Experimental Cerebral Ischemia: The Contribution of the Bethesda Group
Igor Klatzo started his research on cerebral ischemia at the NIH in the 1960s. The mechanism that produces the blood-brain barrier change after ischemia was a focus of interest in Klatzo’s experiments, which used larger mammals. Studies using Mongolian ge
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Abstract Igor Klatzo started his research on cerebral ischemia at the NIH in the 1960s. The mechanism that produces the blood-brain barrier change after ischemia was a focus of interest in Klatzo’s experiments, which used larger mammals. Studies using Mongolian gerbils, started by U. Ito, resulted in several important findings, including observation of the maturation phenomenon in 1975. Using newly developed ischemia models, the mechanism of postischemic neuronal/tissue injury was extensively studied. The cumulative effect was observed after repetitive cerebral ischemia. The protective mechanism of cortical spreading depression after global ischemia was investigated. Projects including in vitro studies of human brain endothelial cells and mucosal tolerance to E-selectin were performed in the Stroke branch after Klatzo retired from the NIH. Klatzo published a biography of Cecil and Oskar Vogt after retirement. He passed away in May 2007 in Gaithersburg, Maryland a few months after he completed the first part of his autobiography. Keywords Igor Klatzo • experimental cerebral ischemia • NIH Igor Klatzo started his research on cerebral ischemia in the 1960s at the NIH. In the first series of studies, postischemic blood-brain barrier (BBB) changes as well as clinicopathological changes were the foci of interest. The first paper in this series of studies using larger mammals was published in 1970 in the first issue of Stroke journal (2), followed by reports on the ultra-structural changes and hemodynamic aspects of postischemic BBB changes (13). Biphasic opening of the BBB during the postischemic phase was reported in 1985 (10). Research studies using Mongolian gerbils were started with U. Ito in the 1970s. Approximately one third of the gerbils developed ischemic symptoms such as circling hemiparesis and seizure after the occlusion of the unilateral T. Kuroiwa (*) Laboratory of Clinical Medicine, Namegata District General Hospital, 98-8 Inouefujii, Namegata, Ibaraki 311-3516, Japan e-mail: [email protected]
common carotid artery (12). By selecting these symptompositive animals (which will develop infarction), it is possible to have animals with a homogeneous intensity of tissue injury. In this series of investigations, the slow appearance of neuronal necrosis in the H2 (CA1) sector was observed. Shorter ischemic insults resulted in delayed appearances of necrosis (3). Blood-brain barrier disruption was also delayed as a result of milder ischemic insult (4). This facet of the response was named the ‘maturation phenomenon’. Energy failure after a short period ischemia also developed slowly over a few days of postischemia, with a tendency to be delayed in the areas suffering milder ischemic insults (11). In Klatzo’s laboratory, several new animal models of cerebral ischemia have been developed and extensively tested. Studies using these new models of ischemia resulted in many interesting observations; after repetitive ischemic insults, a pronounced cumulative effect on brain edema and tissue injury was observed. T
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