**14. Research envisaged using autologous whole blood induced haemorrhage model**

Takehiro Nakamura, MD et al., have studied the effect of Deferoxamine an iron chelator, on brain edema and neurological deficits induced by autologous whole blood intracerebral haemorrhage model in rats. The effect of Deferoxamine was assessed by measuring edema formation in the brain, and neurological deficits were studies using functional tests. 8-hydroxyl-2-deoxyguanosine (8-OHdG), a marker to check the oxidative DNA damage, was estimated using immunohistochemical analysis followed by a western blot test to estimate the amount of redox effector factor–1 and apurinic/ apyrimidinic endonuclease (Ref-1/APE) to assess DNA oxidative damage. Treatment


#### **Table 1.**

*Comparision between invivo cerebral ischemic models.*

with deferoxamine inherited brain edema formation, restored all neurological deficits, and prevented intracerebral haemorrhage-induced changes in 8-OHdG and Ref-1/APE. The results confirmed that deferoxamine might have potential use in decreasing oxidative stress caused by hematoma [82].

Takehiro Nakamura MD has studied the effect of nafamostat mesylate (FUT), a serine protease inhibitor, on brain injury and edema formation using intracerebral haemorrhage model rats. FUT was injected intraperitoneally after 6 hr. of intracerebral haemorrhage. Treatment with FUT reduced brain water content in the basal ganglia region and inhibited 8-hydroxyl-2-deoxyguanosine changes; thus, FUT would be a potential component to treat intracerebral haemorrhage [83].

Takehiro Nakamura, MD et al., have studied the effect of edaravone on brain edema and neurologic deficits using the Intracerebral haemorrhage model in rats. The model was adapted to measure edema size and neurological deficits, and oxidative markers to estimate brain injury. Treatment with edaravone after 2 hr. of ICH (Intracerebral Hemorrhage) successfully ameliorated the formation of brain edema and reduced impact on neurological activity. It also inhibited ICH (Intracerebral Hemorrhage) induced changes in oxidative biomarkers and prevented an oxidative injury. These results recommend Edaravone as an active component in treating ICH (Intracerebral Hemorrhage) [84].

T. Nakamura et al., have studied the effects of endogenous and exogenous estrogen on intracerebral haemorrhage ICH (Intracerebral Hemorrhage) induced brain damage in male and female rats. In the study impact of delayed administration of estradiol on ICH (Intracerebral Hemorrhage) induced brain injury was examined along with dependence on the estrogen receptor. The effect of estradiol on neuronal deficits and brain edema was estimated 24 h after ICH (Intracerebral Hemorrhage) induction. Formation of brain edema was evident in male rats when compared with that of female rats. Estrogen receptor activation takes place in a female after ICH (Intracerebral Hemorrhage). After 2 hr. of ICH (Intracerebral Hemorrhage), estradiol administration to male rats restored neurological deficits, reduced edema formation, and increased Heme oxygenase-1. Treatment with estradiol in male rats was adequate compared to female rats and could be accepted as a potential component in ICH treatment (Intracerebral Hemorrhage) (**Table 1**) [85].

## **15. Conclusion**

*In vivo* experimental model are used widely to understand the underlying physiology involved in different types of human stroke. The pattern of ischemic injury involved would vary in each model. The pathophysiological changes in rodents post-ischemic injury can be compared to that of injury pattern in human stroke. There are several other stroke models, but we have explained the most commonly used methods in this chapter. Based on the investigator's interest, a suitable model can be used to study different types of ischemic strokes.

*Experimental Animal Models of Cerebral Ischemic Reperfusion Injury DOI: http://dx.doi.org/10.5772/intechopen.97592*
