Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Color Doppler US is at present the most reliable noninvasive procedure in the diagnosis of carotid disease and plays a major diagnostic role in the patient at risk for stroke. The anatomofunctional relationships of carotid and vertebrobasilar system suggest a diagnostic combination between Doppler US and transcranial Doppler for complete hemodynamic evaluation of normal and pathologic cerebral vessels. The most relevant disease, as the cause of stroke, is represented by internal carotid atherosclerosis. Mechanisms by which the atheromatous plaque represents a cause of ischemia involve two factors: the embolic factor and the hemodynamic factor. The embolic factor is consequent on unstable plaques and US plays a major role in plaque characterization. Stenotic plaques are the major cause of the hemodynamic factor. Color Doppler US inables quantification of stenosis and selects surgical patients with greater than 70% stenosis. In internal carotid dissection as the acute cause of cerebrovascular insufficiency color Doppler US findings are significant for early diagnosis and follow-up.
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PMID:[The role of Doppler US in the study of carotid system]. 885 21

Clinically significant arterial occlusive disease developed in 26 patients at between 5 months and 44 years (mean(s.d.) 10.7(12.0) years) following radiation therapy. Therapeutic radiation was associated with lesions of the carotid artery (nine patients), subclavian-axillary arteries (seven) and the abdominal aorta and its branches (10). Clinical presentations included transient ischemic attack, stroke, vertebrobasilar insufficiency, carotid bruit, upper- or lower-extremity ischemia and renovascular hypertension. Surgery for cerebrovascular insufficiency included carotid endarterectomy with vein patch, interposition grafting or subclavian-to-carotid bypass. Carotid or subclavian-to-axillary bypass was performed for upper-extremity ischemia. A combination of endarterectomy and Dacron or saphenous vein grafts was used for infrarenal reconstruction. Tunnels were placed orthotopically. Musculocutaneous flaps assisted in healing selected wounds. Ureteral catheters were useful adjuncts in abdominal vascular reconstructions. There were no operative deaths, strokes or amputations. One patient had recurrent transient ischemic attacks following subclavian-to-carotid bypass. The mean(s.d.) postoperative follow-up was 48.1(39.6) months. Patients presenting with end-organ ischemia following radiation therapy can be managed successfully with aggressive surgical revascularization using a broad spectrum of reconstructive techniques.
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PMID:Management of arterial occlusive disease following radiation therapy. 886 26

The effects of chronic cerebrovascular ischemia on memory function and cytochrome oxidase (CO) activity were investigated. Cerebrovascular insufficiency was induced by permanent bilateral carotid artery ligation (2-VO) in 19 month old rats. Sham surgery in no-vessel occlusion (no-VO) rats were used for controls. Memory function was tested 1 week prior to surgery and then weekly for 21 days using the Morris water maze. Regional brain activity of CO was measured 4 weeks after surgery by quantitative histochemistry. Histologic examination of brain slices was used to evaluate any neuropathology present. Results showed that 2-VO rats were significantly impaired in the water maze task at each testing period with respect to no-VO controls. In addition, CO activity in 2-VO rats was markedly reduced only in the dorsal CA1 region of the hippocampus and in the posterior parietal cortex. These brain regions are involved in visuo-spatial memory mechanisms. Analysis of other brain regions in 2-VO rats did not reveal further CO activity changes. There were no damaged or loss of neurons in 2-VO or no-VO groups in any region examined, including CA1 and posterior parietal cortex. The CA1 region however, is known to undergo neuronal loss 25 weeks after chronic 2-VO suggesting that this vascular insult can induce a slowly-evolving cascade consisting of neuronal damage, atrophy and death. The present findings indicate that reduced CO activity in CA1 and posterior parietal regions can predict neural damage and atrophy prior to structural perikaryal pathology following chronic brain ischemia. In addition, the data shows that neuronal energy metabolic deficiency may initiate visuo-spatial memory impairment in this aging rat model.
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PMID:Reduced cytochrome oxidase and memory dysfunction after chronic brain ischemia in aged rats. 908 Apr 58

