Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stroke-prone spontaneously hypertensive rats (SHRSPs) are vulnerable to ischemia and delayed neuronal death (DND) of hippocampus pyramidal cells when bilateral carotid arteries are occluded for only 10 min. Since this occlusion induces just mild ischemia, the resulting DND may be an appropriate animal model for dementia in patient with essential hypertension exposed to small ischemic insults. This study was designed to compare the effects of the antihypertensive drugs lercanidipine, nicardipine, lisinopril, valsartan, and hydralazine on occlusion-induced DND in SHRSPs. Drugs were administered for 2 weeks, from 15 to 17 weeks of age. 0.1% Nicardipine and 0.01 or 0.03% lercanidipine were administered in the SP diet (about 61.3, 5.7, and 18.8 mg/kg/day, respectively), and the remaining drugs were administered at 10 mg/kg/day using the mini-osmotic pump. The animals were operated on at 16 weeks of age, and DND was analyzed by histological examination 1 week later. Systolic blood pressure was measured at 15, 16, and 17 weeks of age. For chronic treatment, Calcium-channel blockers were administered from 8 to 17 weeks of age. All antihypertensive drugs significantly lowered systolic blood pressure at 16 weeks of age. Hydralazine and lisinopril were associated with the greatest reduction; however, lercanidipine, nicardipine, and valsartan effectively reduced systolic blood pressure to within a medium range. DND was significantly inhibited only by 0.03% lercanidipine. Chronic treatment with 0.03% lercanidipine also protected pyramidal neurons. The results of this study demonstrate that the long-acting, lipophilic Calcium-channel blocker lercanidipine inhibits occlusion-induced DND in SHRSPs and that lercanidipine may effectively reduce dementia induced by small ischemic insults in patients with essential hypertension.
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PMID:Lercanidipine rescues hippocampus pyramidal neurons from mild ischemia-induced delayed neuronal death in SHRSP. 2125 46

Hypertensive emergencies, though uncommon in children, are potentially life threatening. While targeting blood pressure reduction to below the 90th percentile for age, gender and height, mean arterial blood pressure should be gradually lowered by one-fourth of the planned reduction over 8-12 h, a further fourth over the next 8-12 h, and the final 50% over the 24 h after that. Frequent invasive or non-invasive blood pressure monitoring is essential, as is monitoring for sensorial alteration and loss of papillary reflexes. Few antihypertensive agents have been examined in children. Continuous intravenous infusions of short acting drugs such as nitroprusside, labetalol and nicardipine are preferred to intravenous boluses of hydralazine or diazoxide. If severe symptoms are absent, oral agents such as nifedipine, clonidine, minoxidil, hydralazine, labetalol, captopril, and prazosin may be used. Nicardipine and labetalol are particularly suited in emergencies with intracranial bleeding or ischemic stroke, while furosemide, sodium nitroprusside and nitroglycerine are useful in congestive cardiac failure. Therapy with oral antihypertensive drugs should be instituted within 6-12 h of parenteral therapy, and the latter gradually withdrawn over the next 12-48 h. Oral agents have limited application as primary therapy, except when administration of intravenous infusion is likely to be delayed. This article provides a summary of the clinical approach to evaluation and management of severe symptomatic hypertension in children.
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PMID:Hypertensive emergencies in children. 2127 5

Acute cerebrovascular diseases (ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage) affect 780,000 Americans each year. Physicians who care for patients with these conditions must be able to recognize when acute hypertension requires treatment and should understand the principles of cerebral autoregulation and perfusion. Physicians should also be familiar with the various pharmacologic agents used in the treatment of cerebrovascular emergencies. Acute ischemic stroke frequently presents with hypertension, but the systemic blood pressure should not be treated unless the systolic pressure exceeds 220 mm Hg or the diastolic pressure exceeds 120 mm Hg. Overly aggressive treatment of hypertension can compromise collateral perfusion of the ischemic penumbra. Hypertension associated with intracerebral hemorrhage can be treated more aggressively to minimize hematoma expansion during the first 3 to 6 hours of illness. Subarachnoid hemorrhage is usually due to aneurysmal rupture; systolic blood pressure should be kept <150 mm Hg to prevent re-rupture of the aneurysm. Nicardipine and labetalol are recommended for rapidly treating hypertension during cerebrovascular emergencies. Sodium nitroprusside is not recommended due to its adverse effects on cerebral autoregulation and intracranial pressure. Hypoperfusion of the injured brain should be avoided at all costs.
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PMID:Blood pressure control in acute cerebrovascular disease. 2136 52

Nicardipine is a dihydropyridine calcium-channel blocker that is frequently used in the acute treatment of hypertension in the emergency department (ED). Reflex sympathetic tachycardia is a well-described side effect of this medication. Two experimental studies and 1 anesthesia case report, however, have previously described nicardipine-induced bradycardia as a very rare side effect. We report the case of an elderly patient with an acute ischemic stroke who developed nicardipine-induced bradycardia in the ED.
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PMID:Bradycardia caused by intravenous nicardipine in an elderly patient with acute ischemic infarct. 2637 31


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