The Experts below are selected from a list of 1989 Experts worldwide ranked by ideXlab platform
Luc Huyghens - One of the best experts on this subject based on the ideXlab platform.
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Postischemic mild hypothermia reduces neurotransmitter release and astroglial cell proliferation during reperfusion after asphyxial cardiac arrest in rats
Brain Research, 2004Co-Authors: Said Hachimi-idrissi, A. Van Hemelrijck, Alex Michotte, Ilse Smolders, Sophie Sarre, Guy Ebinger, Luc Huyghens, Yvette MichotteAbstract:The present study investigated whether postischemic mild hypothermia attenuates the ischemia-induced striatal glutamate (GLU) and dopamine (DA) release, as well as astroglial cell proliferation in the brain. Anesthetized rats were exposed to 8 min of asphyxiation, including 5 min of cardiac arrest. The cardiac arrest was reversed to restoration of spontaneous circulation (ROSC), by brief external Heart Massage and ventilation within a period of 2 min. After the insult and during reperfusion, the extracellular glutamate and dopamine overflow increased to, respectively, 3000% and 5000% compared with the baseline values in the normothermic group and resulted in brain damage, ischemic neurons and gliosis. However, when hypothermia was induced for a period of 60 min after the insult and restoration of spontaneous circulation, the glutamate and dopamine overflows were not significantly different from that in the sham group. Histological analysis of the brain showed that postischemic mild hypothermia reduced brain damage, ischemic neurons, as well as astroglial cell proliferation. Thus, postischemic mild hypothermia reduces the excitotoxic process, brain damage, as well as astroglial cell proliferation during reperfusion. Moreover, these results emphasize the trigger effect of dopamine on the excitotoxic pathway.
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The effect of mild hypothermia and induced hypertension on long term survival rate and neurological outcome after asphyxial cardiac arrest in rats
Resuscitation, 2001Co-Authors: Said Hachimi-idrissi, Luc Corne, Luc HuyghensAbstract:Abstract Study objective: we studied the long-term effect of a combined treatment with resuscitative mild hypothermia and induced hypertension on survival rate and neurological outcome after asphyxial cardiac arrest (CA) in rats. Methods: 36 male Wistar rats, were randomised into three groups: Group I ( n =10): anaesthetised with halothane and N 2 O/O 2 (70/30%) had vessel cannulation but no asphyxial CA; mechanical ventilation was continued to 1 h. Group II ( n =13): under the same anaesthetic conditions and vessel cannulation, was subjected to asphyxial CA of 8 min, reversed by brief external Heart Massage and followed by mechanical ventilation to 1 h post restoration of spontaneous circulation (ROSC). Group III ( n =13): received the same insult and resuscitation as described in group II, but in contrast to the previous group, a combination treatment of hypothermia (34°C) and induced hypertension was started immediately after ROSC and maintained for 60 min ROSC. Survival rate and neurological deficit (ND) scores were determined before arrest, at 2 and 24 h, and each 24-h up to 4 weeks after ROSC. Results: Baseline variables were the same in the three groups. Comparison of the asphyxial CA groups (groups II and III), showed an increased, although not statistically significant, survival rate at 72 h after ROSC in group III, and it became highly significant at 4 weeks after ROSC. The ND scores were the same in both asphyxial CA groups (groups II and III). Conclusions: Resuscitative mild hypothermia and induced hypertension after asphyxial CA in rats is associated with a better survival rate. This beneficial effect persisted for 4 weeks after ROSC.
H. M. Wisniewski - One of the best experts on this subject based on the ideXlab platform.
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Reassessment of a new model of complete cerebral ischemia in rats
Acta Neuropathologica, 1991Co-Authors: R. Pluta, A. S. Lossinsky, M. J. Mossakowski, L. Faso, H. M. WisniewskiAbstract:The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.5 or 10 min, with survival periods that lasted from 3 min to 7 days. A special metal hook-like device was inserted into the chest cavity at the third intercostal spaces for occluding the cardiac vessel bundle. The effect of this procedure was total cessation of systemic circulation, i.e., clinical death. In 52% of animals with 10-min clinical death, resuscitation (external Heart Massage and artificial ventilation) restored Heart activity. When brain circulation was restored respiratory activity, pain reaction, corneal reflex, bioelectric activity of the cortex, and normal activities of the rats returned. Scanning electron microscopy was applied to study the effect of ischemia on the vessel wall and endothelial cells (EC). Ischemia produced a remarkable increase in the numbers of microvilli and pit-like invaginations on the luminal EC surface. The luminal wall surface of many of the microvessels (MV) formed ridges. Frequently, microthrombi of varying sizes were observed. The most prominent changes were noted from 3 min to 6 h of recirculation, and they correlated with hypoperfusion after ischemia. Seven days later, these changes completely disappeared. The data presented here indicate that progressive hypoperfusion after ischemia occurs with significant alterations fusion after ischemia occurs with significant alterations in the MV walls. These studies collectively suggest that the focal responses in select MVs may be associated with receptor molecule up-regulation of some, but not all, affected ECs. Our data provide further characterization of a new and unique chronic model of brain ischemia that can be applied to relevant clinical studies.
