Temperature Changes of greater or equal to 1 degree Celsius Alter Functional Neurologic Outcome and Histopathology in a Canine Model of Complete Cerebral Ischemia

Wass, C. Thomas; Lanier, William L.; Hofer, Roger E.; Scheithauer, Bernd W.; Andrews, April

doi:10.1097/00000542-199508000-00013

Cited by 236 publications

(93 citation statements)

References 38 publications

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“…Future work would also involve graded hypothermia studies. It would be informative to show neuron activity under gradient hypothermia and relate it to neurological outcome, as clinically it is shown that moderate (30 -32°C) and mild (32-34°C) hypothermia is neurologically beneficial, with increasing benefits as the temperature lowers (Wass et al 1995;Xia and Xia 2011), but deep hypothermia (27-30°C) is detrimental (Steen et al 1979). We also would like to link the electrophysiological changes to the metabolic changes as well as altered neurochemical activity, for example, glutamate excitotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia

Wu¹,

Xiong²,

Jia

et al. 2012

Journal of Neurophysiology

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Wu D, Xiong W, Jia X, Geocadin RG, Thakor NV. Short-and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia. J Neurophysiol 107: 1164 -1171, 2012. First published December 7, 2011 doi:10.1152/jn.00681.2011Evoked potentials recorded from the somatosensory cortex have been shown to be an electrophysiological marker of brain injury in global hypoxic ischemia (HI). The evoked responses in somatosensory neurons carry information pertaining to signal from the ascending pathway in both the subcortical and cortical areas. In this study, origins of the subcortical and cortical signals are explored by decomposing the evoked neuronal activities into short-and long-latency responses (SLR and LLR), respectively. We evaluated the effect of therapeutic hypothermia on SLR and LLR during early recovery from cardiac arrest (CA)-induced HI in a rodent model. Twelve rats were subjected to CA, after which half of them were treated with hypothermia (32-34°C) and the rest were kept at normal temperature (36 -37°C). Evoked neuronal activities from the primary somatosensory cortex, including multiunit activity (MUA) and local field potential (LFP), were continuously recorded during injury and early recovery. Results showed that upon initiation of injury, LLR disappeared first, followed by the disappearance of SLR, and after a period of isoelectric silence SLR reappeared prior to LLR. This suggests that cortical activity, which primarily underlies the LLR, may be more vulnerable to ischemic injury than SLR, which relates to subcortical activity. Hypothermia potentiated the SLR but suppressed the LLR by delaying its recovery after CA (hypothermia: 38.83 Ϯ 5.86 min, normothermia: 23.33 Ϯ 1.15 min; P Ͻ 0.05) and attenuating its amplitude, suggesting that hypothermia may selectively downregulate cortical activity as an approach to preserve the cerebral cortex. In summary, our study reveals the vulnerability of the somatosensory neural structures to global HI and the differential effects of hypothermia on these structures.

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Section: Discussionmentioning

confidence: 99%

Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia

Wu¹,

Xiong²,

Jia

et al. 2012

Journal of Neurophysiology

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“…Furthermore, it has been shown that even small temperature differences affect the extent of cerebral injury (Wass et al, 1995) Selective brain hypothermia results in temperature gradients within the brain (Gelman et al, 1997;Kuhnen et al, 1999;Schwartz et al, 1996a). However, the effect of regional temperature differences on regional CBF under conditions of SBH had not been studied until now.…”

Section: Discussionmentioning

confidence: 99%

Coupling of Cerebral Blood Flow and Oxygen Metabolism in Infant Pigs during Selective Brain Hypothermia

