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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Study of the blood platelet functional activity and intensity of hemolysis in 41 patients with transient disorders of cerebral circulation and comparison of the results with the corresponding indices in healthy individuals, in 40 patients with hypertensive disease free of crisis, and in 25 patients with cerebral atherosclerosis led to the conclusion that the character of cerebral stroke is already determined in the pre-stroke period. It depends on the functional state of the blood platelets in many respects. In patients with hypertensive disease in a period clear of crisis, for instance, there is a tendency towards hypoaggregation possible associated with the presence of latent hemolysis. Platelet hypofunction progresses in the period of hypertensive encephalopathy and still more during its transformation into hemorrhagic stroke. On the contrary, in patients with atherosclerosis but no symptoms of cerebral ischemia the adhesion-aggregation activity of the platelets does not differ essentially from that in healthy individuals. With the development of signs of ischemia of the brain, the platelet activity grows considerably, particularly when transient cerebral circulatory disorders transform into ischemic stroke.
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PMID:[Importance of the thrombocytes and hemolytic syndrome in the pathogenesis of transient cerebral circulatory disorders in hypertension patients]. 63 13

The introduction of vascular micro-surgical techniques has allowed to treat cerebral ischemia, through extra-intra-cranial anastomosis, when the causative arterial lesions have a surgically unfavorable location. Thirty patients underwent brain revascularization through extra-intra-cranial micro-anastomosis between the superficial temporal artery (branch of the external carotid artery) and a cortical branch of the middle cerebral artery. Twenty five patients had definite sensitive and motor deficits. Five patients, on the other hand, underwent preventive surgery because of transient cerebral ischemia. In our series, the global rate of the microanastomosis patency is 78%. When the anastomosis is patent, 85% of the cases with motor deficits are cured or improved. The results are even more favorable in case of transient cerebral ischemia, for the anastomosis in such cases was always patent. None of these later patients had ischemia attacks with a one-year follow-up.
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PMID:[Cerebral ischemia, treatment by vascular micro surgical technique: intra-extra cranial anastomosis (author's transl)]. 66 67

The effects of severe cerebral ischemia on postischemic brain perfusion were examined in a series of pentobarbital-anesthetized cats. Ischemia of 15 or 30 minutes' duration was produced by occlusion of both common carotid arteries and the basilar artery and was coupled with mild systemic hypotension. A 90-minute period of normotensive postischemic recirculation was permitted in some animals. In 9 of 10 animals studied at the end of the ischemic insult and not allowed to recover, blood flow in the cerebral hemispheres was greatly reduced, with minimal flow (0.01 to 0.11 ml gm-1 min-1) persisting only in scattered perisulcal regions in 4 animals. Following 15 minutes of ischemia, blood flow was restored uniformly during recirculation, though at subnormal levels (31 to 35% of control). In contrast, 30 minutes of prior ischemia led to marked heterogeneities of local cerebral perfusion during recirculation, with multiple zones of persistent severe ischemia. Thus, while recirculation was suboptimal following both 15 and 30 minutes of ischemia, the 30-minute insult led to focal postischemic perfusion abnormalities that were sufficiently severe to make the possibility of functional recovery appear unlikely.
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PMID:Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation. 67 14

The clinical features of 102 cases with transient attacks due to cerebral ischemia were evaluated, and 94 out of 102 cases were followed for an average of 6 years. 1) The clinical study makes comparisons between two groups of patients grouped under the somewhat new definition of Reversible Ischemic Attacks (RIA): classical Transient Ischemic Attacks (TIA) and Stroke with Full Recovery (SFR), in which a complete recovery took place over a longer period, on the average 3 weeks. 2) SFR constitutes the 34.31% of the total cases with transient ischemic episodes. In the carotid district the onset was more frequently gradual in SFR than in TIA and aphasia more frequent in TIA than in SFR. Multiple attacks prevailed in TIA over the SFR group. The definition of transient attack due to ischemia is discussed. 3) Completed strokes occurred in 11 cases (11.7%) with RIA. Hypertension and cardiac disease were significantly frequent in cases with subsequent stroke. The conclusion was reached that TIA is a symptom, not a pathological state, and TIA should be considered an important symptom but not a specific harbinger of completed stroke.
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PMID:Clinical features and long-term follow-up of patients with reversible ischemic attacks (RIA). 69 35

