ramipril and Brain-Ischemia

In the list of named numerical neuro-ophthalmological syndromes, such as one-and-a-half syndrome and others, we report for the first time twenty-and-a-half syndrome, which is characterized by one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy (1.5 + 7 + 7 + 5 = 20.5) in a patient with ischemic stroke.. A 45-year-old Asian Hindu woman presented with vomiting and imbalance of 1 day's duration. She had left-sided ataxic hemiparesis with one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy. Magnetic resonance imaging of her brain revealed acute non-hemorrhagic infarct in the right posterolateral aspect of pons and medulla, with normal brain vessels angiography. We described her disorder as twenty-and-a-half syndrome. She was put on antiplatelet therapy.. Twenty-and-a-half syndrome is reported for the first time. It is due to posterior circulation stroke; in our case, it was due to lacunar infarcts in the pons and medulla, manifesting as one-and-a-half syndrome with bilateral seventh and right fifth nerve palsy.

Topics: Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Atorvastatin; Brain; Brain Ischemia; Cranial Nerve Diseases; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Magnetic Resonance Imaging; Middle Aged; Paresis; Physical Therapy Modalities; Platelet Aggregation Inhibitors; Ramipril; Stroke; Syndrome

Topics: Anticoagulants; Brain Ischemia; Churg-Strauss Syndrome; Endocardium; Female; Fibrinolytic Agents; Humans; Middle Aged; Ramipril; Thrombosis

Topics: Animals; Antihypertensive Agents; Benzimidazoles; Benzoates; Brain Ischemia; Cerebral Arteries; Drug Therapy, Combination; Hypertension; Male; Ramipril; Random Allocation; Rats; Rats, Inbred SHR; Telmisartan; Vasodilation

We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSH t) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Brain Injuries; Brain Ischemia; Chronic Disease; Disease Models, Animal; Free Radicals; Glutathione; Glutathione Disulfide; Malondialdehyde; Neuroglia; Ramipril; Rats; Rats, Sprague-Dawley

Drugs interfering with the renin-angiotensin system (RAS) have been shown to reduce the incidence of stroke in patients at risk and to afford neuroprotection in experimental brain ischemia. This study aimed to compare potential neuroprotective effects of systemic pretreatment with the angiotensin receptor blocker, candesartan, and the angiotensin-converting enzyme (ACE)-inhibitor, ramipril, in normotensive Wistar rats after focal cerebral ischemia, with special emphasis on the regulation of neurotrophins.. Equipotent subcutaneous doses of candesartan and ramipril were determined via inhibition of pressor responses to intravenously injected angiotensin II (Ang II) or angiotensin I (Ang I), respectively. Accordingly, animals were treated with candesartan (0.1 mg/kg body weight, twice daily), ramipril (0.01 and 0.1 mg/kg body weight, twice daily) or vehicle (0.9% saline, twice daily), respectively, 5 days prior to middle cerebral artery occlusion (MCAO) with reperfusion. Severity of stroke was estimated via infarct size [magnetic resonance imaging (MRI) 48 h after MCAO] and neurological outcome (24 h, 48 h after MCAO). Measurements of neurotrophins/receptors in brain tissue were performed 48 h after MCAO.. Pretreatment with candesartan and ramipril (low dose) did not reduce blood pressure during MCAO, whereas ramipril high dose did. Candesartan, but not ramipril at any dose, significantly reduced stroke volume and improved neurological outcome. Poststroke mRNA and protein of the neurotrophin receptor, TrkB, were significantly elevated in animals treated with candesartan, but not ramipril.. Systemic pretreatment with a sub-hypotensive, RAS-blocking dose of candesartan affords neuroprotection after focal ischemia, associated with increased activity of the neurotrophin BDNF/TrkB system. Ramipril at sub-hypotensive and hypotensive, RAS-blocking doses showed no significant neuroprotective effects.

Topics: Animals; Antihypertensive Agents; Benzimidazoles; Biphenyl Compounds; Brain Ischemia; Brain-Derived Neurotrophic Factor; Disease Models, Animal; Incidence; Male; Pilot Projects; Ramipril; Rats; Rats, Wistar; Receptor, trkB; Renin-Angiotensin System; Reverse Transcriptase Polymerase Chain Reaction; Stroke; Tetrazoles