The protective effect of hypothermia on reversibility in the neuronal function of the hippocampal slice during long lasting anoxia

Okada, Yasuhiro; Tanimoto, Michinori; Yoneda, Kazushi

doi:10.1016/0304-3940(88)90520-4

Cited by 48 publications

(17 citation statements)

References 7 publications

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“…The magnitude of neuronal cell protection at 24 hr declined to 60–65% with mild and moderate hypothermia, whereas the greatest protection was seen with deep hypothermia. These findings are compatible with the two animal studies by Young et al (1983) and Okada et al (1988). Both of these studies show the highest degree of neuroprotection with deep hypothermia (21°C).…”

Section: Discussionsupporting

confidence: 94%

“…The results of these culture experiments may not be readily applicable in clinical practice. Although there is now convincing evidence that deep hypothermia (21–27°C) significantly attenuates brain damage during global cerebral ischemia (Young et al, 1983; Okada et al, 1988), temperatures of mild hypothermia are widely used in clinical practice. In fact, a more important reason is that cooling below 30°C causes undesirable complications that include myocardial ischemia, arrhythmias, coagulopathies, delayed recovery from anesthesia, and altered disposition of drugs.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective effect of hypothermia at defined intraischemic time courses in cortical cultures

Varathan

Shibuta

Shimizu

et al. 2001

J of Neuroscience Research

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Many experimental and clinical studies have shown that hypothermia confers cerebroprotective benefits against ischemic insults. Because of the many conflicting reports on hypothermic neuroprotection, we undertook this cellular study to identify the optimal temperature or a range of temperatures for maximal neuroprotection at different times (6-24 hr) during ischemic insults. Cultured Wistar rat cortical neurons were exposed to oxygen deprivation at defined times and temperatures (37 degrees C normothermia, 32 degrees C mild hypothermia, 27 degrees C moderate hypothermia, 22 degrees C deep hypothermia, and 17 degrees C profound hypothermia). The survival rate of neurons was evaluated by assessing viable neurons on photomicrographs. The normothermic group demonstrated a significantly lower survival rate of cultured neurons (6 hr, 80.3% +/- 2.7%; 12 hr, 56.1% +/- 2.1%; 18 hr, 34.2% +/- 1%; 24 hr, 18.1% +/- 2.2%) compared to hypothermic groups (P < 0.001). The survival rate for the profound hypothermic group was significantly reduced (P < 0.01) compared to other hypothermic groups (at 17 degrees C: 12 hr, 85.9% +/- 2.5%, 18 hr, 74.7% +/- 3.7%, 24 hr, 58.7% +/- 2.7%). Almost equal survival rates were observed among mild, moderate, and deep hypothermic groups following <18 hr exposure to hypoxia, but the deep hypothermic group showed a significantly higher survival rate (84.1% +/- 1.6%; P < 0.001) when subjected to hypoxia for 24 hr. In conclusion, hypothermia offers marked neuroprotection against hypoxia, but attenuation of neuronal cell death was less with profound hypothermia compared to mild, moderate, and deep hypothermia. Deep hypothermia affords maximal protection of neurons compared to mild and moderate hypothermia during long-lasting hypoxia (>18 hr).

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of hypothermia at defined intraischemic time courses in cortical cultures

Varathan

Shibuta

Shimizu

et al. 2001

J of Neuroscience Research

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“…The reliability of the present image analysis can be supported further by the results on experimental ischemia (deprivation of oxygen and glucose). Previous investigations, including ours, have demonstrated that the membrane potential of CA1 pyramidal neurons during exposure to ischemic conditions showed a stereotyped response characterized by an initial hyperpolarization, followed by rapid and then sustained depolarization, called anoxic depolarization (Fujiwara et al, 1987;Okada et al, 1988;Schurr et al, 1989;Tanaka et al, 1997). There is general agreement that, in the initial hyperpolarization, an increase in K ϩ conductance is generated (Leblond and Krnjevic, 1989;Ben-Ari, 1990;Yamamoto et al, 1997).…”

Section: Discussionmentioning

confidence: 83%

Novel method for quantification of brain cell swelling in rat hippocampal slices

Nakajima

Nakamura

Ogawa

et al. 2004

J of Neuroscience Research

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We have developed a novel device for the quantification of edematous morphology changes in acute brain slices. We can also carry out real-time monitoring of detailed hippocampal cells. The device we developed is based on infrared differential interference contrast microscopy (IR-DIC) and a custom-made real-time computerized image-analysis system for quantification of the morphological dynamics of cells in slice preparations. We applied the coefficient of variation (CV) of light intensity in IR-DIC images to evaluate the change in morphological dynamics. We examined three kinds of edema in the CA1 region of rat hippocampal acute slices under conditions of hypotonic, strong excitation, and experimental ischemia, together with field excitatory postsynaptic potential (fEPSP) recording from radiatum in CA1 the region. There were notable close relationships among the edema formations, the light transmittance, the extent of changes in CV, and features of fEPSP during the three different insults. The present results indicate that CV is a reliable quantification index for edema formation in brain tissue and confirm that applying CV for the analysis in addition to the light transmittance analysis presents additional important information on brain tissue swelling.

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“…Comparable effects have been reported in vitro, where mild hypothermia provides a powerful protective effect. 41 This profound temperature sensitivity suggests that moderate reductions in temperature may induce significant reductions in release. We have found that mild spinal cord hypothermia (34°C) before aortic occlusion completely prevented glutamate release in the dorsal horn but only partially blocked the release of taurine observed during reperfusion.…”

Section: Mechanism Of Hypothermia-mediated Protectionmentioning

confidence: 99%

Effect of graded hypothermia (27 degrees to 34 degrees C) on behavioral function, histopathology, and spinal blood flow after spinal ischemia in rat.

Maršala

Vanický

Yaksh

1994

Stroke

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Background and PurposeWe used a rat model of reversible spinal ischemia to assess the effect of spinal cord temperature on the development of neurological and histopathologic changes after 20 minutes of reversible aortic occlusion. Spinal cord blood flow and CO 2 reactivity was tested by using laser Doppler before and 60 minutes after ischemia.Methods In halothane (l%)-anesthetized rats, the spinal cord temperature as assessed by using thermocouple in the paraspinal muscles was lowered to 34°, 31°, or 27°C. After ischemia, spinal cord temperature was raised to 37°C for the next 30 minutes. Animals were maintained in this normothermic condition for 8 hours, after which motor and sensory function were assessed. All animals were then anesthetized and perfused with 10% formalin for light microscopic analysis of spinal cords.Results In normothermic animals, 20 minutes of ischemia resulted in a loss of CO 2 reactivity and hind limb paraplegia

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The protective effect of hypothermia on reversibility in the neuronal function of the hippocampal slice during long lasting anoxia

Cited by 48 publications

References 7 publications

Neuroprotective effect of hypothermia at defined intraischemic time courses in cortical cultures

Neuroprotective effect of hypothermia at defined intraischemic time courses in cortical cultures

Novel method for quantification of brain cell swelling in rat hippocampal slices

Effect of graded hypothermia (27 degrees to 34 degrees C) on behavioral function, histopathology, and spinal blood flow after spinal ischemia in rat.

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