The state of systemic circulation, collapsed or preserved defines the need for hyperoxic or normoxic resuscitation in neonatal mice with hypoxia–ischemia

Matsiukevich, Dzmitry; Randis, Tara M.; Utkina-Sosunova, Irina; Polin, Richard A.; Ten, Vadim S.

doi:10.1016/j.resuscitation.2009.11.024

Cited by 23 publications

(16 citation statements)

References 23 publications

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“…The pathophysiology of the brain injury in this model is ischemia-reperfusion [20]. Briefly, mice were anesthetized with isoflurane (2 vol % for induction and 0.8 vol % maintenance) and a permanent ligation of the right carotid artery was made under dissecting microscopy.…”

Section: Methodsmentioning

confidence: 99%

Nelfinavir Inhibits Intra-Mitochondrial Calcium Influx and Protects Brain against Hypoxic-Ischemic Injury in Neonatal Mice

et al. 2013

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Nelfinavir (NLF), an antiretroviral agent, preserves mitochondrial membranes integrity and protects mature brain against ischemic injury in rodents. Our study demonstrates that in neonatal mice NLF significantly limits mitochondrial calcium influx, the event associated with protection of the brain against hypoxic-ischemic insult (HI). Compared to the vehicle-treated mice, cerebral mitochondria from NLF-treated mice exhibited a significantly greater tolerance to the Ca2+-induced membrane permeabilization, greater ADP-phosphorylating activity and reduced cytochrome C release during reperfusion. Pre-treatment with NLF or Ruthenium red (RuR) significantly improved viability of murine hippocampal HT-22 cells, reduced Ca2+ content and preserved membrane potential (Ψm) in mitochondria following oxygen-glucose deprivation (OGD). Following histamine-stimulated Ca2+ release from endoplasmic reticulum, in contrast to the vehicle-treated cells, the cells treated with NLF or RuR also demonstrated reduced Ca2+ content in their mitochondria, the event associated with preserved Ψm. Because RuR inhibits mitochondrial Ca2+ uniporter, we tested whether the NLF acts via the mechanism similar to the RuR. However, in contrast to the RuR, in the experiment with direct interaction of these agents with mitochondria isolated from naïve mice, the NLF did not alter mitochondrial Ca2+ influx, and did not prevent Ca2+ induced collapse of the Ψm. These data strongly argues against interaction of NLF and mitochondrial Ca2+ uniporter. Although the exact mechanism remains unclear, our study is the first to show that NLF inhibits intramitochondrial Ca2+ flux and protects developing brain against HI-reperfusion injury. This novel action of NLF has important clinical implication, because it targets a fundamental mechanism of post-ischemic cell death: intramitochondrial Ca2+ overload → mitochondrial membrane permeabilization → secondary energy failure.

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Section: Methodsmentioning

confidence: 99%

Nelfinavir Inhibits Intra-Mitochondrial Calcium Influx and Protects Brain against Hypoxic-Ischemic Injury in Neonatal Mice

et al. 2013

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“…[216][217][218][219][220][221][222][223] 222 One demonstrated more rapid restoration of cerebral blood flow but no difference in histologic brain injury scores. 224 For the critical outcome of oxidative injury, we found 10 animal studies reported on oxidative injury with varying results 212,213,216,[219][220][221][222][223][225][226][227] (very-low-quality evidence, downgraded for potential bias, inconsistency, and indirectness). Six studies (pigs/mice) demonstrated no difference in various oxidative injury markers, 212,213,[219][220][221]224 3 (lambs/ rats) demonstrated more oxidative damage from using 100% O 2 including apoptosis, 216,222,226 and a pig study reported less striatal and hippocampal apoptosis with 100% O 2 compared with 21% O 2 .…”

Section: Consensus On Sciencementioning

confidence: 99%

Part 7: Neonatal Resuscitation

Perlman¹,

Wyllie²,

Kattwinkel³

et al. 2015

Pediatrics

237

291

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“…The SaO 2 probe was wrapped around the neck. Changes in CBF during hypoxemia and reoxygenation were recorded using laser Doppler flowmeter (Peliflux 5000, Sweden), as we described (Matsiukevich et al, 2010). In brief, the Doppler probe via 15-20 cm fiberoptic extention was attached with tissue glue to the skull in the projection of the right cortex (2 mm posterior and 3 mm lateral to bregma).…”

Section: Measurements Of Heart Rate Oxygen Saturation and Cerebral Bmentioning

confidence: 99%

Mild intermittent hypoxemia in neonatal mice causes permanent neurofunctional deficit and white matter hypomyelination

Juliano

Sosunov

Niatsetskaya

et al. 2015

Experimental Neurology

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The state of systemic circulation, collapsed or preserved defines the need for hyperoxic or normoxic resuscitation in neonatal mice with hypoxia–ischemia

Abstract: Background-The return of spontaneous circulation (ROSC) is a primary goal of resuscitation. For neonatal resuscitation the International Liaison Committee on Resuscitation (ILCOR) recommends oxygen concentrations ranging from 21% to 100%.

Cited by 23 publications

References 23 publications

Nelfinavir Inhibits Intra-Mitochondrial Calcium Influx and Protects Brain against Hypoxic-Ischemic Injury in Neonatal Mice

Nelfinavir Inhibits Intra-Mitochondrial Calcium Influx and Protects Brain against Hypoxic-Ischemic Injury in Neonatal Mice

Part 7: Neonatal Resuscitation

Mild intermittent hypoxemia in neonatal mice causes permanent neurofunctional deficit and white matter hypomyelination

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