Depth of delayed cooling alters neuroprotection pattern after hypoxia-ischemia
Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham‐normothermia (38.5–39°C); (Gro...
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Published in | Annals of neurology Vol. 58; no. 1; pp. 75 - 87 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.07.2005
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Abstract | Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham‐normothermia (38.5–39°C); (Group ii) sham‐33°C; (Group iii) HI‐normothermia; (Group iv) HI‐35°C; and (Group v) HI‐33°C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35°C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33°C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33°C, 35°C resulted in more viable neurons in deep GM, whereas 33°C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient‐specific hypothermia protocols by combining systemic and selective cooling. Ann Neurol 2005;58:75–87 |
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AbstractList | Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham-normothermia (38.5-39 degrees C); (Group ii) sham-33 degrees C; (Group iii) HI-normothermia; (Group iv) HI-35 degrees C; and (Group v) HI-33 degrees C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35 degrees C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33 degrees C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33 degrees C, 35 degrees C resulted in more viable neurons in deep GM, whereas 33 degrees C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient-specific hypothermia protocols by combining systemic and selective cooling. Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham-normothermia (38.5-39 degrees C); (Group ii) sham-33 degrees C; (Group iii) HI-normothermia; (Group iv) HI-35 degrees C; and (Group v) HI-33 degrees C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35 degrees C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33 degrees C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33 degrees C, 35 degrees C resulted in more viable neurons in deep GM, whereas 33 degrees C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient-specific hypothermia protocols by combining systemic and selective cooling. Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham-normothermia (38.5-39 degree C); (Group ii) sham- 33 degree C; (Group iii) HI-normothermia; (Group iv) HI-35 degree C; and (Group v) HI-33 degree C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35 degree C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33 degree C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33 degree C, 35 degree C resulted in more viable neurons in deep GM, whereas 33 degree C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient-specific hypothermia protocols by combining systemic and selective cooling. Ann Neurol 2005; 58:75-87 Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham‐normothermia (38.5–39°C); (Group ii) sham‐33°C; (Group iii) HI‐normothermia; (Group iv) HI‐35°C; and (Group v) HI‐33°C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35°C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33°C resulted in a 55% increase in neuronal viability in cortical GM (p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33°C, 35°C resulted in more viable neurons in deep GM, whereas 33°C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient‐specific hypothermia protocols by combining systemic and selective cooling. Ann Neurol 2005;58:75–87 Abstract Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham‐normothermia (38.5–39°C); (Group ii) sham‐33°C; (Group iii) HI‐normothermia; (Group iv) HI‐35°C; and (Group v) HI‐33°C. Groups iii through v were subjected to transient HI insult. Groups ii, iv, and v were cooled to their target rectal temperatures between 2 and 26 hours after resuscitation. Experiments were terminated at 48 hours. Compared with normothermia, hypothermia at 35°C led to 25 and 39% increases in neuronal viability in cortical gray matter (GM) and deep GM, respectively (both p < 0.05); hypothermia at 33°C resulted in a 55% increase in neuronal viability in cortical GM ( p < 0.01) but no significant increase in neuronal viability in deep GM. Comparing hypothermia at 35 and 33°C, 35°C resulted in more viable neurons in deep GM, whereas 33°C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient‐specific hypothermia protocols by combining systemic and selective cooling. Ann Neurol 2005;58:75–87 |
Author | Sakata, Yasuko Cady, Ernest B. Iwata, Sachiko Bainbridge, Alan Noone, Martina A. Sellwood, Mark W. De Vita, Enrico Iwata, Osuke Wyatt, John S. Raivich, Gennadij Thornton, John S. O'Brien, Frances E. Scaravilli, Francesco Peebles, Donald Ordidge, Roger Robertson, Nicola J. |
