Experimental Brain Injury and Delayed Hypothermia

Rosomoff, Hubert L.; Shulman, Kenneth I.; Raynor, Richard B.; Grainger, William

doi:10.1097/00132586-196108010-00012

Cited by 15 publications

(13 citation statements)

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“…36 Mild hypothermia might attenuate the deleterious reoxygenation chemical cascades, without blocking recovery of ATP and metabolic processes. 11 Clinical trials of resuscitative mild (i.e., not risky) cerebral hypothermia seem justified, not only for cardiac arrest cases, 1112 in whom cooling must be accomplished within 15-30 minutes of reperfusion, 37 but also after experimental focal brain ischemia, 38 -39 brain trauma, 40 " 42 and hemorrhagic shock. 43 Clinical trials of mild resuscitative hypothermia for acutely comatose patients, starting in the prehospital setting, must not only determine clinically feasible and rapidly effective cooling methods 12 -18 but also must apply routine monitoring in emergency care of brain temperature as T ty or nasopharyngeal temperature and core temperature as esophageal temperature, to prevent cardiac temperature of <32°C and cerebral temperature of >38°C; even mild hyperthermia can damage the already damaged brain further.…”

Section: -35mentioning

confidence: 99%

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

Weinrauch

Šafář

Tisherman

et al. 1992

Stroke

212

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Background and Purpose: Mild cerebral hypothermia (34°C) induced immediately after cardiac arrest improves outcome. Deep postarrest hypothermia (15°C) has not been studied.Methods: We used our dog model of normothermic ventricular fibrillation (no blood flow) of 12.5 minutes, reperfusion by brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 72 hours. Head surface cooling and bypass cooling were performed from start of reperfusion to 1 hour. Five groups of six dogs each were compared: group I, normothermic controls; group II, deep hypothermia (15°C); group III, moderate hypothermia (30°C); group IV, mild hypothermia (34°C); and group V, mild hypothermia with head surface cooling begun during no flow.Results: In control group I, five dogs remained comatose (overall performance category [OPC] 4) and one severely disabled (OPC 3). In group II, four dogs achieved OPC 4 and two dogs OPC 3 (NS versus group I). Compared with group I, OPCs were better in group III (p<0.05), group IV (p<0.05), and group V (p<0.05). Neurological deficit scores were also better in groups III, IV, and V than in groups I or II (p<0.05). Total brain histological damage scores were better in group III (p-0.02), group IV (p=0.06), and group V (p<0.05) than in group I. In group II, OPC and neurological deficit scores were the same and histological damage scores numerically worse than in group I and all were worse than in groups III, IV, and V (p<0.05). Cardiovascular complications and myocardial morphological damage in groups II and III were worse than in groups I, IV, and V (p<0.05).Conclusions: Mild or moderate cerebral hypothermia induced immediately after cardiac arrest improves cerebral outcome, more likely when initiated during arrest, whereas deep postarrest hypothermia can worsen cerebral and cardiac outcome. (Stroke 1992;23:1454-1462 KEY WORDS • anoxia • cerebral ischemia • hypothermia • dogs

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Section: -35mentioning

confidence: 99%

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

Weinrauch

Šafář

Tisherman

et al. 1992

Stroke

212

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“…[1][2][3][4] The results of early studies of hypothermia in humans with brain injury were inconclusive. [5][6][7][8][9] Subsequent testing established 32°C as the safe limit for hypothermia in humans with brain injury.…”

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Lack of Effect of Induction of Hypothermia after Acute Brain Injury

Clifton¹,

et al. 2001

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“…The mechanism by which hypothermia protects the ischémie or traumatized brain (i.e., when induced before and maintained during an insult) or resuscitates the brain (i.e., when induced to reverse an insult and support recovery) is multifaceted (Bigelow et al, 1950;Rosomoff and Holaday, 1954;Stone et al, 1956;Rosomoff, 1959;Rosomoff et al, 1960;Rosomoff and Safar, 1965;Kramer et al, 1968;Michenfelder and Theye, 1970;Astrup et al, 1980;Dempsey et al, 1987;Busto et al, 1989a;Chopp et al, 1989;Baiping et al, 1994;Goss et al, 1995;Rosomoff et al, 1996;Safar, 1996;Whalen et al, 1996;Kochanek et al, 1997;Marion et al, 1997).…”

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confidence: 99%

Moderate Hypothermia for 48 Hours After Temporary Epidural Brain Compression Injury in a Canine Outcome Model

Ebmeyer

Šafář²,

Radovsky³

et al. 1998

Journal of Neurotrauma

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In a previous study with this dog model, post-insult hypothermia of 31 degrees C for 5 h prevented secondary intraventricular pressure (IVP) rise, but during 35 degrees C or 38 degrees C, one-half of the dogs developed delayed IVP rise to brain death. We hypothesized that 31 degrees C extended to 48 h would prevent brain herniation. Using epidural balloon inflation, we increased contralateral IVP to 62 mm Hg for 90 min. Controlled ventilation was to 72 h and intensive care to 96 h. Group 1 dogs (n = 10) were normothermic controls (37.5 degrees C). Group 2 dogs (n = 10) were surface-cooled from 15 to 45 min of balloon inflation and maintained at moderate hypothermia (31 degrees C) to 48 h. Rewarming was from 48 to 72 h. Four additional dogs of hypothermia Group 2 had to be excluded from analysis for pneumonia and/or bleeding diathesis. After balloon deflation, IVP increased to 20 mm Hg or greater at 154 +/- 215 (range 15-720) min following the insult in Group 1 and at 1394 +/- 1191 (range 210-3420) min in Group 2 (p = 0.004), still during 31 degrees C but without further increase during hypothermia. Further IVP rise led to brain death in Group 1 in 6 of 10 dogs at 44 +/- 18 (range 21-72) h (all during controlled ventilation); and in Group 2, in 6 of 10 dogs at 87 +/- 11 (range 72-96) h (p = 0.001), all after rewarming, during spontaneous breathing. Survival to 96 h was achieved by 4 of 10 dogs in Group 1, and by 7 of 10 dogs in Group 2 (NS). Three of the six brain deaths in Group 2 occurred at 96 h. The macroscopically damaged brain volume was only numerically smaller in Group 2. The vermis downward shift was 6.8 +/- 3.5 mm in Group 1, versus 4.7 +/- 2.2 mm in Group 2 (p = 0.05). In an adjunctive study, in 4 additional normothermic dogs, hemispheric cerebral blood flow showed post-insult hypoperfusion bilaterally but no evidence of hyperemia preceding IVP rise to brain death. In conclusion, in this model, moderate hypothermia during and for 48 h after temporary epidural brain compression can maintain a low IVP during hypothermia but cannot prevent lethal brain swelling after rewarming and may cause coagulopathy and pulmonary complications.

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Experimental Brain Injury and Delayed Hypothermia

Cited by 15 publications

References 0 publications

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

Lack of Effect of Induction of Hypothermia after Acute Brain Injury

Moderate Hypothermia for 48 Hours After Temporary Epidural Brain Compression Injury in a Canine Outcome Model

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