Neuronal damage in rat brain and spinal cord after cardiac arrest and massive hemorrhagic shock*

Kudo, Yoshifumi; Ohtaki, Hirokazu; Dohi, Kenji; Yin, Li; Nakamachi, Tomoya; Endo, S.; Yofu, Sachiko; Hiraizumi, Yutaka; Miyaoka, Hiroaki; Shioda, Seiji

doi:10.1097/01.ccm.0000242522.48734.64

Cited by 33 publications

(21 citation statements)

References 36 publications

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“…Our results point out that maintenance of cortical CBF is essential in managing the bleeding patient to improve neurological outcome [6,7,9]. Moreover, our results emphasize that oxygen supply after hemorrhage may protect the brain from hypoxia as ventilation with 100% oxygen during controlled hypovolemia maintained oxygen saturation of the blood.…”

Section: Discussionmentioning

confidence: 55%

“…The sub-population most at risk for severe trauma and hemorrhage are people under 45 years [1]. The long-term functional outcome is largely determined by the degree of brain damage resulting from shock-associated cerebral hypoperfusion [6,7]. Although redistribution mechanisms maintain cerebral perfusion constant over a wide range of reduced blood pressures [8], this centralization of the circulation under shock conditions does not effectively prevent from cerebral injury [9].…”

Section: Introductionmentioning

confidence: 99%

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Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling

Schiffner

Bischoff

Rakers

et al. 2017

IJMS

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Background: Maintenance of brain circulation during shock is sufficient to prevent subcortical injury but the cerebral cortex is not spared. This suggests area-specific regulation of cerebral blood flow (CBF) during hemorrhage. Methods: Cortical and subcortical CBF were continuously measured during blood loss (≤50%) and subsequent reperfusion using laser Doppler flowmetry. Blood gases, mean arterial blood pressure (MABP), heart rate and renal blood flow were also monitored. Urapidil was used for α1A-adrenergic receptor blockade in dosages, which did not modify the MABP-response to blood loss. Western blot and quantitative reverse transcription polymerase chain reactions were used to determine adrenergic receptor expression in brain arterioles. Results: During hypovolemia subcortical CBF was maintained at 81 ± 6% of baseline, whereas cortical CBF decreased to 40 ± 4% (p < 0.001). Reperfusion led to peak CBFs of about 70% above baseline in both brain regions. α1A-Adrenergic blockade massively reduced subcortical CBF during hemorrhage and reperfusion, and prevented hyperperfusion during reperfusion in the cortex. α1A-mRNA expression was significantly higher in the cortex, whereas α1D-mRNA expression was higher in the subcortex (p < 0.001). Conclusions: α1-Adrenergic receptors are critical for perfusion redistribution: activity of the α1A-receptor subtype is a prerequisite for redistribution of CBF, whereas the α1D-receptor subtype may determine the magnitude of redistribution responses.

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Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling

Schiffner

Bischoff

Rakers

et al. 2017

IJMS

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“…Animals experiencing 12 minutes of hemorrhagic shock followed by 5 minutes of cardiac arrest showed severe neuronal damage in the Cornu Ammonis field CA1 region of the hippocampus, severe hind-limb paralysis and neuronal damage in the lumbar spinal cord 6 hours to 7 days after resuscitation [55]. In view of the results of this experiment, it was suggested that hind-limb paralysis after global ischemia might result from spinal cord damage.…”

Section: Sequels and Delayed Neuronal Cell Damage Following Cardiac Amentioning

confidence: 70%

“…Though it is not known whether oseltamivir causes this type of sequels, I believe that the clinical courses of these three cases are compatible with that of the neurological sequels following global ischemia [3,22,55]. However various other disorders such as acute disseminated encephalomyelitis (ADEM) [23,31], Rett syndrome [71,93] and various causes of apparent life threatening events (ALTE) in infants [61] should be differentiated as a cause.…”

Section: Sequels and Delayed Neuronal Cell Damage Following Cardiac Amentioning

confidence: 99%

“…A wide spectrum of neurological sequels may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes characterized by amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke [3] including paraplegia [22] or lower-limb paralysis [55].…”

Section: Sequels and Delayed Neuronal Cell Damage Following Cardiac Amentioning

confidence: 99%

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Fatal neuropsychiatric adverse reactions to oseltamivir: Case series and overview of causal relationships

Hama¹

2008

International Journal of Risk and Safety in Medicine

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Background: Infection-associated encephalopathies such as Reye's syndrome have been one of the major public health problems in many countries. The not dissimilar neuropsychiatric adverse reactions, including deaths, observed with Tamiflu (oseltamivir phosphate: OP) have been another current problem especially in Japan.Methods: Among the cases with neuropsychiatric adverse reactions to Tamiflu on which I was consulted, those cases in which medical charts, autopsy records and/or prescription certificates were available were analyzed and described. In order to obtain a complete view of the spectrum of neuropsychiatric adverse reactions attributed to Tamiflu and of existing knowledge of the causal relationship, adverse reaction case reports and accounts of personal experiences were collected using PubMed, Japonica Centra Revuo Medicina, the websites of MHLW, PMDA and FDA and other Internet sources. Information on animal toxicity and clinical trial findings was derived from the texts of the officially approved data sheet for Tamiflu.Results and discussion: This paper reports eight cases in total: five of these died and three survived. Two died as a result of accidents resulting from abnormal behaviour. Three others died suddenly during sleep (two infants and one adult). One of the infants and the adult were found at autopsy to have severe lung oedema. A 14-year-old boy experienced agitation, cyanosis, loss of consciousness and seizures but recovered completely, while a 10-month-old girl showed retarded development and mental retardation after initially appearing to recover from the acute event involving loss of consciousness and seizure. A 15-year-old boy had a delayed onset of complications but developed prolonged neuropsychiatric adverse reactions after taking an almost complete course of Tamiflu; in this case the symptoms lasted for two weeks.Following our review of known clinical cases of this type, which included 80 fatalities (among them 50 instances of sudden death and 8 cases of accidental death consequential upon abnormal behaviour, and in the light of our study of animal experiments and the latest laboratory findings, we propose to classify adverse reactions to Tamiflu as follows:(1) Sudden onset adverse reactions typically occurring after taking one or two doses of Tamiflu; these result from the central nervous system suppressant action of oseltamivir, a pro-drug of oseltamivir carboxylate (OCB: an active metabolite). The group includes cases of sudden death during sleep or associated with respiratory suppression, sudden onset of abnormal behaviour and occurrence of other neuropsychiatric disorders having an acute onset but a short duration.(2) Delayed onset adverse reactions occurring after taking several doses or a full course of Tamiflu, probably caused by OCB. Examples include delayed onset neuropsychiatric reactions with prolonged duration, pneumonia, sepsis, bleeding and hyperglycemia.(3) Allergic and miscellaneous reactions involving various organs. The mechanisms underlying the adverse reactions to ...

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Ultrastructural Study on the Demyelination of the White Matter in the Rat Spinal Cord after Cardiac Arrest and Massive Hemorrhagic Shock

Yin

Kudo

Ohtaki

et al.

Breathing, Feeding, and Neuroprotection

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Neuronal damage in rat brain and spinal cord after cardiac arrest and massive hemorrhagic shock*

Cited by 33 publications

References 36 publications

Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling

Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling

Fatal neuropsychiatric adverse reactions to oseltamivir: Case series and overview of causal relationships

Ultrastructural Study on the Demyelination of the White Matter in the Rat Spinal Cord after Cardiac Arrest and Massive Hemorrhagic Shock

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