Author_xml | – sequence: 1 givenname: Osuke surname: Iwata fullname: Iwata, Osuke email: oiwata@medphys.ucl.ac.uk organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 2 givenname: John S. surname: Thornton fullname: Thornton, John S. organization: Department of Medical Physics and Bioengineering, University College London, London, United Kingdom – sequence: 3 givenname: Mark W. surname: Sellwood fullname: Sellwood, Mark W. organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 4 givenname: Sachiko surname: Iwata fullname: Iwata, Sachiko organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 5 givenname: Yasuko surname: Sakata fullname: Sakata, Yasuko organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 6 givenname: Martina A. surname: Noone fullname: Noone, Martina A. organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 7 givenname: Frances E. surname: O'Brien fullname: O'Brien, Frances E. organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 8 givenname: Alan surname: Bainbridge fullname: Bainbridge, Alan organization: Department of Medical Physics and Bioengineering, University College London, London, United Kingdom – sequence: 9 givenname: Enrico surname: De Vita fullname: De Vita, Enrico organization: Department of Medical Physics and Bioengineering, University College London, London, United Kingdom – sequence: 10 givenname: Gennadij surname: Raivich fullname: Raivich, Gennadij organization: Perinatal Brain Research Group, Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, London, United Kingdom – sequence: 11 givenname: Donald surname: Peebles fullname: Peebles, Donald organization: Perinatal Brain Research Group, Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, London, United Kingdom – sequence: 12 givenname: Francesco surname: Scaravilli fullname: Scaravilli, Francesco organization: Division of Neuropathology, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom – sequence: 13 givenname: Ernest B. surname: Cady fullname: Cady, Ernest B. organization: Department of Medical Physics and Bioengineering, University College London, London, United Kingdom – sequence: 14 givenname: Roger surname: Ordidge fullname: Ordidge, Roger organization: Department of Medical Physics and Bioengineering, University College London, London, United Kingdom – sequence: 15 givenname: John S. surname: Wyatt fullname: Wyatt, John S. organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom – sequence: 16 givenname: Nicola J. surname: Robertson fullname: Robertson, Nicola J. organization: Department of Paediatrics and Child Health, Royal Free and University College Medical School, The Rayne Institute, London, United Kingdom |
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Effects of isoflurane ve 2004; 22 2001; 344 1990; 10 2004; 61 1994; 654 1993; 61 2002; 110 1995; 37 1997; 272 1997; 42 2002; 51 1997; 41 1999; 46 1995; 217 1996; 74 1999; 88 2001; 49 2001; 108 2003; 53 2003; 111 2003; 54 1998; 88 1997; 8 1990; 85 1992; 7 1986; 1 1997; 99 2001 1994; 181 2000; 10 1997; 15 1984; 56 2002; 88 1994; 36 2005; 32 1998; 10 1992; 2 2003; 285 2003; 45 1991; 131 2004; 100 1997; 336 1989; 20 1995; 15 1997; 23 2000; 20 1999; 67 1999; 20 1995; 2 1996; 16 1989; 25 2003; 31 1994; 87 1991; 6 2001; 128 1995; 7 1990; 21 2002; 29 1989; 97 1997; 769 2002; 20 2005; 365 2000; 106 2004; 56 2001; 8 1995; 43 1996; 40 1998; 5 1998; 102 2003; 23 e_1_2_6_51_2 e_1_2_6_72_2 e_1_2_6_53_2 e_1_2_6_74_2 e_1_2_6_30_2 e_1_2_6_70_2 e_1_2_6_19_2 e_1_2_6_13_2 e_1_2_6_34_2 e_1_2_6_59_2 e_1_2_6_11_2 e_1_2_6_32_2 e_1_2_6_17_2 e_1_2_6_38_2 e_1_2_6_55_2 e_1_2_6_15_2 e_1_2_6_36_2 e_1_2_6_57_2 e_1_2_6_62_2 e_1_2_6_20_2 e_1_2_6_41_2 Watanabe T (e_1_2_6_49_2) 1989; 97 Takahashi T (e_1_2_6_58_2) 1999; 20 e_1_2_6_60_2 e_1_2_6_7_2 e_1_2_6_9_2 e_1_2_6_5_2 Cervos‐Navarro J (e_1_2_6_24_2) 1991; 6 e_1_2_6_47_2 e_1_2_6_28_2 e_1_2_6_43_2 e_1_2_6_66_2 e_1_2_6_26_2 e_1_2_6_45_2 e_1_2_6_68_2 e_1_2_6_50_2 e_1_2_6_73_2 e_1_2_6_52_2 e_1_2_6_75_2 Thornton JS (e_1_2_6_76_2) 2004; 22 e_1_2_6_31_2 e_1_2_6_71_2 e_1_2_6_18_2 Frank SM (e_1_2_6_46_2) 1997; 272 e_1_2_6_12_2 e_1_2_6_35_2 e_1_2_6_10_2 e_1_2_6_33_2 e_1_2_6_16_2 e_1_2_6_39_2 e_1_2_6_54_2 e_1_2_6_77_2 e_1_2_6_14_2 e_1_2_6_37_2 e_1_2_6_56_2 e_1_2_6_61_2 Vannucci RC (e_1_2_6_3_2) 1990; 85 e_1_2_6_63_2 e_1_2_6_42_2 e_1_2_6_40_2 Eger EI (e_1_2_6_64_2) 1984; 56 e_1_2_6_8_2 e_1_2_6_29_2 e_1_2_6_4_2 e_1_2_6_6_2 Volpe JJ (e_1_2_6_22_2) 2001 e_1_2_6_23_2 e_1_2_6_48_2 e_1_2_6_69_2 e_1_2_6_2_2 e_1_2_6_21_2 e_1_2_6_65_2 e_1_2_6_27_2 e_1_2_6_44_2 e_1_2_6_67_2 e_1_2_6_25_2 |
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Snippet | Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the... Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the... Abstract Hypothermia after perinatal hypoxia‐ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To... |
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SubjectTerms | Animals Animals, Newborn Biological and medical sciences Disease Models, Animal Female Hypothermia, Induced Hypoxia-Ischemia, Brain - pathology Hypoxia-Ischemia, Brain - therapy Male Medical sciences Nerve Degeneration - prevention & control Neurology Neurons - pathology Neuropharmacology Neuroprotective agent Pharmacology. Drug treatments Swine Temperature Vascular diseases and vascular malformations of the nervous system |
Title | Depth of delayed cooling alters neuroprotection pattern after hypoxia-ischemia |
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