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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulation to the brain is greatly affected by hypertension and by its treatment. Neurologic dysfunction is prominent among the complications of increased arterial pressure and is also most susceptible to preventive antihypertensive therapy. The upward resetting of the limits of autoregulation of cerebral blood flow in hypertension is probably due largely to structural thickening of the walls (hyaline arteriosclerosis) of the resistance vessels. Other consequences of hypertensive vascular lesions in the brain include increased formation of atheroma, lacunae and lacunar infarction, cerebral infarction, multi-infarct dementia and Binswanger's disease. There is also an association between hypertension and hemorrhagic strokes, namely, subarachnoid and intracerebral hemorrhage. Brain lesions are also prominent in malignant hypertension and hypertensive encephalopathy. Antihypertensive treatment, especially if intensive, can result in boundary zone ischemia in the brain if arterial pressure decreases steeply.
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PMID:Morphologic changes during hypertension. 264 56

The authors report a case of brain abscess following cerebral infarction. A 73-year-old man was admitted to our clinic with symptoms of right hemiparesis and total aphasia. CT scan revealed abnormal low density area in the left fronto-temporo-parietal region. Cerebral angiography demonstrated occlusion of the left middle cerebral artery at the M1 portion. On the 16th hospital day, an episode of generalized seizure with high fever appeared, and intermittent high fever persisted thereafter. Two months after admission, CT scan revealed several cystic lesions with marked ring enhancement at the site of cerebral infarction, suggesting multiple abscesses. Aspirations of left frontal and parietal abscesses were accomplished and the cultures of the pus disclosed Proteus vulgaris. Due to progressive hydrocephalus, a ventriculoperitoneal shunt was constructed one month later. Repeated CT scans showed a gradual diminution of the abscesses. It is considered that the blood-brain barrier is broken and the local immunological system against bacteria may be weakened when the brain is damaged by ischemia. Brain abscess seems to be developed in such circumstances even under the influence of transient bacteremia which originates in other parts of the body. Therefore the possibility of cerebral abscess should be suspected if patients with cerebral infarction suffer from the symptoms such as fever, neck stiffness or disturbance of consciousness.
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PMID:[Brain abscess following cerebral infarction: a case report]. 267 75

After focal cerebral infarction by occluding the middle cerebral artery (MCA) of the rat, the neuronal death occurred in the ipsilateral thalamic neurons, because axons of the thalamic neurons were injured by infarction and retrograde degeneration occurred in the thalamic neurons. However, cortical neurons adjacent to the infarction survived despite their axons injured by ischemia. We employed immunohistochemical staining for 200 kilodalton (kD) neurofilament (NF), in order to study those responses of cortical and thalamic neurons against axonal injury caused by focal cerebral infarction. In the sham operated rats the immunoreactivity to the anti-200 kD NF antibody was only detected in the axon but not in the cell bodies and dendrites. At 3 days after MCA occlusion, axonal swelling proximal to the site of ischemic injury was found in the caudoputamen and internal capsule of the ipsilateral side. At 7 days after occlusion, cell bodies and dendrites of the neurons in the ipsilateral cortex and thalamus were strongly stained with anti-NF antibodies. At 2 weeks after occlusion these responses disappeared in the cortex, but lasted in the thalamus. These phenomena are caused by stasis of the slow axonal transport, because the NF is transported by slow axonal transport. In the cortical neurons impairment of slow axonal transport recovered in the early phase after injury, but in the thalamic neurons the impairment prolonged up to 3 weeks after occlusion. The early recovery of axonal transport from ischemia seemed to be essential for survival of neurons after ischemic axonal injury.
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PMID:[Ischemic axonal injury and its recovery after focal cerebral ischemia]. 267 26

