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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.

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

Effects of levosimendan treatment on the autoregulatory index. Values after transient MCAO (reperfusion) were compared to values before ischemia (baseline) (*** p < 0.001 vs. levosimendan).
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Figure 3: Effects of levosimendan treatment on the autoregulatory index. Values after transient MCAO (reperfusion) were compared to values before ischemia (baseline) (*** p < 0.001 vs. levosimendan).

Mentions: Although HR and MAP did change significantly over time (p = 0.001), no differences between the groups could be observed (Figure 2A/B). There was a significant interaction between time and group for CBF (p = 0.001). Post-hoc analysis showed significantly lower CBF values in the levosimendan group at 20 and 30 min after reperfusion (Figure 2C). ARI demonstrated no differences between the groups (0.37 ± 0.31 vs. 0.32 ± 0.18) before ischemia. During reperfusion, ARI remained unchanged after levosimendan treatment (0.35 ± 0.22; Figure 3) but it increased in the control group (1.71 ± 0.68; p = 0.001), an indication of abrogated autoregulation.


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)

Effects of levosimendan treatment on the autoregulatory index. Values after transient MCAO (reperfusion) were compared to values before ischemia (baseline) (*** p < 0.001 vs. levosimendan).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750823&req=5

Figure 3: Effects of levosimendan treatment on the autoregulatory index. Values after transient MCAO (reperfusion) were compared to values before ischemia (baseline) (*** p < 0.001 vs. levosimendan).
Mentions: Although HR and MAP did change significantly over time (p = 0.001), no differences between the groups could be observed (Figure 2A/B). There was a significant interaction between time and group for CBF (p = 0.001). Post-hoc analysis showed significantly lower CBF values in the levosimendan group at 20 and 30 min after reperfusion (Figure 2C). ARI demonstrated no differences between the groups (0.37 ± 0.31 vs. 0.32 ± 0.18) before ischemia. During reperfusion, ARI remained unchanged after levosimendan treatment (0.35 ± 0.22; Figure 3) but it increased in the control group (1.71 ± 0.68; p = 0.001), an indication of abrogated autoregulation.

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