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Levosimendan limits reperfusion injury in a rat middle cerebral artery occlusion (MCAO) model.

Hein M, Zoremba N, Bleilevens C, Bruells C, Rossaint R, Roehl AB - BMC Neurol (2013)

Bottom Line: Although levosimendan limited the infarct size and brain swelling by 40% and 53%, respectively, no effect on neurological outcome or mortality could be demonstrated.Upregulation of tumor necrosis factor α and intercellular adhesion molecule 1 was significantly impeded.Levosimendan demonstrated significant neuroprotective properties in a rat model of transient brain ischemia by reducing reperfusion injury.

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ABSTRACT

Background: Neuroprotective strategies in ischemic stroke are an important challenge in clinical and experimental research as an adjunct to reperfusion therapy that may reduce neurologic injury and improve outcome. The neuroprotective properties of levosimendan in traumatic brain injury in vitro, transient global brain ischemia and focal spinal cord ischemia suggest the potential for similar effects in transient brain ischemia.

Methods: Transient brain ischemia was induced for 60 min by intraluminal occlusion of the middle cerebral artery in 40 male Wistar rats under general anesthesia with s-ketamine and xylazine and with continuous monitoring of their blood pressure and cerebral perfusion. Five minutes before inducing reperfusion, a levosimendan bolus (24 μg kg -1) was administered over a 20 minute period. Infarct size, brain swelling, neurological function and the expression of inflammatory markers were quantified 24 hours after reperfusion.

Results: Although levosimendan limited the infarct size and brain swelling by 40% and 53%, respectively, no effect on neurological outcome or mortality could be demonstrated. Upregulation of tumor necrosis factor α and intercellular adhesion molecule 1 was significantly impeded. Cerebral blood flow during reperfusion was significantly reduced as a consequence of sustained autoregulation.

Conclusions: Levosimendan demonstrated significant neuroprotective properties in a rat model of transient brain ischemia by reducing reperfusion injury.

No MeSH data available.


Related in: MedlinePlus

Additional effects of levosimendan treatment on neurological injury during MCAO. Differences between groups for brain swelling (A), serum levels of s-100ß (B) and neurological testing (C) after 24 hours were displayed (* p <0.05 vs. control; ** p < 0.01 vs. control).
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Figure 5: Additional effects of levosimendan treatment on neurological injury during MCAO. Differences between groups for brain swelling (A), serum levels of s-100ß (B) and neurological testing (C) after 24 hours were displayed (* p <0.05 vs. control; ** p < 0.01 vs. control).

Mentions: The total infarct volume was 239 ± 83 mm3 in the control group and 128 ± 42 mm3 in the levosimendan-treated group (p = 0.01). This difference was discernible in the cortex (142 ± 79 vs. 72 ± 36 mm3; p = 0.03) and the striatum (97 ± 38 vs. 56 ± 21 mm3; p = 0.02) in all slices (Figure 4A). Infarct size reduction was noted in the cortex medially and temporally and in the striatum from the center (Figure 4B/C). Total brain swelling was less pronounced after levosimendan treatment compared to the control group (63 ± 38 vs. 134 ± 43 mm3; p = 0.004; Figure 5A). Moreover, significantly lower serum levels of s-100ß were measured 24 hours after reperfusion in the levosimendan group versus the control group (1.19 ± 0.64 vs. 2.20 ± 1.75 ng mL-1; p = 0.02; Figure 5B). The low neurological test scores attained by both groups are indicative of a relevant functional deficit with no statistically significant differences between the groups (p = 0.12; Figure 5C).


Levosimendan limits reperfusion injury in a rat middle cerebral artery occlusion (MCAO) model.

Hein M, Zoremba N, Bleilevens C, Bruells C, Rossaint R, Roehl AB - BMC Neurol (2013)

Additional effects of levosimendan treatment on neurological injury during MCAO. Differences between groups for brain swelling (A), serum levels of s-100ß (B) and neurological testing (C) after 24 hours were displayed (* p <0.05 vs. control; ** p < 0.01 vs. control).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC3750823&req=5

Figure 5: Additional effects of levosimendan treatment on neurological injury during MCAO. Differences between groups for brain swelling (A), serum levels of s-100ß (B) and neurological testing (C) after 24 hours were displayed (* p <0.05 vs. control; ** p < 0.01 vs. control).
Mentions: The total infarct volume was 239 ± 83 mm3 in the control group and 128 ± 42 mm3 in the levosimendan-treated group (p = 0.01). This difference was discernible in the cortex (142 ± 79 vs. 72 ± 36 mm3; p = 0.03) and the striatum (97 ± 38 vs. 56 ± 21 mm3; p = 0.02) in all slices (Figure 4A). Infarct size reduction was noted in the cortex medially and temporally and in the striatum from the center (Figure 4B/C). Total brain swelling was less pronounced after levosimendan treatment compared to the control group (63 ± 38 vs. 134 ± 43 mm3; p = 0.004; Figure 5A). Moreover, significantly lower serum levels of s-100ß were measured 24 hours after reperfusion in the levosimendan group versus the control group (1.19 ± 0.64 vs. 2.20 ± 1.75 ng mL-1; p = 0.02; Figure 5B). The low neurological test scores attained by both groups are indicative of a relevant functional deficit with no statistically significant differences between the groups (p = 0.12; Figure 5C).

Bottom Line: Although levosimendan limited the infarct size and brain swelling by 40% and 53%, respectively, no effect on neurological outcome or mortality could be demonstrated.Upregulation of tumor necrosis factor α and intercellular adhesion molecule 1 was significantly impeded.Levosimendan demonstrated significant neuroprotective properties in a rat model of transient brain ischemia by reducing reperfusion injury.

View Article: PubMed Central - HTML - PubMed

ABSTRACT

Background: Neuroprotective strategies in ischemic stroke are an important challenge in clinical and experimental research as an adjunct to reperfusion therapy that may reduce neurologic injury and improve outcome. The neuroprotective properties of levosimendan in traumatic brain injury in vitro, transient global brain ischemia and focal spinal cord ischemia suggest the potential for similar effects in transient brain ischemia.

Methods: Transient brain ischemia was induced for 60 min by intraluminal occlusion of the middle cerebral artery in 40 male Wistar rats under general anesthesia with s-ketamine and xylazine and with continuous monitoring of their blood pressure and cerebral perfusion. Five minutes before inducing reperfusion, a levosimendan bolus (24 μg kg -1) was administered over a 20 minute period. Infarct size, brain swelling, neurological function and the expression of inflammatory markers were quantified 24 hours after reperfusion.

Results: Although levosimendan limited the infarct size and brain swelling by 40% and 53%, respectively, no effect on neurological outcome or mortality could be demonstrated. Upregulation of tumor necrosis factor α and intercellular adhesion molecule 1 was significantly impeded. Cerebral blood flow during reperfusion was significantly reduced as a consequence of sustained autoregulation.

Conclusions: Levosimendan demonstrated significant neuroprotective properties in a rat model of transient brain ischemia by reducing reperfusion injury.

No MeSH data available.


Related in: MedlinePlus