We measured cerebral oxygen extraction, cerebral blood flow(CBF), and cerebral metabolic rate (CMRO2) in comatose patients during the first 60 hours after resuscitation from cardiac arrest. Each patient was studied 2 or 3 times. CBF was determined by a modification of the Kety-Schmidt method using inhaled Xenon133. Over the study period jugular venous oxygen tension and saturation rose, while the oxygen content difference between arterial and jugular venous blood fell, indicating a progressive increase in the ratio of CBF to metabolism CBF and CMRO2 measurements confirmed this. Between 2 and 6 hours after resuscitation both measurements were severely but proportionately depressed to less than 50% of normal. After 6 hours CBF was increased disproportionately to CMRO2 so that a relative hyperemia developed and persisted for the duration of the study. Although regional inhomogeneity of flow and regional ischemia cannot be ruled out, we have found no evidence for global cerebral ischemia between 2 and 60 hours post-resuscitation as an explanation for failure of recovery. In man following cardiac arrest restoration of levels of global cerebral blood flow, which can be considered adequate relative to the depressed metabolic state of the tissue, is achieved within 2 hours of resuscitation.
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PMID:Cerebral blood flow and metabolism in man following cardiac arrest. 74 88

Hypo- and hypercapnia produced in dogs had no effect on the level of endogenous prostaglandin-like substances (PLS) bioassayed continuously in sagittal sinus blood. Increased release of endogenous PLS, predominantly of prostaglandin E-like substance into cerebral venous blood occurred in conditions injurious to brain, such as hypoxia cerebral ischemia and embolism. It may be concluded that increased output of PLS into cerebral venous blood is not related to functional changes in cerebral blood flow, but results from cerebral and/or cerebrovascular damage. Enchanced generation of endogenous prostaglandins and their release into cerebral venous blood preceed the development of structural alterations evoked by hypoxia and ischemia in brain.
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PMID:Release of prostaglandin--like substances into cerebral venous blood in conditions injurious to brain in the dog. 74 12

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95

Cerebral ischemia and infarction have been produced in the Rhesus monkey using an autologous clot embolization technique. Preliminary findings suggest that cerebral arteriography may be used to study experimental cerebral infarction and ischemia, and the resulting cerebral edema and also that cerebral arteriography may be used as a tool for the evaluation of various types of therapy now used clinically in the treatment of these entities. The present experimental study in the monkey suggests that whereas steroid therapy initiated immediately following the onset of cerebral ischemia reduces morbidity and hastens clinical recovery, pretreatment with steroids in these same cases of cerebral ischemia may be hazardous and may increase the risk of cerebral infarction.
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PMID:Experimental cerebral infarction in the monkey. Radiographic evaluation of steroid therapy. 82 Jun 68

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Records of 248 patients undergoing aortoiliac reconstruction for occlusive disease between 1957 and 1975 were reviewed. Carotid bruits were ausculted in 35 patients (14%). Five of the patients with bruits also were thought to have symptoms of transient ischemia. Strokes occurred after operation in four of the 248 patients (1.6%). No patient with a previously noted bruit developed postoperative stroke. Two patients with transient cerebral ischemia and no confirmed bruit before operation did develop postoperative strokes. Cerebral angiography was performed in 18 of the patients with carotid bruits. Two of these patients underwent carotid endarterectomy prior to aortoiliac reconstruction. None of these 18 patients developed strokes following their carotid surgery of aortoiliac reconstruction. A third patient with no bruit but with retinal cholesterol emboli also underwent arteriography and endarterectomy without complication. The results suggest that the asymptomatic carotid bruit alone does not indicate an increased risk of stroke during aortoiliac reconstruction. The authors conclude that their experience does not support prophylactic carotid endarterectomy in the asymptomatic patient prior to aortoiliac reconstruction.
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PMID:Carotid bruit as a risk factor in aortoiliac reconstruction. 85 Aug 72


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