rats

et al. 2006

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“…The contralateral hemisphere also exhibited a small (~5%) yet significant decrease in CBF i on average. Other investigators have observed similar reductions in flow after ligation in neonatal and adult rats [26–28]. We highlight that although CBF i was reduced, it is most likely still above critical levels needed for metabolic demand, given that carotid ligation alone does not produce cell damage in neonatal rats [29].…”

Section: Discussionsupporting

confidence: 60%

In vivo Monitoring of Cerebral Hemodynamics in the Immature Rat: Effects of Hypoxia-Ischemia and Hypothermia

et al. 2015

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Background: Neonatal hypoxic-ischemic (HI) encephalopathy occurs in 1-4 per 1,000 live term births and can cause devastating neurodevelopmental disabilities. Currently, therapeutic hypothermia (TH) is the only treatment with proven efficacy. Since TH is associated with decreased cerebral metabolism and cerebral blood flow (CBF), it is important to assess CBF at the bedside. Diffuse correlation spectroscopy (DCS) has emerged as a promising optical modality to noninvasively assess an index of CBF (CBF_i) in both humans and animals. In this initial descriptive study, we employ DCS to monitor the evolution of CBF_i following HI with or without TH in immature rats. We investigate potential relationships between CBF and subsequent cerebral damage. Methods: HI was induced on postnatal day 10 or 11 rat pups by right common carotid artery ligation followed by 60-70 min hypoxia (8% oxygen). After HI, the pups recovered for 4 h under hypothermia (HI-TH group, n = 23) or normothermia (HI-N group, n = 23). Bilateral measurements of hemispheric CBF_i were made with DCS in unanesthetized animals at baseline, before HI, and 0, 1, 2, 3, 4, 5, and 24 h after HI. The animals were sacrificed at either 1 or 4 weeks, and brain injury was scored on an ordinal scale of 0-5 (0 = no injury). Results: Carotid ligation caused moderate bilateral decreases in CBF_i. Following HI, an initial hyperemia was observed that was more prominent in the contralateral hemisphere. After initiation of TH, CBF_i dropped significantly below baseline levels and remained reduced for the duration of TH. In contrast, CBF_i in the HI-N group was not significantly decreased from baseline levels. Reductions in CBF_i after 4 h of TH were not associated with reduced damage at 1 or 4 weeks. However, elevated ipsilateral CBF_i and ipsilateral-to-contralateral CBF_i ratios at 24 h were associated with worse outcome at 1 week after HI. Conclusions: Both HI and TH alter CBF_i, with significant differences in CBF_i between hypothermic and normothermic groups after HI. CBF_i may be a useful biomarker of subsequent cerebral damage.

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“…This hyperemia could be related to the great vasodilation of the local vascular network because collateral recruitment in adult was only effective after a few hours [23], [24]. In contrast, we did not find evidence of such hyperemia at early re-flow in our rat pups, in agreement with data showing that the CBF responses to hypoxia-ischemia and reperfusion differ depending on postnatal age, with hyperemia in juvenile but not neonatal rats [25]. Probably this is a reflection of a smaller vasodilation magnitude in pups consecutive to the very early (within 10 min) effective collateral recruitment during ischemia [12] as compared to adults, and its maintenance during early re-flow.…”

Section: Discussionsupporting

confidence: 87%

Ischemic Postconditioning Fails to Protect against Neonatal Cerebral Stroke

et al. 2012

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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.

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Cerebral blood flow response to a hypoxic-ischemic insult differs in neonatal and juvenile rats

Cited by 18 publications

References 34 publications

Evolution of Magnetic Resonance Imaging Changes Associated with Cerebral Hypoxia-Ischemia and a Relatively Selective White Matter Injury in Neonatal Rats

Evolution of Magnetic Resonance Imaging Changes Associated with Cerebral Hypoxia-Ischemia and a Relatively Selective White Matter Injury in Neonatal Rats

In vivo Monitoring of Cerebral Hemodynamics in the Immature Rat: Effects of Hypoxia-Ischemia and Hypothermia

Ischemic Postconditioning Fails to Protect against Neonatal Cerebral Stroke

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