Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol

Bermueller, Christian; Thal, Serge C.; Plesnila, Nikolaus; Schmid-Elsaesser, Robert; Kreimeier, U.; Zausinger, Stefan

doi:10.1016/j.jns.2005.10.016

Cited by 24 publications

(24 citation statements)

References 70 publications

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“…Using a model of subarachnoid hemorrhage (SAH) that induces a massive ipsilateral CBF depression, a 20-min augmentation of CBF by a bolus injection of hyperoncotic/hypertonic fluid was sufficient to induce neuroprotection. Treatment with mannitol and hypertonic solution did not affect CBF, and induced less neuroprotection following SAH (Bermueller et al, 2006), indicating that even a short-term CBF increase early after SAH contributes to neuroprotection. In this way the energy supply has been improved in areas at risk, and lactate may have supported protective processes such as oxidative metabolism (Holloway et al, 2007;Levasseur et al, 2006), free radical scavenging (Groussard et al, 2000), or upregulation of MCT-1 and COX (Hashimoto and Brooks, 2008).…”

Section: Discussionmentioning

confidence: 89%

The Neuroprotective Effect of Lactate Is Not Due to Improved Glutamate Uptake after Controlled Cortical Impact in Rats

Alessandri

Schwandt

Kamada

et al. 2012

Journal of Neurotrauma

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For many years lactate was considered to be a waste product of glycolysis. Data are accumulating that suggest that lactate is an important energy substrate for neurons during activation. In severe traumatic brain injury (TBI) glutamate release and ischemic cerebral blood flow (CBF) are major factors for a mismatch between energy demand and supply and for neuronal cell death. Although ATP and behavior could be improved by lactate treatment after TBI, no histological correlate nor any linkage to better astrocytic glutamate uptake or CBF as possible mechanisms have been described. We subjected male rats to a controlled cortical impact (CCI; 5 m/sec, 2.5 mm). To study the effects of lactate treatment on lesion volume, glutamate release, and CBF, animals were infused with either NaCl or 100 mM lactate for up to 3 h. The role of endogenous lactate was investigated by inhibiting transport with α-cyano-4-hydroxy-cinnamic acid (4-CIN; 90 mg/kg). Lactate treatment 15 min post-CCI reduced lesion volume from 21.1±2.8 mm³ to 12.1±1.9 mm³ at day 2 after CCI. Contusion produced a significant three- to fourfold increase of glutamate in microdialysates, but there was no significant difference between treatments that began 30 min before CCI. In this experiment lesion volume was significantly reduced by lactate at day 7 post-CCI (23.7±4 to 9.3±1-2 mm³). CBF increased immediately after CCI and dropped thereafter below baseline in all animals. Lactate infusion 15 min post-CCI elevated CBF for 20 min in 7 of 10 animals, whereas 7 of 8 NaCl-treated animals showed a further CBF decline. Neuroprotection was achieved by lactate treatment following contusion injury, whereas blocking of endogenous lactate transport exerted no adverse effects. Neuroprotection was not achieved by improved glutamate uptake into astrocytes, but was supported by augmented CBF following CCI. Due to its neuroprotective property, lactate might be a beneficial pharmacological treatment for TBI patients.

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Section: Discussionmentioning

confidence: 89%

The Neuroprotective Effect of Lactate Is Not Due to Improved Glutamate Uptake after Controlled Cortical Impact in Rats

Alessandri

Schwandt

Kamada

et al. 2012

Journal of Neurotrauma

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“…Coronal sections (bregma −1.6 mm) were prepared and stained with Cresyl Violet. The number of surviving neurons in the hippocampus was quantified in a region of interest of 0.4 mm × 0.4 mm as previously described (Bermueller et al, 2006).…”

Section: Quantification Of Ischemic Brain Damagementioning

confidence: 99%

Standardized induction of subarachnoid hemorrhage in mice by intracranial pressure monitoring

Feiler¹,

Friedrich²,

Schöller³

et al. 2010

Journal of Neuroscience Methods

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“…In this and other studies, we were not able to identify brain tissue injury in coronary sections. 5,39 Human trials have shown an association of increased ICP with intraoperative cerebral swelling and worse postoperative Glasgow Coma Scale scores. 12 A correlation of increased mortality was found with reinforced brain edema formation.…”

Section: Discussionmentioning

confidence: 99%

“…37 Histological data 7 days after SAH demonstrated bilateral hippocampal damage. 5,39 Three days might therefore be too short to result in detectable damage in the CA1-3 region. Ongoing pathophysiological processes, such as delayed cerebral vasospasm, may be necessary to produce additional, delayed histological damage.…”

Section: Discussionmentioning

confidence: 99%

Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

Thal¹,

Sporer²,

Kłopotowski

et al. 2009

JNS

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Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: A comparison between small volume resuscitation and mannitol

Cited by 24 publications

References 70 publications

The Neuroprotective Effect of Lactate Is Not Due to Improved Glutamate Uptake after Controlled Cortical Impact in Rats

The Neuroprotective Effect of Lactate Is Not Due to Improved Glutamate Uptake after Controlled Cortical Impact in Rats

Standardized induction of subarachnoid hemorrhage in mice by intracranial pressure monitoring

Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

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