AGE-RELATED CARDIOVASCULAR CHANGES: Age-related changes in vascular structure and function may contribute to isolated systolic hypertension and target-organ damage. These include cardiac hypertrophy, systolic as well as diastolic dysfunction, congestive heart failure, coronary artery disease, cardiac arrhythmias, cerebrovascular diseases, peripheral vascular diseases and renal insufficiency. POTENTIAL ADVANTAGES OF CALCIUM ANTAGONISTS IN THE ELDERLY: Dihydropyridine calcium anatagonists have been advocated as first choice agents for the treatment of hypertension in the elderly on the grounds that (1) they may be more active in lowering blood pressure because of the predominantly low renin status in elderly hypertensives, (2) they may be better tolerated because side effects related to the activation of the sympathetic system may be less frequent because of attenuation of baroflexes during ageing and (3) they may have beneficial effects on a variety of concomitant cardiovascular diseases which are frequently present in the elderly. These assumptions, however are not always proven in clinical practice. ADVANTAGES OF NICARDIPINE: Additional to its potent vasodilatator action, nicardipine has anti-ischemic effects in both the coronary and the cerebral circulation, including antiplatelet and hemorrheological effects, and protection at ther cellular level against calcium overload and ischemia. The results of a large number of studies in cerebrovascular insufficiency suggest that nicardipine, may favourably affect the cerebral circulation and may improve the patient's cognitive function. Nicardipine may decrease left ventricular mass by about 4-12% and may reduce both the frequency and the severity of arrhythmias. The anti-anginal effects of nicardipine are well established. The drug is also able to decrease the progression of new atherosclerotic lesions in coronary arteries and is consequently potentially beneficial in elderly hypertensives with coronary artery disease. Nicardipine has no clinically significant negative inotropic effect. Nevertheless, in congestive heart failure, the use of calcium antagonists is usually not recommended because of the lack of clinical benefit and of possible harmful effects, including sympathetic and renin-angiotensin system stimulation. Although kidney protection may be provided by a strict and long-term control of blood pressure, the effects of nicardipine on long-term protection of renal function are not clear at present. RECENT CONTROVERSY CONCERNING SHORT-ACTING CALCIUM ANTAGONISTS: Much-debated recent case-control studies suggest that hypertensive patients treated with short-acting calcium antagonists may have an increased incidence of myocardial infarction and possibly of cardiovascular and total mortality. However, only well designed prospective comparative trials can answer this question.
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PMID:Concomitant diseases in elderly hypertensives: the position of nicardipine. 912 Jun 65

