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

Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of ketamine such as phencyclidine (PCP) not only exert potent hallucinogenic properties and are widely abused drugs, but often result in hypertensive encephalopathies and death. In view of the paucity of information on the cerebral circulatory actions of barbiturates, ketamine and PCP (and analogs), in-vivo (microcirculatory) and in-vitro studies were undertaken. Barbiturates, in anesthetic concentrations (e.g., 10(-5) to 10(-4) M), were found to exert direct vasodilator actions on cerebral arterial smooth muscle; these relaxant actions appear to be related to inhibition of calcium ion (Ca2+) influx in cerebral vessels. The latter may be important in the salutory actions of barbiturates in brain ischemia, head trauma and cerebrovasospasm. Unlike barbiturates, ketamine was found to exert spasmogenic actions on cerebral arteries, which may aid in explaining the inability of this anesthetic to be of therapeutic value in brain ischemia. PCP and its analogs, as well as other hallucinogenic molecules (e.g., LSD, mescaline) produced spasms in cerebral arterioles, venules and arteries in concentrations which mimic their hallucinogenic potencies. Distinct PCP-like receptors which subserve contraction appear to exist on large as well as microscopic cerebral blood vessels. Spasms induced by PCP, its analogs and ketamine can be readily reversed or prevented completely by calcium channel blockers. The latter agents could be quite useful, clinically, in prevention of cerebral infarction, hypertension and fatality associated with PCP (and analogs) intoxication.
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PMID:Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle. 640 Apr 29

Various therapeutic methods have been attempted for cerebral infarction, but the development of more effective methods is still awaited. We have investigations of the effect of mannitol in preventing the development of cerebral infarction and have reported it effects in clinical cases of operated cerebral aneurysms. In recent years, our attention has been drawn to the so-called red cell substitute, perfluorochemicals (FC), which has a high oxygen-carrying capacity and a small particle less than 0.1 mu. In the present studies, using infarction models in dogs which have previously developed and reported, observations are made on recovery of brain electrical activity in severe ischemia, suppressing brain swelling following recirculation of cerebral blood flow and protection upon the hemorrhagic brain infarction, due to administration of mannitol or FC. These experimental results indicate that the combined administration of mannitol and FC is effective in protecting the brain from cerebral ischemia.
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PMID:[Development of new methods in suppressing brain infarction--combined administration of mannitol and perfluorochemicals (author's transl)]. 645 81

Treatment with an anticoagulant (AC) or acetylsalicylic acid (ASA), chosen at random, was given to 241 patients with symptoms of carotid transient attacks of ischemia, some of whom recovered completely within 24 hours (TIA) while the others had slight residual symptoms (TIA-IR). Cerebral infarction was recorded in 4 patients in each of these treatment groups during a mean follow-up period of 20 months. The incidences of TIA and TIA-IR were also similar in the two groups. Severe hemorrhage occurred more often in the AC group, whereas other side reactions, including gastrointestinal disorders, were more common in the ASA group. Recurrent cerebral ischemic events were significantly more common among the patients that had had greater than or equal to 2 TIAs in the 14 days immediately preceding randomization, and in those with a history of CVS symptoms more than 14 days before randomization, or those with a carotid bruits. In the group experiencing greater than or equal to 2 TIAs in the 14 days prior to randomization the incidence of recurrent cerebral ischemic events was the same for the two types of treatment.
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PMID:Treatment after transient ischemic attacks: a comparison between anticoagulant drug and inhibition of platelet aggregation. 665 49

Over the past ten years, several studies have outlined the importance of high blood viscosity as a pathogenetic factor in ischemic cerebrovascular diseases. Clinical studies have demonstrated that a high blood viscosity due to an elevated hematocrit (greater than 46%) increases the risk of cerebral infarction. Furthermore, in patients with high hematocrit, the cerebral blood flow seems to be lower than in controls and, by removing 200-250 ml of blood by venesection, the cerebral blood flow can be normalized. Several authors have therefore proposed that venesection may be used as a preventive measure in patients at risk for cerebral ischemia with high hematocrit. In addition, studies on experimental brain ischemia have shown that hemodilution reduces the size of the infarction. Therefore, hemodilution has been proposed as an effective measure in the treatment of acute cerebral ischemia. In conclusion, it seems that high blood viscosity is a risk factor in cerebral ischemia although its pathogenetic mechanisms and clinical importance are not yet completely clarified.
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PMID:[Hemorrheological changes in cerebrovascular disease]. 667 95

Improved treatment of associated cardiovascular and hematogenous abnormalities has favorably influenced the incidence and outcome of cerebral vascular disease during the past 25 years. Strong evidence now indicates that attention to the carbohydrate content of the brain also may influence outcome from brain ischemia. With brain lactate levels above approximately 16 mmol per kilogram, ischemia produces tissue infarction; ie, the lesion includes astrocytic and endothelial necrosis as well as neuronal death. We find that equal degrees of ischemia accompanied by lower tissue lactate values produce only selective neuronal damage in predictably vulnerable areas; astrocytes and endothelia are spared and extracellular or progressive postischemic cerebral edema fails to develop. The findings suggest that astrocytes can function to defend brain tissue against the damaging effects of acute anoxia but that during such conditions, they are potentially vulnerable to high tissue lactate levels. Initial clinical evidence suggests that scrupulous attention to blood sugar may reduce the risk of human cerebral infarction after ischemia.
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PMID:What causes infarction in ischemic brain?: The Robert Wartenberg Lecture. 668 61