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Reassessment of a new model of complete cerebral ischemia in rats
Acta Neuropathologica, 1991Co-Authors: R. Pluta, A. S. Lossinsky, M. J. Mossakowski, L. Faso, H. M. WisniewskiAbstract:The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.5 or 10 min, with survival periods that lasted from 3 min to 7 days. A special metal hook-like device was inserted into the chest cavity at the third intercostal spaces for occluding the cardiac vessel bundle. The effect of this procedure was total cessation of systemic circulation, i.e., clinical death. In 52% of animals with 10-min clinical death, resuscitation (external Heart Massage and artificial ventilation) restored Heart activity. When brain circulation was restored respiratory activity, pain reaction, corneal reflex, bioelectric activity of the cortex, and normal activities of the rats returned. Scanning electron microscopy was applied to study the effect of ischemia on the vessel wall and endothelial cells (EC). Ischemia produced a remarkable increase in the numbers of microvilli and pit-like invaginations on the luminal EC surface. The luminal wall surface of many of the microvessels (MV) formed ridges. Frequently, microthrombi of varying sizes were observed. The most prominent changes were noted from 3 min to 6 h of recirculation, and they correlated with hypoperfusion after ischemia. Seven days later, these changes completely disappeared. The data presented here indicate that progressive hypoperfusion after ischemia occurs with significant alterations fusion after ischemia occurs with significant alterations in the MV walls. These studies collectively suggest that the focal responses in select MVs may be associated with receptor molecule up-regulation of some, but not all, affected ECs. Our data provide further characterization of a new and unique chronic model of brain ischemia that can be applied to relevant clinical studies.
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Reassessment of a new model of complete cerebral ischemia in rats. Method of induction of clinical death, pathophysiology and cerebrovascular pathology.
Acta neuropathologica, 1991Co-Authors: R. Pluta, A. S. Lossinsky, M. J. Mossakowski, L. Faso, H. M. WisniewskiAbstract:The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.5 or 10 min, with survival periods that lasted from 3 min to 7 days. A special metal hook-like device was inserted into the chest cavity at the third intercostal spaces for occluding the cardiac vessel bundle. The effect of this procedure was total cessation of systemic circulation, i.e., clinical death. In 52% of animals with 10-min clinical death, resuscitation (external Heart Massage and artificial ventilation) restored Heart activity. When brain circulation was restored respiratory activity, pain reaction, corneal reflex, bioelectric activity of the cortex, and normal activities of the rats returned. Scanning electron microscopy was applied to study the effect of ischemia on the vessel wall and endothelial cells (EC). Ischemia produced a remarkable increase in the numbers of microvilli and pit-like invaginations on the luminal EC surface. The luminal wall surface of many of the microvessels (MV) formed ridges. Frequently, microthrombi of varying sizes were observed. The most prominent changes were noted from 3 min to 6 h of recirculation, and they correlated with hypoperfusion after ischemia. Seven days later, these changes completely disappeared. The data presented here indicate that progressive hypoperfusion after ischemia occurs with significant alterations fusion after ischemia occurs with significant alterations in the MV walls. These studies collectively suggest that the focal responses in select MVs may be associated with receptor molecule up-regulation of some, but not all, affected ECs. Our data provide further characterization of a new and unique chronic model of brain ischemia that can be applied to relevant clinical studies.
Marcel Rigaud - One of the best experts on this subject based on the ideXlab platform.
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Clamshell thoracotomy and open Heart Massage--A potential life-saving procedure can be taught to emergency physicians: An educational cadaveric pilot study.
Injury, 2015Co-Authors: Paul Puchwein, Florian Sommerauer, Hans Clement, Veronika Matzi, Norbert Peter Tesch, Barbara Hallmann, Tim Harris, Marcel RigaudAbstract:Abstract Aims Selected patients in traumatic cardiac arrest may benefit from pre-hospital thoracotomy. Pre-hospital care physicians rarely have surgical training and the procedure is rarely performed in most European systems. Limited data exists to inform teaching and training for this procedure. We set out to run a pilot study to determine the time required to perform a thoracotomy and the a priori defined complication rate. Methods We adapted an existing system operating procedure requiring four instruments (Plaster-of-Paris shears, dressing scissors, non-toothed forceps, scalpel) for this study. We identified a convenience sample of surgically trained and non-surgically trained participants. All received a training package including a lecture, practical demonstration and cadaver experience. Time to perform the procedure, anatomical accuracy and a priori complication rates were assessed. Results The mean total time for the clamshell thoracotomy from thoracic incision to delivery of the Heart was 167 s (02:47 min:sec). There was no statistical difference in the time to complete the procedure or complication rate among surgeons, non-surgeons and students. The complication rate dropped from 36% in the first attempt to 7% in the second attempt but this was not statistically significant. This is a pilot study and small numbers of participants arguably saw it underpowered to define differences between study groups. Conclusion Clamshell thoracotomy can be taught using cadaver models. In this simulated environment, the procedure may be performed rapidly with minimum equipment.