Recent advances in magnetic resonance (MR) imaging and MR spectroscopy (MRS) allow the noninvasive in vivo study of a variety of anatomical, physiological, and biochemical alterations that may occur in different cerebral pathologies. The authors have investigated the use of MR imaging and MRS to monitor the evolution of experimental focal cerebral ischemia in rats. Permanent focal cerebral ischemia was induced in 36 rats, and 12 normal rats were used as a control group. Changes in high-energy phosphate metabolites were followed in vivo using MRS during the 1st hour and at 3 and 6 hours after ischemic insult. Changes in vivo MR images were evaluated at 1, 3, 6, 12, and 24 hours after ischemic insult. Significant decreases (p less than 0.05) in phosphocreatine/inorganic phosphate ratios and intracellular pH values occurred immediately after the induction of ischemia. The presence of an infarcted area seen on MR images was a constant finding at 3 hours after ischemic insult, and was well defined and localized at 12 and 24 hours. The location of areas of infarction seen on MR images correlated well with areas identified histopathologically. The T1 and T2 MR relaxation times were significantly increased 3 hours after ischemic insult and remained prolonged for at least 24 hours. The results show that MR imaging is a sensitive method to measure cerebral infarction, and that MRS is a sensitive measure of changes that occur in the early phases of ischemia, perhaps when cellular changes may still be reversible. At 3 and 6 hours after the ischemic insult, however, 31P-MRS spectra may appear to be "normal" despite the presence of well-documented areas of infarction.
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PMID:Magnetic resonance imaging and 31P magnetic resonance spectroscopy for evaluating focal cerebral ischemia. 292 2

The injury of brachiocephalic artery is uncommon in the blunt trauma and sometimes it was accompanied by other organ damages. We reported a case and reviewed 47 cases in literature. A 28-year-old woman was transferred to our hospital with the blunt chest trauma and the cerebral infarction due to the traffic accident. The cineangiogram showed complete obstruction at the middle portion of brachiocephalic artery and the subclavian steal-carotid recovery phenomenon. Thirty days after trauma, the operation was performed under the monitoring of right superficial temporal arterial pressure. The vessel with intimal defect was plugged by a clot and it was replaced with a Gore-Tex graft during simple occlusion of the right carotid, subclavian and brachiocephalic arteries without any monitoring pressure change. The postoperative course was uneventful and the symptom improved. The review decided that the main cause of the injury is traffic accidents and the cineangiogram is important to find the arterial damage and the monitoring of superficial temporal arterial pressure is helpful to avoid the brain ischemia during operation.
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PMID:[Nonpenetrating brachiocephalic arterial injury]. 304 70

Several new concepts have emerged recently regarding the effects of chronic hypertension on cerebral blood vessels. First, hypertrophy of large cerebral arteries in chronic hypertension attenuates increases in pressure of downstream vessels and protects the cerebral microvasculature. Second, in contrast to large cerebral arteries, which become less distensible during chronic hypertension, distensibility of cerebral arterioles increases during chronic hypertension despite hypertrophy of the arteriolar wall. Third, dilatation of cerebral blood vessels with disruption of the blood-brain barrier, and not vasospasm, appears to be the critical factor in the pathogenesis of hypertensive encephalopathy. This concept is supported by the finding that cerebral edema in stroke-prone spontaneously hypertensive rats is preceded by vasodilatation and disruption of the barrier. Fourth, alterations of endothelium-mediated dilatation may impair vasodilator responses in chronic hypertension and predispose to ischemia. Finally, chronic hypertension impairs dilatation of collateral blood vessels in the cerebral circulation. The implication of this finding is that increased susceptibility to cerebral infarction in chronic hypertension may be related in part to compromised responses of the collateral circulation.
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PMID:Cerebral circulation in chronic arterial hypertension. 304 94

Although approximately 500,000 patients suffer from a stroke each year in the United States, treatment of these patients to date has consisted primarily of prevention, supportive measures, and rehabilitation. The modification of experimental cerebral infarction by new pharmacologic agents, along with encouraging results from the restoration of blood flow to areas of focal ischemia in both laboratory and clinical trials, suggests that a more aggressive approach might be considered in selected patients with acute stroke.
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PMID:Focal cerebral ischemia: pathophysiologic mechanisms and rationale for future avenues of treatment. 309 3

