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Raul Busto - One of the best experts on this subject based on the ideXlab platform.
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detection of free radical activity during transient global ischemia and recirculation effects of intraischemic Brain Temperature modulation
Journal of Neurochemistry, 2002Co-Authors: Mordecai Y T Globus, Raul Busto, Baowan Lin, Holger Schnippering, Myron D GinsbergAbstract:: To obtain direct evidence of oxygen radical activity in the course of cerebral ischemia under different intraischemic Temperatures, we used a method based on the chemical trapping of hydroxyl radical in the form of the stable adducts 2,3- and 2,5-dihydroxybenzoic acid (DHBA) following salicylate administration. Wistar rats were subjected to 20 min of global foreBrain ischemia by two-vessel occlusion plus systemic hypotension (50 mm Hg). Intraischemic striatal Temperature was maintained as normothermic (37°C), hypothermic (30°C), or hyperthermic (39°C) but was held at 37°C before and following ischemia. Salicylate was administered either systemically (200 mg/kg, i.p.) or by continuous infusion (5 mM) through a microdialysis probe implanted in the striatum. Striatal extracellular fluid was sampled at regular intervals before, during, and after ischemia, and levels of 2,3- and 2,5-DHBA were assayed by HPLC with electrochemical detection. Following systemic administration of salicylate, stable baseline levels of 2,3- and 2,5-DHBA were observed before ischemia. During 20 min of normothermic ischemia, a 50% reduction in mean levels of both DHBAs was documented, suggesting a baseline level of hydroxyl radical that was diminished during ischemia, presumably owing to oxygen restriction to tissue at that time. During recirculation, 2,3- and 2,5-DHBA levels increased by 2.5- and 2.8-fold, respectively. Levels of 2,3-DHBA remained elevated during 1 h of reperfusion, whereas the increase in 2,5-DHBA levels persisted for 2 h. The increases in 2,3- and 2,5-DHBA levels observed following hyperthermic ischemia were significantly higher (3.8- and fivefold, respectively). In contrast, no significant changes in DHBA levels were observed following hypothermic ischemia. The postischemic changes in DHBA content observed following local administration of salicylate were comparable to the results obtained with systemic administration, thus confirming that the hydroxyl radicals arose within Brain parenchyma itself. These results provide evidence that hydroxyl radical levels are increased during postischemic recirculation, and this process is modulated by intraischemic Brain Temperature. Hence, these data suggest a possible mechanism for the effects of Temperature on ischemic outcome and support a key role for free radical-induced injury in the development of ischemic damage.
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combating hyperthermia in acute stroke a significant clinical concern
Stroke, 1998Co-Authors: Myron D Ginsberg, Raul BustoAbstract:Background—Moderate elevations of Brain Temperature, when present during or after ischemia or trauma, may markedly worsen the resulting injury. We review these provocative findings, which form the ...
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the significance of Brain Temperature in focal cerebral ischemia histopathological consequences of middle cerebral artery occlusion in the rat
Journal of Cerebral Blood Flow and Metabolism, 1992Co-Authors: Eiharu Morikawa, Myron D Ginsberg, Dalton W Dietrich, Robert C Duncan, Susan Kraydieh, Mordecai Y T Globus, Raul BustoAbstract:The purpose of this study was to determine the effect of selective modulation of Brain Temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague–Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of Brain-Temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36°C × 4 h), (b) permanent MCA occlusion alone (30, 36, or 39°C × 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39°C × 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser–Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36°C groups. In rat...
