𝔖 Bobbio Scriptorium
✦   LIBER   ✦

The mechanism of cerebral hypoxic-ischemic damage

✍ Scribed by Dr. Avital Schurr; Benjamin M. Rigor

Publisher
John Wiley and Sons
Year
1992
Tongue
English
Weight
879 KB
Volume
2
Category
Article
ISSN
1050-9631

No coin nor oath required. For personal study only.

✦ Synopsis

The four most prominent hypotheses on the cellular processes leading to hypoxic-ischemic neuronal damage or death are (1) the lactacidosis hypothesis, (2) the calcium overload hypothesis, (3) the excitotoxic hypothesis, and (4) the oxygen-free radical hypothesis. The authors comment on the evidence in favor of and against each in an attempt to select the one hypothesis that best explains the mechanism of cerebral hypoxic-ischemic damage while withstanding the scrutiny of scientific testing. A major part of this inquiry is derived from in vitro studies that are suited to mechanistic exploration. l h e y conclude that the calcium overload hypothesis is the best qualified in this respect. It is important to note, however, that some of the other hypothetical mechanisms may play a secondary role in exacerbating neuronal damage by accelerating calcium influx and overload.

📜 SIMILAR VOLUMES

Rat model of perinatal hypoxic-ischemic
Rat model of perinatal hypoxic-ischemic brain damage
✍ R.C. Vannucci; J.R. Connor; D.T. Mauger; C. Palmer; M.B. Smith; J. Towfighi; S.J 📂 Article 📅 1999 🏛 John Wiley and Sons 🌐 English ⚖ 41 KB

To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic brain damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces perm

17β-estradiol protects against hypoxic/i
17β-estradiol protects against hypoxic/ischemic white matter damage in the neonatal rat brain
✍ Bettina Gerstner; Joan Lee; Tara M. DeSilva; Frances E. Jensen; Joseph J. Volpe; 📂 Article 📅 2009 🏛 John Wiley and Sons 🌐 English ⚖ 345 KB

## Abstract Developing oligodendrocytes (pre‐OLs) are highly vulnerable to hypoxic‐ischemic injury and associated excitotoxicity and oxidative stress. 17β‐Estradiol plays an important role in the development and function of the CNS and is neuroprotective. The sudden drop in circulating estrogen aft

Multiple congenital anomalies associated
Multiple congenital anomalies associated with in utero exposure of phenytoin: Possible hypoxic ischemic mechanism?
✍ Helen M. Lyon; Lewis B. Holmes; Taosheng Huang 📂 Article 📅 2003 🏛 John Wiley and Sons 🌐 English ⚖ 150 KB 👁 1 views

## Abstract ## BACKGROUND The characteristics of the phenotype of the malformed phenytoin‐exposed infant can help to clarify the mechanism of the drug's teratogenesis. One postulated mechanism is vascular disruption. ## CASE An infant who was exposed to phenytoin as monotherapy throughout pregna

Temporal and anatomical variations of br
Temporal and anatomical variations of brain water apparent diffusion coefficient in perinatal cerebral hypoxic-ischemic injury: Relationships to cerebral energy metabolism
✍ Dr. John S. Thornton; Roger J. Ordidge; Juliet Penrice; Ernest B. Cady; Philip N 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 838 KB

## Abstract Cerebral apparent diffusion coefficients {ADCs) were determined in nine newborn piglets before and for 48 h after transient hypoxia‐ischemia. Phosphorus MRS revealed severely reduced cerebral energy metabolism during the insult and an apparently complete recovery 2 h after resuscitation