Laser Doppler Scanning: How Many Measurements are Required to Assess Regional Cerebral Blood Flow?

Soehle, Martin; Heimann, Axel; Kempski, Oliver

doi:10.1007/978-3-7091-6346-7_36

“…In all animals a skull area frontal to the injury site was thinned out on both hemispheres. CBF was measured by laser Doppler scanning (Soehle et al, 2000). Treatment started 15 min after CCI.…”

Section: Experimental Designmentioning

confidence: 99%

“…For CBF scanning 25 positions were predefined in a grid (1 · 1-mm squares) on the thinned out skull area over each hemisphere (Soehle et al, 2000). During each scan (180 sec) CBF was recorded at each position.…”

Section: Cerebral Blood Flow Scanningmentioning

confidence: 99%

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

Alessandri

¹

,

Schwandt

²

,

Kamada

³

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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“…Assuming that a bilateral decrease of laser-Doppler flow (LDF) reflects a global reduction of CBF, that baseline LDF reflects normal cerebral perfusion and that relative changes of LDF reflect relative changes of CBF in about the same percentage (Soehle et al, 2000;Schmid-Elsaesser et al, 1998), CBF did not fall below ischemic thresholds in any of the SAH-groups (Jones et al, 1981). Accordingly, we found no signs of cerebral infarction.…”

Section: Tissue Damagementioning

confidence: 51%

Impact of various extents of experimental subarachnoid hemorrhage induced by the endovascular filament model on mortality and changes of cerebral blood flow

Westermaier

¹

,

Jauss²,

Vince³

et al. 2011

J Exp Stroke Transl Med

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Objective: Among various animal models of subarachnoid hemorrhage (SAH), the endovascular filament model has been found particularly suitable to investigate acute pathophysiological changes after experimental SAH. Its major drawback, however, are high mortality and high variability of results. The present studies were carried out to examine the impact of various extents of experimental SAH in rats induced by different filament sizes. Methods:In study 1, Sprague-Dawley rats were subjected to vessel perforation with a 3-0, 4-0 or 5-0 monofilament or served as controls (n = 8). Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and local cortical blood flow (LCBF) were continuously monitored for 6 hours after SAH. 24 hours later, the animals were sacrificed to evaluate subarachnoid blood effusion. In study 2, the animals were subjected to SAH using a 3-0 monofilament or served as controls (n = 8). After 7 days, they were sacrificed for quantification of tissue damage.Results: With increasing filament size, the decrease of CPP and LCBF and subarachnoid blood effusion were more pronounced. In all SAH-groups, the decline of LCBF after SAH exceeded the decline of CPP. Hippocampal damage was moderate but consistent. In both studies, the acute mortality was lower than previously reported. Conclusion:With controlled pre-hemorrhage blood pressure values and longer mechanical ventilation mortality can be kept low even if stronger filaments are used. The impact of subarachnoid vessel perforation on pathophysiological changes and blood effusion can be graded by the use of different filament sizes. The persisting mismatch between CPP and LCBF both in major and minor SAH suggests sustained vasoconstriction occurring independent of the extent of hemorrhage.

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“…Assuming that a bilateral decrease of laser-Doppler flow (LDF) reflects a global reduction of CBF, that baseline LDF reflects normal cerebral perfusion and that relative changes of LDF reflect relative changes of CBF in about the same percentage (Soehle et al, 2000;Schmid-Elsaesser et al, 1998), CBF did not fall below ischemic thresholds in any of the SAH-groups (Jones et al, 1981). Accordingly, we found no signs of cerebral infarction.…”

Section: Tissue Damagementioning

confidence: 67%

Impact of various extents of experimental subarachnoid hemorrhage induced by the endovascular filament model on mortality and changes of cerebral blood flow

Westermaier¹,

Jauss²,

Vince³

et al. 2011

Journal of Experimental Stroke and Translational Medicine

View full text Add to dashboard Cite

Objective: Among various animal models of subarachnoid hemorrhage (SAH), the endovascular filament model has been found particularly suitable to investigate acute pathophysiological changes after experimental SAH. Its major drawback, however, are high mortality and high variability of results. The present studies were carried out to examine the impact of various extents of experimental SAH in rats induced by different filament sizes. Methods:In study 1, Sprague-Dawley rats were subjected to vessel perforation with a 3-0, 4-0 or 5-0 monofilament or served as controls (n = 8). Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and local cortical blood flow (LCBF) were continuously monitored for 6 hours after SAH. 24 hours later, the animals were sacrificed to evaluate subarachnoid blood effusion. In study 2, the animals were subjected to SAH using a 3-0 monofilament or served as controls (n = 8). After 7 days, they were sacrificed for quantification of tissue damage.Results: With increasing filament size, the decrease of CPP and LCBF and subarachnoid blood effusion were more pronounced. In all SAH-groups, the decline of LCBF after SAH exceeded the decline of CPP. Hippocampal damage was moderate but consistent. In both studies, the acute mortality was lower than previously reported. Conclusion:With controlled pre-hemorrhage blood pressure values and longer mechanical ventilation mortality can be kept low even if stronger filaments are used. The impact of subarachnoid vessel perforation on pathophysiological changes and blood effusion can be graded by the use of different filament sizes. The persisting mismatch between CPP and LCBF both in major and minor SAH suggests sustained vasoconstriction occurring independent of the extent of hemorrhage.

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Laser Doppler Scanning: How Many Measurements are Required to Assess Regional Cerebral Blood Flow?

Cited by 5 publications

References 8 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

Impact of various extents of experimental subarachnoid hemorrhage induced by the endovascular filament model on mortality and changes of cerebral blood flow

Impact of various extents of experimental subarachnoid hemorrhage induced by the endovascular filament model on mortality and changes of cerebral blood flow

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