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the significance of Brain Temperature in focal cerebral ischemia histopathological consequences of middle cerebral artery occlusion in the rat
Journal of Cerebral Blood Flow and Metabolism, 1992Co-Authors: Eiharu Morikawa, Myron D Ginsberg, Robert C Duncan, Susan Kraydieh, Mordecai Y T Globus, W D Dietrich, Raul BustoAbstract:The purpose of this study was to determine the effect of selective modulation of Brain Temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague-Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of Brain-Temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36 degrees C x 4 h), (b) permanent MCA occlusion alone (30, 36, or 39 degrees C x 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39 degrees C x 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser-Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36 degrees C groups. In rats with permanent MCA occlusion without hypotension, significant differences in infarct volume were again not demonstrable, but an interaction between infarct area and Temperature class was shown by repeated-measures analysis, indicating that hypothermia altered the topographic pattern of the cortical infarct. With 2 h of reversible MCA occlusion, there was a statistically significant reduction in infarct volume in the 30 degrees C group compared to 39 degrees C rats. Although intra- and postischemic CBF were not significantly different among the three Temperature groups, the cortical infarct volume was positively correlated with postischemic CBF. The postischemic CBF, in turn, was positively correlated to the intraischemic Brain Temperature and was negatively correlated to CBF during the ischemic period. These findings demonstrate that moderate manipulations of Brain Temperature have a greater influence on the resulting cortical infarction in the setting of transient focal ischemia than in the context of permanent vascular occlusion.
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therapeutic modulation of Brain Temperature relevance to ischemic Brain injury
Cerebrovascular and brain metabolism reviews, 1992Co-Authors: Linda L Sternau, Mordecai Y T Globus, W D Dietrich, Raul BustoAbstract:Hypothermia was first applied therapeutically as a local anesthetic and later was used to achieve organ protection during procedures necessitating circulatory interruption. Profound whole-body hypothermia, typically carried out in conjunction with extracorporeal bypass, has long been employed during cardiac and neurosurgical operative procedures. More recently, studies in small-animal experimental models of cerebral ischemia have provided persuasive evidence that even small decreases in Brain Temperature confer striking protection against ischemic neuronal injury. By contrast, small elevations of Brain Temperature during ischemia accelerate and extend pathologic changes in the Brain and promote early disruption of the blood-Brain barrier. Hypothermia retards the rate of high-energy phosphate depletion during ischemia and promotes postischemic metabolic recovery. More importantly, mild intraischemic hypothermia markedly attenuates the release of glutamate into the Brain's extracellular space and significantly diminishes the release of dopamine. Similarly, the inhibition of calcium-calmodulin-dependent protein kinase II triggered by normothermic ischemia is prevented by hypothermia, as is the ischemia-induced translocation and inhibition of the key regulatory enzyme protein kinase C. Hypothermia also appears to facilitate the resynthesis of ubiquitin following ischemia. Studies of potential clinical importance have shown that moderate hypothermia is capable of attenuating ischemic damage even if instituted early in the postischemic period. In the setting of focal cerebral ischemia, moderate Brain hypothermia reduces the infarct size (particularly in the setting of reversible middle cerebral artery occlusion); conversely, hyperthermia markedly increases the infarct volume. These studies underscore the importance of monitoring and regulating the Brain Temperature during experimental studies of cerebral ischemia to insure a consistent pathologic outcome and to avoid the false attribution of "pharmacoprotection" to drugs that reduce the body Temperature. The measurement of Brain Temperature is now practicable in neurosurgical patients requiring invasive monitoring, and human studies have shown that cortical and cerebroventricular Temperatures may exceed systemic Temperatures. Mild to moderate decreases in Brain Temperature are neuroprotective in cerebral ischemia, while mild elevations of Brain Temperature are markedly deleterious in the setting of ischemia or injury. It is anticipated that controlled clinical trials of therapeutic Brain Temperature modulation will be undertaken over the next several years.
Charmaine Childs - One of the best experts on this subject based on the ideXlab platform.
