The Keio journal of medicine
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Biography Historical Article
A brief review of Dr F Gotoh's contribution to neuroscience: research in the field of cerebral blood flow and stroke.
Professor Emeritus Fumio Gotoh began and continues his remarkable career in medicine at Keio University. Since his graduation from medical school there in 1951, Dr. Gotoh has devoted himself to neurology, especially in the enigmatic field of stroke science. ⋯ In conjunction with leading authorities, he developed a quantifiable, evidence-based stroke scale which was introduced in the International Journal of Stroke in 2001. Today despite his retirement, Dr. Gotoh continues his work in cerebral blood flow and metabolism.
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The authors examined the correlations between cerebral blood flow (CBF) during the stage of vasospasm following subarachnoid hemorrhage and four parameters, namely, cardiac output (cardiac index), mean arterial blood pressure, age, and the Glasgow coma scale score. Forty-two patients who were diagnosed to have subarachnoid hemorrhage were included in this study, and 50 measurements were performed between day 5 and 12 following the subarachnoid hemorrhage. The CBF was measured by stable xenon-enhanced CT and the mean values of four CBF maps were corrected for a PaCO2 of 34 mm Hg (CBF34). ⋯ Furthermore, we measured the CBF and cerebral perfusion pressure before and after increasing cardiac output in three patients during the stage of vasospasm. The CBF increased by 22.5% +/- 2.9 (SD), with a 42.0% +/- 16.4 increase in the cardiac index, however, no significant change in cerebral perfusion pressure was observed. Therefore, the increase in CBF associated with the increase in cardiac output seems to be attributable to a reduction in the cerebrovascular resistance.
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In 14 patients with severe head injury, the cerebral blood flow (CBF) during mild hypothermia therapy was measured. Their Glasgow Coma Scale scores on admission were 8 or less and the intracranial pressures were greater than 20 mmHg despite conventional therapy. The CBF was measured with two-level stable xenon CT techniques. ⋯ The values of mean CBF and CMRO2 of each group were 25.6 +/- 6.6 vs 24.4 +/- 6.4 ml/100 g/min and 1.26 +/- 0.45 vs 0.79 +/- 0.31 ml/100 g/ml, respectively. There were no statistically significant differences between both groups. Single CBF measurement during this therapy may not be helpful as a factor of prognosis evaluation in patients with severe head injury.
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Based on the concept of the systemic inflammatory response syndrome (SIRS), a one-year retrospective study was carried out among a total of 2389 patients transported to the emergency room by ambulance. With respect to 351 patients who had all data necessary for evaluating SIRS criteria in 369 hospitalized patients, 200 met SIRS criteria within 24 hours of admission (24h-SIRS). The mortality rate for 24h-SIRS patients was significantly higher than that of non-SIRS patients. ⋯ Among 153 patients who had all data necessary for APACHEIII scoring within 24 hours of admission, the mortality rate for SIRS patients whose APACHEIII score was 50 or higher was 40.7%, significantly higher than that of other patients. In conclusion, SIRS criteria were demonstrated to be useful as indicators of severity and for predicting outcome in patients hospitalized through emergency services. Patients who met the following criteria were found to be a high-risk population among hospitalized emergency patients with SIRS: (1) Those who had three or more consecutive days of SIRS. (2) Those whose APACHEIII score was 50 or higher.
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A major mechanism by which the heart adapts to intracellular acidosis during ischemia and recovers from the acidosis after reperfusion is through the sodium-hydrogen exchanger (NHE). There are at least 5 NHE isoforms thus-far identified with the NHE-1 subtype representing the major one found in the mammalian myocardium. This 110 kDa glycoprotein extrudes protons concomitantly with Na influx in a 1:1 stoichiometric relationship rendering the process electroneutral. ⋯ In this regard, we have demonstrated that NHE inhibitors can effectively attenuate the cardiac injury produced by lysophosphatidylcholine and hydrogen peroxide. In addition, it now appears that NHE inhibition reduces apoptosis in the ischemic myocardium, a process which may be of importance in the subsequent development of postinfarction heart failure. In conclusion, NHE represents an important adaptive process in response to intracellular acidosis resulting in a paradoxical contribution to cardiac tissue injury.