Dynamics of Late Neuronal Changes in Global Cerebral Ischemia

Mossakowski, Mirosław Jan; Zelman, Irmina B.

doi:10.1007/978-3-642-77134-7_8

Maturation Phenomenon in Cerebral Ischemia 1992

DOI: 10.1007/978-3-642-77134-7_8

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Dynamics of Late Neuronal Changes in Global Cerebral Ischemia

Mirosław Jan Mossakowski¹,

Irmina B. Zelman²

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Cited by 4 publications

(1 citation statement)

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“…Morphological study of rat brain after clinical death produced by cardiac arrest revealed changes in neurons in various CNS structures during the early posthypoxic period [13,14]. The general pathogenetic mechanisms of postresuscitation encephalopathies were elucidated [1].…”

mentioning

confidence: 99%

Ca2+ Transport into Sarcoplasmic Reticulum and Immediate-Early Response Proteins in the Myocardium of Rats Resuscitated after Systemic Circulatory Arrest

et al. 2005

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Activity of antioxidant defense enzymes and content of stress protein HSP70 in the heart increased in passive and, to a lesser extent, in active rats on day 7 of the postresuscitation period after systemic circulatory arrest. The resistance of membrane structures in the heart to endogenous damaging factors in passive rats was lower than in active animals. The degree of compensation in active rats was much higher than in passive animals at these terms of the postresuscitation period.

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mentioning

confidence: 99%

Ca2+ Transport into Sarcoplasmic Reticulum and Immediate-Early Response Proteins in the Myocardium of Rats Resuscitated after Systemic Circulatory Arrest

et al. 2005

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Hypertrophic synapses as a factor of formation of persistent pathological centers in the brain in the late postresuscitation period

2000

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Clinical death was modelled on albino rats. Synapses in the molecular layer of the cerebral sensorimotor cortex were investigated 1, 2, 3, 4, 5, 6, 7, 8, and 9 months postresuscitation. The total density of synapses peaked and the number of hypertrophic and perforated contacts increased 4, 7, and 9 months after resuscitation. The role of increased number of hypertrophic and perforated contacts in the pathogenesis of postresuscitation encephalopathy is discussed.

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Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period in rats by means of succinic acid

et al. 1997

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Dynamics of Late Neuronal Changes in Global Cerebral Ischemia

Cited by 4 publications

References 6 publications

Ca2+ Transport into Sarcoplasmic Reticulum and Immediate-Early Response Proteins in the Myocardium of Rats Resuscitated after Systemic Circulatory Arrest

Ca2+ Transport into Sarcoplasmic Reticulum and Immediate-Early Response Proteins in the Myocardium of Rats Resuscitated after Systemic Circulatory Arrest

Hypertrophic synapses as a factor of formation of persistent pathological centers in the brain in the late postresuscitation period

Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period in rats by means of succinic acid

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