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report of a consensus meeting on human Brain Temperature after severe traumatic Brain injury its measurement and management during pyrexia
Frontiers in Neurology, 2010Co-Authors: Charmaine Childs, Bridget Harris, Tadeusz Wieloch, Fiona Lecky, G Machin, Nino StocchettiAbstract:Temperature disturbances are common in patients with severe traumatic Brain injury. The possibility of an adaptive, potentially beneficial role for fever in patients with severe Brain trauma has been dismissed, but without good justification. Fever might, in some patients, confer benefit. A cadre of clinicians and scientists met to debate the clinically relevant, but often controversial issue about whether raised Brain Temperature after human traumatic Brain injury (TBI) should be regarded as “good or bad” for outcome. The objective was to produce a consensus document of views about current Temperature measurement and pyrexia treatment. Lectures were delivered by invited speakers with National and International publication track records in thermoregulation, neuroscience, epidemiology, measurement standards and neurocritical care. Summaries of the lectures and workshop discussions were produced from transcriptions of the lectures and workshop discussions. At the close of meeting, there was agreement on four key issues relevant to modern Temperature measurement and management and for undergirding of an evidence-based practice, culminating in a consensus statement. There is no robust scientific data to support the use of hypothermia in patients whose intracranial pressure is controllable using standard therapy. A randomized clinical trial is justified to establish if body cooling for control of pyrexia (to normothermia) vs moderate pyrexia leads to a better patient outcome for TBI patients.
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infra red thermometry the reliability of tympanic and temporal artery readings for predicting Brain Temperature after severe traumatic Brain injury
Critical Care, 2009Co-Authors: Danielle Kirk, Timothy Rainey, Andy Vail, Charmaine ChildsAbstract:Temperature measurement is important during routine neurocritical care especially as differences between Brain and systemic Temperatures have been observed. The purpose of the study was to determine if infra-red temporal artery thermometry provides a better estimate of Brain Temperature than tympanic membrane Temperature for patients with severe traumatic Brain injury. Brain parenchyma, tympanic membrane and temporal artery Temperatures were recorded every 15–30 min for five hours during the first seven days after admission. Twenty patients aged 17–76 years were recruited. Brain and tympanic membrane Temperature differences ranged from -0.8 °C to 2.5 °C (mean 0.9 °C). Brain and temporal artery Temperature differences ranged from -0.7 °C to 1.5 °C (mean 0.3 °C). Tympanic membrane Temperature differed from Brain Temperature by an average of 0.58 °C more than temporal artery Temperature measurements (95% CI 0.31 °C to 0.85 °C, P < 0.0001). At Temperatures within the normal to febrile range, temporal artery Temperature is closer to Brain Temperature than is tympanic membrane Temperature.
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infra red thermometry the reliability of tympanic and temporal artery readings for predicting Brain Temperature after severe traumatic Brain injury
Critical Care, 2009Co-Authors: Danielle Kirk, Timothy Rainey, Andy Vail, Charmaine ChildsAbstract:Introduction Temperature measurement is important during routine neurocritical care especially as differences between Brain and systemic Temperatures have been observed. The purpose of the study was to determine if infra-red temporal artery thermometry provides a better estimate of Brain Temperature than tympanic membrane Temperature for patients with severe traumatic Brain injury.
