Key result
Intracerebroventricular Angiotensin 1-7 reduces infarct size ~59% versus controls in a rat ischemic stroke model.
Why the study?
Stimulation of ACE2, production of Angiotensin 1-7, and activation of the Mas receptor are potential targets for cerebroprotection in ischemic stroke but require demonstration in relevant models.
Does intracerebroventricular Angiotensin 1-7 reduce infarct size and neurological deficits in a rat model of ischemic stroke?
Does intracerebroventricular Angiotensin 1-7 reduce infarct size and neurological deficits in a rat model of ischemic stroke?
Absolute Event Rate: 15.23% vs 36.94%
Central administration of Angiotensin 1-7 provides cerebroprotection by reducing infarct size and neurological deficits in a rat model of ischemic stroke.
Hypothesis-generating for central Ang 1-7 in stroke; prospective human trials needed before any adoption.
Recent progress in cardiovascular therapy suggests that stimulation of Angiotensin Converting Enzyme 2 (ACE2), production of Angiotensin 1‐7 (Ang 1‐7), and activation of the Ang 1‐7 receptor, Mas, are viable targets for disease prevention and treatment. We proposed that central administration of Ang 1‐7 via lateral ventricular cannula will provide cerebroprotection in a rat model of Endothelin‐1 (ET‐1)‐induced middle cerebral artery occlusion (MCAO). Prior to ET‐1 induced MCAO, rats were treated with intracerebroventricular Ang 1‐7 (1µg/h) or artificial Cerebrospinal Fluid (aCSF) for 5 days. Ang 1‐7 treatment reduced neurological deficits and infarct size measured 72 h after MCAO induction. Infarct size was reduced to 15.23 ± 5.77% (n = 9) of ipsilateral gray matter in the Ang 1‐7 treated rats compared with 36.94 ± 7.56% (n = 12) in artificial Cerebrospinal Fluid (aCSF) controls. Neurological deficits were also reduced in Ang 1‐7 treated rats as indicated by a lower Benderson Exam Score of 0.22 ± 0.15 (n = 9) compared to 1.08 ± 0.31 (n = 12) in control rats, a higher Garcia Exam Score of 17.56 ± 0.18 (n = 9) compared to 14.00 ± 1.10 (n = 12) in control rats, and improved sunflower seed eating from 146 ± 23 s and 14 ± 1 (n = 9) shell pieces compared to 293 ± 7 s and 29 ± 1 shell pieces (n = 12) in control rats. This provides the first demonstration of the cerebroprotective properties of Ang 1‐7 during ischemic stroke.
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Mecca et al. (2009) studied Ischemic stroke (n=21). Intracerebroventricular Angiotensin 1-7 vs. Artificial Cerebrospinal Fluid (aCSF) was evaluated on Infarct size (% of ipsilateral gray matter). Intracerebroventricular administration of Angiotensin 1-7 reduced infarct size to 15.23% compared to 36.94% in controls in a rat model of ischemic stroke.
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