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Nobuyoshi Ogata, Yasuhiro Yonekawa, Waro Taki, Reiji Kannagi, Takashi Murachi, Takao Hamakubo, and Haruhiko Kikuchi

T he brain is vulnerable to ischemia, and neurological recovery is dependent on both the severity and duration of the ischemia. Many experimental results have shown that ischemia of 5 to 15 minutes results in an irreversible change in brain function. 2, 6, 16, 17 Various biochemical aspects of experimental cerebral ischemia have been investigated in a number of animal models; however, no reports have demonstrated clear evidence of irreversible changes at an early phase of ischemia. It is suggested that the influx of Ca ++ into the cytoplasm during ischemia

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Yuji Kinuta, Haruhiko Kikuchi, Masatsune Ishikawa, Mieko Kimura, and Yoshinori Itokawa

I t has been recognized that damage in cerebral ischemia is at least partly due to oxidative damage caused by free radical formation and subsequent lipid peroxidation. 11–13 Free radical damage is assumed to be initiated by increased production of the superoxide anion radical and its by-products, which are generated by several autoxidation reactions and some enzymatic reactions. The abrupt increase in these active oxygen species can be very deleterious because lipids, which are abundant in the brain, are vulnerable to peroxidation. 10, 35 To protect against

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Toshiki Yoshimine, Kazuyoshi Morimoto, Joan M. Brengman, Henry A. Homburger, Heitaro Mogami, and Takehiko Yanagihara

astrocytic reaction. A part of the present investigation has been reported elsewhere in abstract form. 22 Materials and Methods Mongolian gerbils (each 60 gm in body weight) were used for the present study. Under general anesthesia with ether, the right common carotid artery was occluded in the neck with a miniature Mayfield aneurysmal clip. 10, 17 The early manifestation of cerebral ischemia was identified by torsion of the neck and circling, 17 and only the gerbils with typical manifestation were selected. After a predetermined ischemic period, the clip was

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Bo K. Siesjö

I n spite of improvements in the prevention of vascular disease, focal cerebral ischemia still represents a major cause of morbidity and mortality. Focal ischemia encompasses cerebrovascular disease (stroke), subarachnoid hemorrhage (SAH), and trauma. Progress has been made in the pharmacological and surgical treatment of SAH; 65, 106 however, there is at present no adequate therapy for stroke and, until very recently, experimental work gave few useful hints. The situation has now changed since exploration of pathophysiological events has prepared the ground

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Kenichi Kono and Tomoaki Terada

treatment of CPA with cerebral ischemia. 4 , 12 We report the first case of adult CPA with cerebral ischemia successfully treated by encephaloduroarteriosynangiosis (EDAS). Case Report History, Examination, and Initial Treatment A 28-year-old man presented with epilepsy in 2008. The patient suffered from simple partial seizures with jerking of the left upper and lower extremities for 1–10 minutes. An electroencephalogram obtained at nonepileptic status showed 9- to 10-Hz waves, no spikes, and no epileptic discharge. On MRI, contrast-enhanced CT, and

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Seppo Juvela

A neurysmal subarachnoid hemorrhage (SAH) is a serious disease with a high mortality rate (40% to 50%) and high morbidity, in spite of recent improvements in surgical and medical treatments. 6, 15, 23 Delayed cerebral ischemia, commonly attributed to vasospasm in large cerebral arteries, is the major cause of death and disability after the primary hemorrhage. 4, 13, 15, 23 The pathogenesis of cerebral vasospasm and delayed ischemia after SAH is unclear and seems to be multifactorial. 4, 26 Therefore, treatment outcome is often unsatisfactory, although the

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Microregional blood flow changes in experimental cerebral ischemia

Effects of arterial carbon dioxide studied by fluorescein angiography and xenon133 clearance

Y. Lucas Yamamoto, Kathryne M. Phillips, Charles P. Hodge, and William Feindel

arterial pCO 2 . 2, 3, 25, 33, 35, 38 In experimental investigations, one of the difficulties in arriving at a satisfactory answer to this particular question stems from the fact that focal cerebral ischemia established by experimental occlusion of the middle cerebral artery is known to produce a zone of cerebral damage which varies in size and severity as judged by histological examination of the fixed brain. 16, 19, 30, 33 Although visual, chemical, and electrographic changes can indicate to some extent the degree of the decrease in cerebral blood flow in the

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Kathleen L. Meyer, Robert J. Dempsey, Mark W. Roy, and David L. Donaldson

E xperimental cerebral ischemia alters central nervous system (CNS) function and leads to infarction. While most studies of ischemia rely on evaluation of the size and distribution of the resulting infarct, in this study we evaluated somatosensory evoked potentials (SEP's) as a means of measuring neurophysiological function in the remaining viable brain during ischemia. The SEP peaks in man and animals are presumed to be generated by specific CNS structures. 1, 3, 7, 11 Evoked potential components that are consistently identifiable, and their presumed

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W. Scott Haddon, Donald S. Prough, Daniel Kong, and Patricia Petrozza

O nly 30% of patients hemodynamically resuscitated from in-hospital cardiac arrest (and the associated global cerebral ischemia) are ultimately discharged from the hospital without significant neurological deficit. 1 Following global cerebral ischemia, animals undergo a short period of relative cerebral hyperperfusion followed by prolonged severe cerebral hypoperfusion. 20 This sustained decrease in cerebral blood flow (CBF) after global cerebral ischemia has been implicated in the progression of neurological deficits following resuscitation. 18 Loss of

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Delbert E. Evans, Philip W. Catron, James J. McDermott, Linda B. Thomas, Arthur I. Kobrine, and Edward T. Flynn

C erebral air embolism in the cat has been used to study the pathophysiology of acute cerebral ischemia. 17–22 Although clinical cases of cerebral air embolism are not common, such cases can occur in individuals during deep-sea diving and in others exposed to increased atmospheric pressure. 10, 11, 15 Cerebral air embolism has been reported during surgery and other invasive procedures when air gains entrance into the systemic circulation. 7, 12, 41 Air embolism has also been used in animals as a model of acute stroke. In comparing the pathophysiology