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human Brain Temperature regulation measurement and relationship with cerebral trauma part 1
British Journal of Neurosurgery, 2008Co-Authors: Charmaine ChildsAbstract:Temperature has a major effect on survival in all animal species. Despite wide variations in climate, organ Temperature is regulated 'tightly' by homeostatic mechanisms controlling heat production and conservation, as well as heat loss. Although less is known about the Temperature of the healthy or injured human Brain, mammalian Brain homeothermy involves interplay between neural metabolic heat production, cerebral blood flow and the Temperature of incoming arterial blood. Recent advances in invasive and non-invasive thermometry have allowed measurement of Brain Temperature to be made in man. In health, small differences only exist between local Brain and body core Temperature. Large (negative) Brain-body Temperature dissociation, observed in some patients after severe Brain damage, does not appear to be a feature of cerebral homeothermy in healthy people. The extent to which changes in Brain Temperature reflect, or 'drive', secondary cerebral pathology remains uncertain in patients with traumatic Brain injury (TBI). Raised Temperature may be due to a regulated readjustment in the hypothalamic 'set-point' in response to inflammation and infection, or it may occur as a consequence of damage to the hypothalamus and/or its pathways. Diagnosis of the mechanism of raised Temperature; fever v. neurogenic hyperthermia (regulated v. unregulated Temperature rise) is difficult to make clinically. Whatever the cause, a 1-2 degrees C rise in Brain or body Temperature, especially when it develops early after injury, is widely regarded as harmful. There is no clear evidence that fever per se leads directly to worsened neurological damage or poor outcome, nor evidence that antipyretic treatments (pharmacological or cold-induced therapies) preserve damaged Brain tissue or result in a better outcome. Part 2 follows part one with a detailed analysis of the evidence for the significance of raised Temperature on outcome after TBI.
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determination of regional Brain Temperature using proton magnetic resonance spectroscopy to assess Brain body Temperature differences in healthy human subjects
Magnetic Resonance in Medicine, 2007Co-Authors: Charmaine Childs, Yrjo Hiltunen, Rishma Vidyasagar, Risto A KauppinenAbstract:Proton magnetic resonance spectroscopy (H-1 MRS) was used to determine Brain Temperature in healthy volunteers. Partially water-suppressed H-1 MRS data sets were acquired at 3T from four different gray matter (GM)/white matter (WM) volumes. Brain Temperatures were determined from the chemical-shift difference between the CH3 of N-acetyl aspartate (NAA) at 2.01 ppm and water. Brain Temperatures in H-1 MRS voxels of 2 x 2 x 2 cm(3) showed no substantial heterogeneity. The volume-averaged Temperature from single-voxel spectroscopy was compared with body Temperatures obtained from the oral cavity, tympanum, and temporal artery regions. The mean Brain parenchyma Temperature was 0.5 degrees C cooler than readings obtained from three extra-Brain sites (P < 0.01). H-1 MRS imaging (MRSI) data were acquired from a slice encompassing the single-voxel volumes to assess the ability of spectroscopic imaging to determine regional Brain Temperature within the imaging slice. Brain Temperature away from the center of the Brain determined by MRSI differed from that obtained by single-voxel MRS in the same Brain region, possibly due to a poor line width (LW) in MRSI. The data are discussed in the light of proposed Brain-body Temperature gradients and the use of H-1 MRSI to monitor Brain Temperature in pathologies, such as Brain trauma.
Ross Bullock - One of the best experts on this subject based on the ideXlab platform.
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the importance of Brain Temperature in patients after severe head injury relationship to intracranial pressure cerebral perfusion pressure cerebral blood flow and outcome
Journal of Neurotrauma, 2002Co-Authors: Jens Soukup, A Zauner, Egon M R Doppenberg, Matthias Menzel, Charlotte Gilman, H F Young, Ross BullockAbstract:Brain Temperature was continuously measured in 58 patients after severe head injury and compared to rectal Temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The Temperature difference between Brain and rectal Temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal Temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean Brain Temperature ranged from 36.9 +/- 0.4 degrees C in the normothermic group to 38.2 +/- 0.5 degrees C in the hyperthermic group, 35.3 +/- 0.5 degrees C in the mild therapeutic hypothermia group, and 34.3 +/- 1.5 degrees C in the hypothermia group without active cooling. The mean DeltaT(br-rect) was positive for patients with a T(br) above 36.0 degrees C (0.0 +/- 0.5 degrees C) and negative for patients during mild therapeutic hypothermia (-0.2 +/- 0.6 degrees C) and also in those with a Brain Temperature below 36 degrees C without active cooling (0.8 +/- -1.4 degrees C) - the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a Brain Temperature between 36.0 degrees C and 37.5 degrees C was 37.8 +/- 14.0 mL/100 g/min. The lowest CBF was measured in patients with a Brain Temperature <36.0 degrees C and a negative Brain-rectal Temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of Brain and rectal Temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the Brain and core Temperature, especially during rapid cooling, strongly supports the use of Brain Temperature measurement if therapeutic hypothermia is considered for head injury care.