At present we apply the three-drug-combination therapy consisting of mannitol, vitamin E and glucocorticoid (betamethasone) in the treatment of cerebral infarction at acute stage with favorable results. However, much of the action mechanism of these drugs remains unelucidated. For the purpose to elucidate the mechanism by which they exert actions and moreover to evaluate the efficacy of this therapy, we conducted experiments using highly ischemic whole brain models of rats. In this model, chemiluminescence value, energy metabolism, water content and concentrations of Na+, K+ were determined with time. During ischemic period chemiluminescence level increased with time, and more remarkable increase was seen after recirculation of the blood flow. However, in the group with administration of the three drugs combination increase in chemiluminescence was inhibited remarkably. In the analysis of intensity of chemiluminescence by wavelengths, the peaks were observed at 480, 520 - 530, 570, 620 - 640 and 680 - 700 nm. These wavelengths were taken to suggest the release of energy (luminescence) associated with the transition of singlet oxygen to the grounded state during the breakdown of the lipid hydroperoxide. By addition of vitamin E or beta-carotene (quencher of singlet oxygen) on the brain homogenate in vitro, luminescence was remarkably inhibited over whole ranges of wavelength. Determination of adenine nucleotide and carbohydrate revealed that these three drugs combination promoted their recovery at the period of recirculation of the blood flow after ischemia. In particular, increase in lactate was inhibited from the period of ischemia with prevention of progression of lactic acidosis. Moreover, in the group with administration of the three drugs combination and the group with administration of 20% or isotonic mannitol the increase in the cortical water content following recirculation of the blood flow was inhibited. From these result it is considered that each of the three drugs shows not only inhibition of lipid peroxidation as radical scavengers but also protective effect on lowering of activities of ion channel (Na+, K+-ATPase, etc.) by the free radicals.
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PMID:[The protective effect of mannitol, vitamin E, and glucocorticoid in experimental cerebral ischemia--influence on lipid peroxidation, energy metabolism and brain edema]. 311 28

A new method for brain resuscitation following acute focal ischemic insult has been developed in this laboratory. The technique utilizes a surrogate route to supply cerebral metabolites and employs highly oxygenated fluorocarbons (OFNS), which are efficient gas transport and exchange agents, perfused through the ventriculo-subarachnoid spaces. We previously described a return of aerobic metabolism and EEG after severe global ischemia by oxygenated perfusions and now report treatment-induced reduction in the size of experienced cerebral infarction. Twenty-eight cats were anesthetized (choralose and urethane), tracheotomized and placed in a stereotactic frame. Physiologic adjustments assured arterial blood pCO2 28-35 Torr, pO2 100-150 Torr pH 7.4 and glucose less than 200 mg%. The left middle cerebral artery was exposed transorbitally and temporarily clipped along with both common carotids for 2 h. One hour later (3 h after ischemic onset) the treated group were perfused by the ventriculo-cisternal route either with OFNS [pO2 = 600 Torr; 3 ml/min 6 h, 2 ml/min 2 h, 1 ml/min 2 h, 0.5 ml/min 2 h at 10 mm Hg intracranial pressure (ICP)] or with the vehicle perfusate. Eighteen to twenty hours after the ischemic insult the animals were sacrificed. Sections of fresh brain of 0.5 mm thickness were incubated in 1% triphenyl tetrazolium chloride. The infarcted areas were confirmed with classic neuropathologic techniques. Areas of infarction (expressed in cm3 and as % of the brain) were measured using a planimeter. OFNS-treated brains contained 80% less infarcted tissue than the vehicle-perfused or untreated stroked animals. The infarcted areas were significantly treatment reduced (P less than 0.05 ANOVA and Bonferroni tests).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Focal cerebral ischemia: reduction in size of infarcts by ventriculo-subarachnoid perfusion with fluorocarbon emulsion. 315 23

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.
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PMID:Enhanced in vivo platelet activation in subtypes of ischemic stroke. 316 Dec 20


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