Among 75 patients in whom internal carotid artery (ICA) occlusion was discovered on angiography, 5 presented with transient ischemic attacks (TIAs) without suffering a stroke. Although neurological examination was normal, all had evidence for one (in one instance two) hypodense lesion suggesting infarction contralateral to the neurological dysfunction on computed tomography (CT). These infarcts were small and deeply located, being indistinguishable from lacunes in most cases. We suggest that cerebral infarction with transient signs ( CITS ) may be a usual finding in patients with ICA occlusion who suffer isolated TIAs. In these cases, CITS may correspond to incomplete cerebral necrosis related to a well-developed collateral supply, or to recurrent ischemia in the region of an old "silent" infarct. CITS should be differentiated from TIAs, which may be diagnosed only in absence of visible structural lesion.
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PMID:Cerebral infarction with transient signs (CITS): do TIAs correspond to small deep infarcts in internal carotid artery occlusion? 672 84

It has previously been thought difficult to produce hemorrhagic infarction in animals. Using the thalamic infarction model in the dog, the production of hemorrhagic infarction can be achieved consistently. In this study, the protective effect of mannitol and/or artificial blood (perfluorochemicals) on the hemorrhagic infarction was investigated. Adult mongrel dogs weighing about 10 kg each were used. Following temporal craniotomy, thalamic ischemia was produced by occluding four trunk arteries (the internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries). Dogs which showed EEG changes indicative of thalamic ischemia were used in further experiments. The dogs were divided into 4 groups: (I) non-treated, (II) mannitol-treated, (III) fluorochemical-treated and (IV) mannitol and fluorochemical-treated. All dogs in each group underwent 6 hours of vascular occlusion followed by 1 hour recirculation. In order to evaluate the degree of hemorrhagic infarction, classification into 4 grades was done. Grade O: pale infarction without microscopical bleeding; Grade I: pale infarction wit microscopical bleeding; Grade II: a few sites of macroscopical petecheal bleeding; and Grade III: diffuse macroscopital petecheal bleeding. In the non-treated animals, autopsied brains showed hemorrhagic infarction in all cases. In mannitol-treated animals, some protective effect was found, especially in cases in which mannitol was administered within 60 minutes following occlusion. Hemorrhagic infarction was not suppressed in any of the fluorochemical-treated animals, but there was no hemorrhagic infarction in any of the animals treated with both mannitol and fluorochemicals. The present results are thought to indicate that these drugs administered together are effective in the treatment of hemorrhagic cerebral infarction.
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PMID:[The protective effect of mannitol and artificial blood (perfluorochemicals) on hemorrhagic infarction -- experimental study (author's transl)]. 679 84

Various therapeutic methods have been attempted for cerebral infarction, but the development of more effective methods is still awaited. We have investigations of the effect of mannitol in preventing the development of cerebral infarction and have reported it effects in clinical cases of operated cerebral aneurysms. In recent years, our attention has been drawn to the so-called red cell substitute, perfluorochemicals (FC), which has a high oxygen-carrying capacity and a small particle less than 0.1 mu. In the present studies, using infarction models in dogs which have previously developed and reported, observations are made on the recovery of brain electrical activity in sever ischemia, suppressing brain swelling following recirculation of cerebral blood flow and protection upon the hemorrhagic brain infarction, due to administration of mannitol or FC. These experimental results indicate that the combined administration of mannitol and FC is effective in protecting the brain from cerebral ischemia.
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PMID:[Development of new methods in suppressing brain infarction--combined administration of mannitol and perfluorochemicals (author's transl)]. 679 78

We already reported in our experimental studies that mannitol acts to inhibit cerebral infarction. The purpose of this study was to investigate the efficacy of mannitol as assessed in terms of rCBF. The experiments were carried out with the thalamic infarction model in dogs, an experimental model developed and reported by us previously. The rCBF in the thalamus was measured by the initial slope method of hydrogen clearance curves. Following administration of 20% mannitol (2 g/kg) over a period of 10 minutes, slight increases in rCBF occurred during arterial occlusion. However the effect was more pronounced in mild than in severe ischemia. The length of time required for rCBF to return to its premedication level was almost 60 minutes.
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PMID:[Effect of mannitol on rCBF in canine thalamic ischemia-an experimental study (author's transl)]. 680 Mar 86

A considerable body of evidence suggests that posttraumatic disturbances of the cerebral circulation contribute to poor neurological outcome after blunt head injury, especially when regional cerebral blood flow (rCBF) falls to the ischemic range (below 17 ml/100 gm/min). Cerebral infarction concentrated in the arterial boundary regions has been described in patients who died. Since arterial boundary zones are the cortical areas most susceptible to cerebral ischemia, the authors have investigated the relationship between neurological outcome and the anatomic pattern of rCBF values in the acute phase. The bolus-injection xenon-133 washout technique was used to measure rCBF in 35 regions of the hemisphere during the 1st week after head injury. Eighty-eight hemispheres were studied in 80 patients whose Glasgow Coma Scale (GCS) score was less than 8 on admission to the neurosurgical department. A characteristic pattern of rCBF was found in patients who later died of neurological complications, or who survived in a persistent vegetative state, with low flows in regions conforming to the arterial boundary zones. These patients also had lower average global cerebral blood flow (CBF), GCS scores, and cerebral perfusion pressure compared with those who recovered, with or without neurological deficits; the latter group had an rCBF pattern similar to that of normal individuals. There was little change in the GCS score between the time of hospital admission and CBF measurement, suggesting that the major neurological injury had occurred prior to admission. It was not possible to determine whether boundary-zone ischemia preceded neurological deterioration, but the rCBF pattern of boundary-zone flow deprivation was clearly related to poor neurological outcome. These observations suggest that elevated intracranial pressure and arterial hypotension were important etiological factors. Measures to protect regional cerebral perfusion should be instituted as early as possible after injury, preferably before the patient reaches the hospital.
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PMID:Cerebral circulation after head injury. Part 4: Functional anatomy and boundary-zone flow deprivation in the first week of traumatic coma. 688 57


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