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the importance of Brain Temperature in patients after severe head injury relationship to intracranial pressure cerebral perfusion pressure cerebral blood flow and outcome
Journal of Neurotrauma, 2002Co-Authors: Jens Soukup, A Zauner, Egon M R Doppenberg, Matthias Menzel, Charlotte Gilman, H F Young, Ross BullockAbstract:Brain Temperature was continuously measured in 58 patients after severe head injury and compared to rectal Temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The Temperature difference between Brain and rectal Temperature was also calculated. Mild hypothermia (34-36°C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal Temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean Brain Temperature ranged from 36.9 ± 0.4°C in the normothermic group to 38.2 ± 0.5°C in the hyperthermic group, 35.3 ± 0.5°C in the mild therapeutic hypothermia group, and 34.3 ± 1.5°C in the hypothermia group without active cooling. The mean ΔTbr-rect was positive for patients with a Tbr above 36.0°C (0.0 ± 0.5°C) and negative for patients during mild therapeutic hypothermia (-0.2 ± 0.6°C) and also in those with a Brain Temperature below 36°C without active cooling (0.8 ± -1.4°C) - the ...
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relationship between Brain Temperature Brain chemistry and oxygen delivery after severe human head injury the effect of mild hypothermia
Neurological Research, 2002Co-Authors: J Soukup, Egon M R Doppenberg, Charlotte Gilman, Ross Bullock, A Zauner, M Menzel, H F YoungAbstract:We studied Brain Temperature and the effect of mild hypothermia in 58 patients after severe head injury (SHI). Brain tissue oxygen tension (ptiO2), carbon dioxide tension (ptiCO2), tissuie pH (pHti) and Temperature (T.br) were measured using a multiparameter probe. Microdialysis was performed to measure glucose, lactate, glutamate, and aspartate in the extracellular fluid. Mild hypothermia (34 degrees-36 degrees C) was employed in 33 selected patients who had persistent increased intracranial pressure (ICP > 20 mmHg). Mild induced hypothermia decreased Brain oxygen significantly from 33 +/- 24 mmHg to 30 +/- 22 mmHg (p < 0.05). The ptiCO2 (46 +/- 8 mmHg) was also significantly lower during mild hypothermia (40.4 +/- 4.0 mmHg), p < 0.0001). The pHti increased from 7.13 +/- 0.15 to 7.24 +/- 0.10 (p < 0.0001) under hypothermic conditions. Induced hypothermia may protect patients from secondary ischemic events by lowering the critical ptiO2 threshold, reducing anaerobic metabolism, and decreasing the release of excitatory aminoacids. However, patients with spontaneous Brain hypothermia on admission (Tbr < 36.0 degrees C) showed significantly higher levels of glutamate as well as lactate, compared to all other patients, and had a worse outcome. Spontaneous Brain hypothermia carries a poor prognosis, and was characterized by markedly abnormal Brain metabolic indices.
Myron D Ginsberg - One of the best experts on this subject based on the ideXlab platform.