EGb 761 is a standardized extract of dried leaves of Ginkgo biloba containing 24% ginkgo-flavonol glycosides, 6% terpene lactones such as ginkgolides A, B, C, J and bilobalide. Its broad spectrum of pharmacological activities allows it to be in adequacy to the numerous pathological requirements--hemodynamic, hemorheological, metabolic--which occur in cerebral, retinal, cochleovestibular, cardiac or peripheral ischemia. Moreover, EGb 761 has direct effects against necrosis and apoptosis of neurons and improves neural plasticity as evidenced in vestibular compensation. At the molecular and the cellular levels, some evidence obtained with animal models indicates that EGb 761 can interact as a free radical-scavenger and a inhibitor of lipid peroxidation with all, or nearly all reactive oxygen species; maintains ATP content by a protection of mitochondrial respiration and preservation of oxidative phosphorylations; exerts arterial and venous vasoregulator effects involving the release of endothelial factors and the catecholaminergic system. Moreover, EGb 761 regulates ionic balance in damaged cells and exerts a specific and potent Platelet-activating factor antagonist activity. Numerous well-controlled clinical studies, realized in Europe and in USA, have revealed that EGb 761 is an effective therapy for a wide variety of disturbances of cerebral function, ranging from cerebral impairment of ischemic vascular origins (i.e. multi infarct dementia), early cognitive decline to mild-to-moderate cases of the more severe types of senile dementias (including Alzheimer's disease) or mixed origins (i.e. psychoorganic origin). Improvement of signs and symptoms have been demonstrated for cognitive functions, particularly for memory loss, attention, alertness, vigilance, arousal and mental fluidity. Some clinical studies have showed that EGb 761 treatment may improve the capacity of geriatric patients to cope with the stressful demands of daily life. The explanation is a dual stress-alleviating action of EGb 761: its facilitates behavioral adaptation to stress and may decrease the excess of cortisol release to stress. Moreover, EGb 761 shows a specific neuroprotective effects to hippocampic cells. Regarding the visual system, experimental studies have shown that EGb 761 can inhibit or reduce the functional retinal impairments resulting from ischemia-reperfusion, photo-degeneration, diabetic or proliferative retinopathy. Clinical studies have revealed that EGb 761 may be useful in treating visual activity impairments and damages to the visual field associated with chronic cerebrovascular insufficiency, senile macular degeneration and diabete mellitus. Regarding the vestibular and auditory systems, experimental and clinical studies have shown the efficacy of EGb 761 in treating hypoacusis, tinnitus, vertigo, dizziness and other symptoms of vestibulocochlear disorders. At least, adequatly controlled studies in patients with peripheral arterial occlusive disease have provided good evidence for therapeutic efficacy in intermittent claudication. The future of EGb 761 is undoubtedly in the promise in slowing the progression of Alzheimer's disease. Indeed, two recent american clinical studies have shown the efficacy and safety of EGb 761 in patients with mild to severe Alzheimer's disease and multi-infarct dementia. In clinical terms, progression of symptoms was delayed by approximately 6 months. Actually new clinical studies are undertaken in USA and Europe. At the dawn of the third millenium (the Sixth for Ginkgo biloba) we propose a state of art about it.
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PMID:[Ginkgo biloba extract (EGb 761). State of knowledge in the dawn of the year 2000]. 1048 50

Chronic cerebrovascular ischemia is an important cerebrovascular disorder leading to progression of the functional neurological deficite--to cognitive impairment in the first place. The main reason for the above condition is a stenotic affection of major arteries of the head. In the treatment of patients presenting with the above pathology, we used mildronate (10% infusion solution, 10 ml, for up to 10 days followed by tablets, 750 mg per day for 20 days). As clinical and paraclinical monitoring was conducted of the condition of patients with making use of X-ray computerized tomography, electroencephalography, ultrasonic dopplerography of extra- and intracranial arteries, an assessment was done of findings from the neuropsychological testing. A positive effect is shown on the degree of neurological symptomatology, hemodynamic, electrophysiological, neuropsychological characteristics of the pathology in question. The drug is recommended for use in the treatment of stage II chronic cerebrovascular insufficiency originated and gone ahead because of a stenotic affection of major arteries of the head.
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PMID:[Use of mildronate for the treatment of patients with circulatory encephalopathy against a background of stenosis of major arteries of the head]. 1461 18

Restoration of blood flow to an ischemic brain region is associated with generation of reactive oxygen species with consequent reperfusion injury. Chronic cerebral hypoperfusion induced by permanent occlusion of bilateral common carotid arteries in rats is associated with behavioral and histopathological alterations. Nimodipine, a dihydropyridine calcium channel antagonist, has potent vasodilatory effect on cerebral vessels and increases cerebral blood flow. We analyzed whether nimodipine reduces injury caused by transient forebrain ischemia and long-term cerebral hypoperfusion. Bilateral common carotid occlusion for 30 min followed by 45 min reperfusion resulted in a two-fold increase in lipid peroxidation and superoxide dismutase activity. Nimodipine pretreatment (4 mg/kg, i.p.) brought down these levels by 30 and 23%, respectively. Long-term cerebral hypoperfusion in rats caused a propensity towards anxiety and listlessness (open field paradigm) accompanied by deficits of learning and memory (Morris' water maze testing). Additionally, histopathological observation in hypoperfused brains revealed reactive changes in the form of perivascular inflammation, gliosis and astrocytosis. Nimodipine treatment significantly alleviated these changes in behavioral and histopathological parameters. Our data confirm the protective role of nimodipine in ischemia reperfusion injury. Moreover, it suggests the beneficial role of nimodipine in cerebrovascular insufficiency states and dementia.
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PMID:Nimodipine attenuates biochemical, behavioral and histopathological alterations induced by acute transient and long-term bilateral common carotid occlusion in rats. 1464 94

