Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model: Changes in cyanotic myocardial antioxidant system

Nakanishi, Kōji; Inoue, Masahiro; Sugawara, E; Sano, Shunji

doi:10.1016/s0022-5223(97)70024-2

Cited by 12 publications

(11 citation statements)

References 27 publications

(6 reference statements)

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“…The concentration of O 2 inside the chamber was maintained at 10% by mixing air and nitrogen and was monitored using an oxygen analyzer (Miniox II; Catalyst Research Corporation; Owings Mills, MD). The degree of hypoxia was based on rodent models of CHD [8,34]. Excess humidity from the chamber was eliminated using calcium bisulphate (Drierite; W.A.…”

Section: Induction Of Postnatal Chronic Hypoxiamentioning

confidence: 99%

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

Raman

Tkáč

Ennis

et al. 2005

Developmental Brain Research

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The cognitive deficits observed in children with cyanotic congenital heart disease suggest involvement of the developing hippocampus. Chronic postnatal hypoxia present during infancy in these children may play a role in these impairments. To understand the biochemical mechanisms of hippocampal injury in chronic hypoxia, a neurochemical profile consisting of 15 metabolite concentrations and 2 metabolite ratios in the hippocampus was evaluated in a rat model of chronic postnatal hypoxia using in vivo 1 H NMR spectroscopy at 9.4 T. Chronic hypoxia was induced by continuously exposing rats (n = 23) to 10% O 2 from postnatal day (P) 3 to P28. Fifteen metabolites were quantified from a volume of 9-11 Al centered on the left hippocampus on P14, P21, and P28 and were compared with normoxic controls (n = 14). The developmental trajectory of neurochemicals in chronic hypoxia was similar to that seen in normoxia. However, chronic hypoxia had an effect on the concentrations of the following neurochemicals: aspartate, creatine, phosphocreatine, GABA, glutamate, glutamine, glutathione, myoinositol, N-acetylaspartate (NAA), phosphorylethanolamine, and phosphocreatine/creatine (PCr/Cr) and glutamate/glutamine (Glu/Gln) ratios ( P b 0.001 each, except glutamate, P = 0.04). The increased PCr/Cr ratio is consistent with decreased brain energy consumption. Given the well-established link between excitatory neurotransmission and brain energy metabolism, we postulate that elevated glutamate, Glu/Gln ratio, and GABA indicate suppressed excitatory neurotransmission in an energy-limited environment. Decreased NAA and phosphorylethanolamine suggest reduced neuronal integrity and phospholipid metabolism. The altered hippocampal neurochemistry during its development may underlie some of the cognitive deficits present in human infants at risk of chronic hypoxia. D 2005 Elsevier B.V. All rights reserved.Theme: Other systems of the CNS Topic: Brain metabolism and blood flow

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Section: Induction Of Postnatal Chronic Hypoxiamentioning

confidence: 99%

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

Raman

Tkáč

Ennis

et al. 2005

Developmental Brain Research

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“…The model is characterized by polycythemia due to increased production of erythropoietin, 20 RV hypertrophy, 21 decreased weight gain, and overall failure to thrive. 14 Ohigashi et al reported that nitric oxide and cGMP may interact in modulating hypoxic stimulation of erythropoietin production in exhypoxic polycythemic mice and erythropoietin-producing Hep3B cells. 22 On the preischemia measurement, the coronary fl ow was significantly increased in the hypoxic group relative to that in The postischemia heart rate, LVDP, max dp/dt, and coronary fl ow were calculated as the percent of their respective preischemia values *P < 0.05 the normoxic group.…”

Section: Discussionmentioning

confidence: 99%

“…It was fi ltered through a cellulose acetate membrane (pore size 0.45 μm) to remove any particulate contaminants. 14 Figure 1 shows the schema of the Langendorff apparatus employed in this study.…”

Section: Isolated Perfused Rat Heartmentioning

confidence: 99%

Tolerance of the developing cyanotic heart to ischemia-reperfusion injury in the rat

Fujii

Ishino

Tomii

et al. 2010

Gen Thorac Cardiovasc Surg

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“…23,24 It has also been used as a model for primary pulmonary hypertension. 10 Chronic hypoxia induces suprasystemic RV systolic pressure as a result of high pulmonary vascular resistance and subsequent significant RV hypertrophy.…”

Section: Implications Of the Datamentioning

confidence: 99%

Impact of chronic cyanosis and reoxygenation on the microheterogeneity of the myocardial blood flow: digital radiographic study in neonatal rats

Tomii

Honjo

Matsumoto

et al. 2011

Gen Thorac Cardiovasc Surg

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Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model: Changes in cyanotic myocardial antioxidant system

Abstract: Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.

Cited by 12 publications

References 27 publications

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

Tolerance of the developing cyanotic heart to ischemia-reperfusion injury in the rat

Impact of chronic cyanosis and reoxygenation on the microheterogeneity of the myocardial blood flow: digital radiographic study in neonatal rats

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