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detection of free radical activity during transient global ischemia and recirculation effects of intraischemic Brain Temperature modulation
Journal of Neurochemistry, 2002Co-Authors: Mordecai Y T Globus, Raul Busto, Baowan Lin, Holger Schnippering, Myron D GinsbergAbstract:: To obtain direct evidence of oxygen radical activity in the course of cerebral ischemia under different intraischemic Temperatures, we used a method based on the chemical trapping of hydroxyl radical in the form of the stable adducts 2,3- and 2,5-dihydroxybenzoic acid (DHBA) following salicylate administration. Wistar rats were subjected to 20 min of global foreBrain ischemia by two-vessel occlusion plus systemic hypotension (50 mm Hg). Intraischemic striatal Temperature was maintained as normothermic (37°C), hypothermic (30°C), or hyperthermic (39°C) but was held at 37°C before and following ischemia. Salicylate was administered either systemically (200 mg/kg, i.p.) or by continuous infusion (5 mM) through a microdialysis probe implanted in the striatum. Striatal extracellular fluid was sampled at regular intervals before, during, and after ischemia, and levels of 2,3- and 2,5-DHBA were assayed by HPLC with electrochemical detection. Following systemic administration of salicylate, stable baseline levels of 2,3- and 2,5-DHBA were observed before ischemia. During 20 min of normothermic ischemia, a 50% reduction in mean levels of both DHBAs was documented, suggesting a baseline level of hydroxyl radical that was diminished during ischemia, presumably owing to oxygen restriction to tissue at that time. During recirculation, 2,3- and 2,5-DHBA levels increased by 2.5- and 2.8-fold, respectively. Levels of 2,3-DHBA remained elevated during 1 h of reperfusion, whereas the increase in 2,5-DHBA levels persisted for 2 h. The increases in 2,3- and 2,5-DHBA levels observed following hyperthermic ischemia were significantly higher (3.8- and fivefold, respectively). In contrast, no significant changes in DHBA levels were observed following hypothermic ischemia. The postischemic changes in DHBA content observed following local administration of salicylate were comparable to the results obtained with systemic administration, thus confirming that the hydroxyl radicals arose within Brain parenchyma itself. These results provide evidence that hydroxyl radical levels are increased during postischemic recirculation, and this process is modulated by intraischemic Brain Temperature. Hence, these data suggest a possible mechanism for the effects of Temperature on ischemic outcome and support a key role for free radical-induced injury in the development of ischemic damage.
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combating hyperthermia in acute stroke a significant clinical concern
Stroke, 1998Co-Authors: Myron D Ginsberg, Raul BustoAbstract:Background—Moderate elevations of Brain Temperature, when present during or after ischemia or trauma, may markedly worsen the resulting injury. We review these provocative findings, which form the ...
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the significance of Brain Temperature in focal cerebral ischemia histopathological consequences of middle cerebral artery occlusion in the rat
Journal of Cerebral Blood Flow and Metabolism, 1992Co-Authors: Eiharu Morikawa, Myron D Ginsberg, Dalton W Dietrich, Robert C Duncan, Susan Kraydieh, Mordecai Y T Globus, Raul BustoAbstract:The purpose of this study was to determine the effect of selective modulation of Brain Temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague–Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of Brain-Temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36°C × 4 h), (b) permanent MCA occlusion alone (30, 36, or 39°C × 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39°C × 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser–Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36°C groups. In rat...
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the significance of Brain Temperature in focal cerebral ischemia histopathological consequences of middle cerebral artery occlusion in the rat
Journal of Cerebral Blood Flow and Metabolism, 1992Co-Authors: Eiharu Morikawa, Myron D Ginsberg, Robert C Duncan, Susan Kraydieh, Mordecai Y T Globus, W D Dietrich, Raul BustoAbstract:The purpose of this study was to determine the effect of selective modulation of Brain Temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague-Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of Brain-Temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36 degrees C x 4 h), (b) permanent MCA occlusion alone (30, 36, or 39 degrees C x 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39 degrees C x 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser-Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36 degrees C groups. In rats with permanent MCA occlusion without hypotension, significant differences in infarct volume were again not demonstrable, but an interaction between infarct area and Temperature class was shown by repeated-measures analysis, indicating that hypothermia altered the topographic pattern of the cortical infarct. With 2 h of reversible MCA occlusion, there was a statistically significant reduction in infarct volume in the 30 degrees C group compared to 39 degrees C rats. Although intra- and postischemic CBF were not significantly different among the three Temperature groups, the cortical infarct volume was positively correlated with postischemic CBF. The postischemic CBF, in turn, was positively correlated to the intraischemic Brain Temperature and was negatively correlated to CBF during the ischemic period. These findings demonstrate that moderate manipulations of Brain Temperature have a greater influence on the resulting cortical infarction in the setting of transient focal ischemia than in the context of permanent vascular occlusion.