Walter

Bauer

Kuhnen

et al. 2000

J Cereb Blood Flow Metab

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Summary:Studies documenting the cerebral hemodynamic consequences of selective brain hypothermia (SBH) have yielded conflicting data. Therefore, the authors have studied the effect of SBH on the relation of cerebral blood flow (CBF) and CMRO 2 in the forebrain of pigs. Selective brain hypothermia was induced in seven juvenile pigs by bicarotid perfusion of the head with extracorporally cooled blood. Cooling and stepwise rewarming of the brain to a T brain of 38°C, 25°C, 30°C, and 38°C at normothermic T trunk (38°C) decreased CBF from 71 ± 12 mL 100 g −1 min −1 at normothermia to 26 ± 3 mL 100 g −1 min −1 and 40 ± 12 mL 100 g −1 min −1 at a T brain of 25°C and 30°C, respectively. The decrease of CMRO 2 during cooling of the brain to a T brain of 25°C resulted in a mean Q 10 of 2.8. The ratio between CBF and CMRO 2 was increased at a T brain of 25°C indicating a change in coupling of flow and metabolism. Despite this change, regional perfusion remained coupled to regional temperatures during deep cerebral hypothermia. The data demonstrate that SBH decreases CBF and oxygen metabolism to a degree comparable with the cerebrovascular and metabolic effects of systemic hypothermia. The authors conclude that, irrespective of a change in coupling of blood flow and metabolism during deep cerebral hypothermia, cerebral metabolism is a main determinant of CBF during SBH. Key Words: Selective brain hypothermia-Cerebral flowmetabolism coupling-Microspheres-Pig.There is considerable evidence that hypothermia is a useful intrainsult and postinsult treatment modality for brain injury caused by hypoxia-ischemia, trauma, or neonatal asphyxia (Dietrich, 1992, Gunn et al., 1998bWass et al., 1996). Moreover, systemic hypothermia is routinely used during cardiopulmonary bypass in cardiovascular surgery (McCullough et al., 1999;Jonas, 1998). Because systemic hypothermia causes potentially hazardous side effects (for review see Schubert, 1995), selective brain hypothermia (SBH) is being looked at more intensively with respect to feasibility and cerebroprotective effects (Gunn et al., 1997;Kuluz et al., 1992;Schwartz et al., 1996b).Hypothermic cerebral protection is mediated in part by a reduction of cerebral metabolism (Lanier, 1995). Numerous animal and human studies have shown that systemic hypothermia decreases cerebral blood flow (CBF) and CMRO 2 (Greeley et al., 1993;Michenfelder et al., 1991). However, very few studies have addressed the cerebrovascular and cerebral metabolic responses to SBH. Currently there is no study documenting the physiologic effects of SBH on CMRO 2 and, consequently, on the coupling of CBF and CMRO 2 . Furthermore, investigations documenting the hemodynamic consequences of SBH have reported seemingly conflicting data on the cerebrovascular effects of SBH. A single study in rats has shown that external head cooling results in an increase of CBF (Kuluz et al., 1993). Based on this study it has been concluded that the method of cooling (systemic vs. selective) may be a key factor in determining the cerebral he...

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“…Using these conventional body sites, temperatures greater than 38.5°C are commonly encountered during neurocritical care [2,3] and cause concern. In animal models of cerebral ischaemia [4][5][6][7] and trauma [8,9] a rise in body core temperature in excess of 38°C is associated with increased neuronal damage. In stroke patients a rise in body temperature independently predicts poor outcome [10] and increased mortality [11][12][13][14] but when the human brain is injured by trauma, the evidence for a relationship between raised body temperature and worse neurological outcome is not as clear [15,16].…”

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confidence: 99%

Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury*

Childs

Vail

Protheroe³

et al. 2005

Anaesthesia

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SummaryTheoretical models suggest that small differences only exist between brain and body temperature in health. Once the brain is injured, brain temperature is generally regarded to rise above body temperature. However, since reports of the magnitude of the temperature gradient between brain and body vary, it is still not clear whether conventional body temperature monitoring accurately predicts brain temperature at all times. In this prospective, descriptive study, 20 adults with severe primary brain trauma were studied during their stay in the neurointensive care unit. Brain temperature ranged from 33.4 to 39.9°C. Comparisons between paired brain and rectal temperature measurements revealed no evidence of a systematic difference [mean difference )0.04°C (range )0.13 to 0.05°C, 95% CI), p = 0.39]. Contrary to popular belief, brain temperature did not exceed systemic temperature in this relatively homogeneous patient series. The mean values masked inconsistent and unpredictable individual brain-rectal temperature differences (range 1.8 to )2.9°C) and reversal of the brain-body temperature gradient occurred in some patients. Brain temperature could not be predicted from body temperature at all times. Brain temperature is seldom measured during routine neurointensive care but there is a long-held assumption that since the temperatures of healthy internal organs differ only slightly [1], temperature measurements of the rectum, bladder, pulmonary artery and tympanum can be used as surrogates for brain temperature. Using these conventional body sites, temperatures greater than 38.5°C are commonly encountered during neurocritical care [2,3] and cause concern. In animal models of cerebral ischaemia [4][5][6][7] and trauma [8,9] a rise in body core temperature in excess of 38°C is associated with increased neuronal damage. In stroke patients a rise in body temperature independently predicts poor outcome [10] and increased mortality [11][12][13][14] but when the human brain is injured by trauma, the evidence for a relationship between raised body temperature and worse neurological outcome is not as clear [15,16]. However, it is assumed that the deleterious metabolic, inflammatory and biochemical mechanisms associated with raised body temperature in animal models of stroke and trauma may operate similarly in the brain injured human [17]. This assumption underpins current opinion that even a small increase in body temperature (1-2°C) above normal (37°C) accelerates ischaemic damage and increases the size of the primary brain lesion [9,18] and should therefore be prevented [13].Little is known about human brain temperature, but theoretical models suggest that during normothermia the temperature of the brain is close to that of internal carotid arterial blood before the blood enters the circle of Willis [19]. In man, direct measurement of brain temperature Anaesthesia, 2005, 60, pages 759-765

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Temperature Changes of greater or equal to 1 degree Celsius Alter Functional Neurologic Outcome and Histopathology in a Canine Model of Complete Cerebral Ischemia

Cited by 236 publications

References 38 publications

Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia

Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia

Coupling of Cerebral Blood Flow and Oxygen Metabolism in Infant Pigs during Selective Brain Hypothermia

Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury*

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