Central renin angiotensin system has an important role on the cerebral microcirculation and
metabolism. Our previous work showed that inhibition of angiotensin converting enzyme (ACE) activity prior to
induction of ischemia protected the brain from severe ischemia/reperfusion (I/R) injuries. This study evaluated the
impacts of post-ischemic inhibition of ACE, enalapril, on brain infarction in normotensive rats. Methods: Rats
were anesthetized with chloral hydrate (400 mg/kg). Focal cerebral ischemia was induced by 60-min intraluminal
occlusion of right middle cerebral artery (MCA). Intraperitoneal injection of enalapril (0.03 or 0.1 mg/kg) was done
after MCA reopening (reperfusion). Neurological deficit score (NDS) was evaluated after 24 h and the animals
randomly assigned for the assessments of infarction, absolute brain water content (ABWC) and index of brain
edema. Results: Severe impaired motor functions (NDS = 2.78 ± 0.28), massive infarction (cortex = 214 ± 19 mm3,
striatum = 86 ± 5 mm3) and edema (ABWC = 83.1 ± 0.46%) were observed in non-treated ischemic rats. Nonhypotensive
dose of enalapril (0.03 mg/kg) significantly reduced NDS (1.5 ± 0.22), infarction (cortex = 102 ± 16
mm3, striatum = 38 ± 5 mm3) and edema (ABWC = 80.9 ± 0.81%). Enalapril at dose of 0.1 mg/kg significantly
lowered arterial pressure could not improve NDS (2.0 ± 0.45) and reduce infarction (cortex = 166 ± 26 mm3,
striatum = 71 ± 11 mm3). Conclusion: Post-ischemic ACE inhibition in the normotensive rats without affecting
arterial pressure protects the brain from reperfusion injuries; however, this beneficial action is masked by
hypotension