Kuniaki Ogasawara - One of the best experts on this subject based on the ideXlab platform.
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apparent Brain Temperature imaging with multi voxel proton magnetic resonance spectroscopy compared with cerebral blood flow and metabolism imaging on positron emission tomography in patients with unilateral chronic major cerebral artery steno occlusive disease
Neuroradiology, 2017Co-Authors: Takamasa Nanba, Yoshichika Yoshioka, Makoto Sasaki, Shunrou Fujiwara, Kazunori Terasaki, Hideaki Nishimoto, Toshiyuki Murakami, Ikuko Uwano, Kuniaki OgasawaraAbstract:The purpose of the present study was to determine whether apparent Brain Temperature imaging using multi-voxel proton magnetic resonance (MR) spectroscopy correlates with cerebral blood flow (CBF) and metabolism imaging in the deep white matter of patients with unilateral chronic major cerebral artery steno-occlusive disease. Apparent Brain Temperature and CBF and metabolism imaging were measured using proton MR spectroscopy and 15O-positron emission tomography (PET), respectively, in 35 patients. A set of regions of interest (ROIs) of 5 × 5 voxels was placed on an MR image so that the voxel row at each edge was located in the deep white matter of the centrum semiovale in each cerebral hemisphere. PET images were co-registered with MR images with these ROIs and were re-sliced automatically using image analysis software. In 175 voxel pairs located in the deep white matter, the Brain Temperature difference (affected hemisphere − contralateral hemisphere: ΔBT) was correlated with cerebral blood volume (CBV) (r = 0.570) and oxygen extraction fraction (OEF) ratios (affected hemisphere/contralateral hemisphere) (r = 0.641). We excluded voxels that contained ischemic lesions or cerebrospinal fluid and calculated the mean values of voxel pairs in each patient. The mean ΔBT was correlated with the mean CBF (r = − 0.376), mean CBV (r = 0.702), and mean OEF ratio (r = 0.774). Apparent Brain Temperature imaging using multi-voxel proton MR spectroscopy was correlated with CBF and metabolism imaging in the deep white matter of patients with unilateral major cerebral artery steno-occlusive disease.
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Brain Temperature measured using proton mr spectroscopy detects cerebral hemodynamic impairment in patients with unilateral chronic major cerebral artery steno occlusive disease comparison with positron emission tomography
Stroke, 2009Co-Authors: Daiya Ishigaki, Kuniaki Ogasawara, Yoshichika Yoshioka, Kohei Chida, Makoto Sasaki, Shunrou Fujiwara, Masakazu Kobayashi, Kenji Yoshida, Kazunori Terasaki, Takashi InoueAbstract:Background and Purpose— Brain Temperature is determined by the balance between heat produced by cerebral energy turnover and heat removed by cerebral blood flow. The purpose of the present study was to investigate whether Brain Temperature measured noninvasively using proton MR spectroscopy can detect cerebral hemodynamic impairment in patients with unilateral chronic internal carotid or middle cerebral artery occlusive disease when compared with positron emission tomography. Methods— Brain Temperature, cerebral blood flow, and metabolism were measured using proton MR spectroscopy and 15O-positron emission tomography, respectively, in 21 normal subjects and 37 patients. Positron emission tomography images were coregistered with MR images and resliced automatically using image analysis software. Regions of interest placed in both cerebral hemispheres on MR images were automatically superimposed in these resliced positron emission tomography images. Results— A significant correlation was observed between br...