Previous studies have demonstrated that Z-Ligustilide (LIG), a characterized phthalide constituent present in numerous medical Umbelliferae plants, has significant neuroprotective effects in transient forebrain ischemia and permanent cerebral focal ischemia. The present study further investigated the effect of LIG on chronic cerebral hypoperfusion. Male Wistar rats were subjected to permanent ligation of both common carotid arteries (2VO). On Days 8-12 postsurgery, rat cognition was assessed in the Morris water maze. Rats with significantly impaired acquisition of spatial information were randomly allocated to three groups and orally administered LIG (10 or 40 mg/kg/day) or volume-matched vehicle on Days 13-40 post-2VO surgery. The sham-operated group served as controls. After long-term treatment with LIG, the impaired animals' behavioral, biochemical, and histopathological features were examined. Compared to the sham-operated group, significant cognitive impairment was observed in the vehicle-treated group 40 days after 2VO. Shortened mean escape latency was detected in the Morris water maze in rats treated with LIG (p<0.01 vs. vehicle-treated group) during the same trial days. Chronic 2VO-induced pathological changes included neuronal loss and an increase of glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes in the hippocampus. These effects were prevented with LIG treatment (p<0.01 vs. vehicle-treated group). LIG also significantly reduced malondialdehyde levels and increased superoxide dismutase activity in ischemic brain tissue (p<0.05 and p<0.01 vs. vehicle-treated group). In addition, LIG significantly increased choline acetyltransferase activity and inhibited acetylcholinesterase activity in ischemic brain tissues (p<0.05 and p<0.01 vs. vehicle-treated group). The present data demonstrate that LIG significantly prevented chronically hypoperfused cognitive deficits and brain damage at least partly through an antioxidant effect and improved cholinergic activity. The present findings suggest that LIG may have therapeutic potential in treating vascular dementia and cerebrovascular insufficiency.
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PMID:Postischemic administration of Z-Ligustilide ameliorates cognitive dysfunction and brain damage induced by permanent forebrain ischemia in rats. 1788 86

Possible effect of an ethanolic root extract of Pongamia pinnata (L) Pierre (P. pinnata) on oxidant-antioxidant status and histopathological changes in acute ischemia-reperfusion injury in the rat forebrain have been investigated. Further, its effect was also assessed on long-term cerebral hypoperfusion-induced changes in anxiety, cognitive and histopathological parameters. Cerebral post-ischemic reperfusion is known to be associated with generation of free radicals. In the present study, bilateral common carotid artery occlusion (BCCAO) for 30 min followed by 45 min reperfusion produced increases in lipid peroxidation, superoxide dismutase (SOD) activity and a fall in the total tissue sulfhydryl (T-SH) levels. The ethanolic extract of roots of P. pinnata (50 mg kg(-1), po for 5 days) attenuated the ischemia-reperfusion-induced increase in lipid peroxidation, SOD activity and a fall in T-SH levels. The extract also ameliorated histopathological changes and inflammatory cell infiltration in the frontoparietal region of the rat brain. The extract (50 mg kg(-1), po for 15 days) was also found to alleviate the long-term hypoperfusion-induced anxiety and listlessness (open field paradigm). There was an improvement of learning and memory deficits (Morris' water maze testing). It also attenuated reactive changes in forebrain histology like gliosis, lymphocytic infiltration, astrocytosis and cellular edema. Results suggest protective role of P. pinnata in ischemia-reperfusion injury and cerebrovascular insufficiency states.
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PMID:Effect of ethanolic extract of root of Pongamia pinnata (L) pierre on oxidative stress, behavioral and histopathological alterations induced by cerebral ischemia--reperfusion and long-term hypoperfusion in rats. 1794 35

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.
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PMID:Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat. 1799 15


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