enalapril and Infarction--Middle-Cerebral-Artery

Over 80% of patients exhibit an acute increase in blood pressure (BP) following stroke. Current clinical guidelines make no distinction in BP management between patients with or without prior hypertension. Spontaneously hypertensive (SH) rats were preinstrumented with telemeters to record BP, intracranial pressure, and brain tissue oxygen in the predicted ischemic penumbra for 3 days before and 10 days after transient middle cerebral artery occlusion (n=8 per group) or sham (n=5). Before stroke, BP was either left untreated or chronically treated to a normotensive level (enalapril 10 mg/kg per day). Poststroke elevations in BP were either left uncontrolled, controlled (to the prestroke baseline level), or overcontrolled (to a normotensive level) via subcutaneous infusion of labetalol. Baseline values of intracranial pressure and brain tissue oxygen were similar between all groups, whereas BP was lower in treated SH rats (144±3 versus 115±5 mm Hg;

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Blood Pressure; Brain; Brain Chemistry; Brain Ischemia; Enalapril; Hypertension; Infarction, Middle Cerebral Artery; Intracranial Hypertension; Male; Movement Disorders; Oxygen; Random Allocation; Rats; Rats, Inbred SHR; Recovery of Function; Time Factors

Angioedema orolingual tras trombolisis intravenosa.

Topics: Adrenal Cortex Hormones; Aged, 80 and over; Angioedema; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Bradykinin; Capillary Permeability; Cerebral Cortex; Drug Synergism; Drug Therapy, Combination; Enalapril; Female; Fibrinolytic Agents; Histamine Antagonists; Humans; Hypertension; Infarction, Middle Cerebral Artery; Infusions, Intravenous; Thrombolytic Therapy; Tissue Plasminogen Activator

There is evidence that acutely elevated blood pressure (BP) after stroke is associated with increased cerebral hemorrhage and edema. Previous experiments in our laboratory have shown that candesartan 1 mg/kg administered after reperfusion in a model of hypertension after experimental ischemic stroke reduces neurovascular damage and improves outcome. These results could be either mediated by BP lowering or a BP-independent cerebrovascular protective effect.. To determine the contribution of BP lowering to the neurovascular protection previously reported with candesartan after stroke.. Male Wistar rats (280-305 g) underwent 3 h of middle cerebral artery occlusion (MCAO). At reperfusion, either hydralazine 1 mg/kg (n = 8), enalapril 5 mg/kg (n = 7) or enalapril 10 mg/kg (n = 8) were administered intravenously. BP was measured by telemetry for 2 days before and 24 h after MCAO. After neurological function was assessed, brain tissue was processed for infarct size and hemoglobin content analyses.. Mean arterial pressure (MAP) increased from 92 to 124 mmHg immediately upon MCAO and decreased to 112 mmHg after reperfusion, remaining elevated for 24 h (P < 0.0001) in the saline group. Hydralazine reduced MAP (P = 0.048) and infarct size (53 versus 30%, P = 0.0083), and there was a trend towards decreased hemoglobin content. Enalapril 5 mg/kg did not significantly change MAP or other outcomes. Enalapril 10 mg/kg reduced MAP (P < 0.0001) and infarct size (53 versus 29%, P = 0.003). There was an intermediate effect on both hemoglobin content and neurological function, neither one was significant. The time course of BP lowering varied with each treatment.. Acute BP lowering after reperfusion in acute ischemic stroke is an effective strategy to achieve neurovascular protection. The rate, extent and mechanism of BP lowering may determine the magnitude of protection.

Topics: Analysis of Variance; Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Area Under Curve; Benzimidazoles; Biomarkers; Biphenyl Compounds; Blood Pressure; Brain Ischemia; Cerebrovascular Circulation; Circadian Rhythm; Disease Models, Animal; Dose-Response Relationship, Drug; Enalapril; Hemoglobins; Hydralazine; Infarction, Middle Cerebral Artery; Male; Rats; Rats, Wistar; Reperfusion; Telemetry; Tetrazoles

The effects of an angiotensin II type 1 (AT1) receptor blocker (ARB) on ischemic brain damage induced by middle cerebral artery (MCA) occlusion were compared with those of an angiotensin converting enzyme (ACE) inhibitor. Treatment of male C57BL/6J mice with an ARB, candesartan, reduced the brain ischemic area and neurological deficit after MCA occlusion at a non-hypotensive dose. In contrast, an ACE inhibitor, enalapril, did not reduce the brain ischemic area, and neurological deficit even at a hypotensive dose. Candesartan improved the reduction of brain surface blood flow after MCA occlusion, and inhibited the increase in superoxide production both in the cortex and brain arterial wall at non-hypotensive and hypotensive doses. However, enalapril did not affect the changes in blood flow and superoxide production in the brain after MCA occlusion. AT2 receptor expression in the ischemic area was increased at 3 h after MCA occlusion by pretreatment with candesartan, but not that with enalapril. AT1 receptor expression was neither affected by candesartan nor by enalapril. These results suggest that candesartan attenuated ischemic brain damage, at least partly, through inhibition of oxidative stress.

Topics: Analysis of Variance; Animals; Antihypertensive Agents; Benzimidazoles; Biphenyl Compounds; Blood Pressure; Brain; Brain Ischemia; Cerebrovascular Circulation; Dose-Response Relationship, Drug; Enalapril; Histocompatibility Antigens; Immunohistochemistry; Infarction, Middle Cerebral Artery; Male; Mice; Mice, Inbred C57BL; Oxidative Stress; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Superoxides; Tetrazoles; Tetrazolium Salts