Said Hachimi-idrissi - One of the best experts on this subject based on the ideXlab platform.
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Postischemic mild hypothermia reduces neurotransmitter release and astroglial cell proliferation during reperfusion after asphyxial cardiac arrest in rats
Brain Research, 2004Co-Authors: Said Hachimi-idrissi, A. Van Hemelrijck, Alex Michotte, Ilse Smolders, Sophie Sarre, Guy Ebinger, Luc Huyghens, Yvette MichotteAbstract:The present study investigated whether postischemic mild hypothermia attenuates the ischemia-induced striatal glutamate (GLU) and dopamine (DA) release, as well as astroglial cell proliferation in the brain. Anesthetized rats were exposed to 8 min of asphyxiation, including 5 min of cardiac arrest. The cardiac arrest was reversed to restoration of spontaneous circulation (ROSC), by brief external Heart Massage and ventilation within a period of 2 min. After the insult and during reperfusion, the extracellular glutamate and dopamine overflow increased to, respectively, 3000% and 5000% compared with the baseline values in the normothermic group and resulted in brain damage, ischemic neurons and gliosis. However, when hypothermia was induced for a period of 60 min after the insult and restoration of spontaneous circulation, the glutamate and dopamine overflows were not significantly different from that in the sham group. Histological analysis of the brain showed that postischemic mild hypothermia reduced brain damage, ischemic neurons, as well as astroglial cell proliferation. Thus, postischemic mild hypothermia reduces the excitotoxic process, brain damage, as well as astroglial cell proliferation during reperfusion. Moreover, these results emphasize the trigger effect of dopamine on the excitotoxic pathway.
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The effect of mild hypothermia and induced hypertension on long term survival rate and neurological outcome after asphyxial cardiac arrest in rats
Resuscitation, 2001Co-Authors: Said Hachimi-idrissi, Luc Corne, Luc HuyghensAbstract:Abstract Study objective: we studied the long-term effect of a combined treatment with resuscitative mild hypothermia and induced hypertension on survival rate and neurological outcome after asphyxial cardiac arrest (CA) in rats. Methods: 36 male Wistar rats, were randomised into three groups: Group I ( n =10): anaesthetised with halothane and N 2 O/O 2 (70/30%) had vessel cannulation but no asphyxial CA; mechanical ventilation was continued to 1 h. Group II ( n =13): under the same anaesthetic conditions and vessel cannulation, was subjected to asphyxial CA of 8 min, reversed by brief external Heart Massage and followed by mechanical ventilation to 1 h post restoration of spontaneous circulation (ROSC). Group III ( n =13): received the same insult and resuscitation as described in group II, but in contrast to the previous group, a combination treatment of hypothermia (34°C) and induced hypertension was started immediately after ROSC and maintained for 60 min ROSC. Survival rate and neurological deficit (ND) scores were determined before arrest, at 2 and 24 h, and each 24-h up to 4 weeks after ROSC. Results: Baseline variables were the same in the three groups. Comparison of the asphyxial CA groups (groups II and III), showed an increased, although not statistically significant, survival rate at 72 h after ROSC in group III, and it became highly significant at 4 weeks after ROSC. The ND scores were the same in both asphyxial CA groups (groups II and III). Conclusions: Resuscitative mild hypothermia and induced hypertension after asphyxial CA in rats is associated with a better survival rate. This beneficial effect persisted for 4 weeks after ROSC.
Gunnar Kroesen - One of the best experts on this subject based on the ideXlab platform.
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Cardiopulmonary resuscitation after thoracic surgery: echocardiographic observations.
Resuscitation, 1994Co-Authors: Peter Mair, Wilhelm Furtwaengler, Michael Baubin, Josef Berger, Gunnar KroesenAbstract:We report echocardiographic observations during external chest compression in a patient with marked abnormalities in thoracic anatomy following emergency surgery of aortic arch aneurysm. Transesophageal echocardiography demonstrated direct right ventricular, aortic and left atrial compression, only minimal left ventricular compression and an open mitral valve during closed chest Heart Massage. Colour flow doppler demonstrated forward blood flow across the mitral valve and along the left ventricular outflow tract during the compression phase. Echocardiographic findings indicate that factors apart from simple cardiac pump mechanism contributed to blood flow during cardiopulmonary resuscitation (CPR) in this postoperative patient after a major thoracic surgical intervention.
