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

In order to study if rapid elevation of blood pressure is associated with cerebral ischemia, anesthetized (70% N2O) and artificially ventilated rats were subjected to angiotensin-induced hypertension. After a 5 min hypertensive period, cerebral cortex tissue was frozen in situ for subsequent measurements of labile glycolytic metabolites, ammonia, and organic phosphates. The degree of hypertension induced, which gave evidence of blood-brain barrier damage in 7 of 8 rats, did not affect the tissue concentrations of labile metabolites. It is concluded that ischemia does not contribute to the barrier damage, nor is it likely to be the cause of the clinical symptoms that may occur in conscious rats in the same experimental model.
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PMID:Brain energy metabolism in angiotensin-induced acute hypertension in rats. 88 9

The present experiments were undertaken to measure postischemic regional cerebral blood flow (rCBF) and oxygen utilization rate (CMRo2) in rats anesthetized with either 70% N2O or phenobarbital (150 mg x kg-1). In previous studies we have found that extensive restitution of cerbral energy metabolites occurs after 30 min of complete cerebral ischemia irrespective of the type of anesthesia used. Following 30 min of pronounced, incomplete ischemia, however, a comparable restitution of cerebral energy state was obtained in deeply anesthetized (phenobarbital 150 mg x kg-1) but not in superfically anesthetized (70% N2O) rats. The objectives of the present investigation were (1) to study whether postischemic cerebral blood flow was higher in barbiturate-anesthetized animals during the initial recirculation period, and (2) to investigate if the protective effects of phenobarbital previously observed could be attributed to a decrease in CMRo2. In both groups of animals a considerable variability in postischemic rCBF was observed between different animals. However, no signs of gross inhomogeneity in blood flow were found and no consistent differences in flow values between the two groups of animals were observed. Since the measured postischemic CMRo2 were identical in both groups of animals and since cerebral venous oxygen contents were above normal the results leave little support to the assumption that, in the present model of transient, incomplete cerebral ischemia, failure of recovery of cerebral metabolism (N2O group) is primarily due to impaired recirculation, nor do they indicate that the protective effects of barbiturates is due to their ability to reduce rate of cerebral energy utilization.
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PMID:Postischemic cerebral blood flow and oxygen utilization rate in rats anesthetized with nitrous oxide or phenobarbital. 92 Feb 15

Systemic disorders (eg, cardiac, hematologic) are commonly recognized as predisposing and sometimes actual precipitating events in cerebral ischemia. From available studies, the incidence of precipitation is not clear. To determine this, we undertook a comprehensive investigation of all patients with ischemic brain disease for a one-year period. Results reveal that brain ischemia is more commonly precipitated by systemic illness than usually supposed, particularly transient ischemic attacks of the vertebrobasilar circulation and completed infarcts in the carotid distribution. Cardiac disorders outnumber all other precipitating events. As they are more amenable to therapy than atherosclerosis, a diligent search for such precipitating events is warranted in patients with ischemic symptoms.
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PMID:Associated systemic factors in cerebrovascular ischemia. 93 99

Cerebral ischemia was induced by occlusion of the left common carotic artery in adult Mongolian gerbils. The period of occlusion was 3, 6, or 18 h. Horseradish peroxidase (HRP) was intravenously injected in animals with clear neurological signs 1 h release of the clip. The HRP was allowed to circulate for 5 min. Fixation was carried out by perfusion with aldehydes. Tissue, incubated for peroxidatic activity, from the left side of the brain was treated for electron microscopy. During the postischemic period enhanced permeability was demonstrated in the brains of all animals. The amount of HRP transferred into the neuropil depended on the duration of ischemia. Thus the gerbils with 18 h occlusion showed the greatest content. The cells comprising the neuropil adjacent to vessels were studied and the degree of the pathological changes described below was increased proportionally to the time period of occlusion. The intercellular spaces, often filled with peroxidase, were expanded and the astrocytes swollen, especially the endfeet. Sometimes the astrocytes were pervious to HRP. The neurons were also swollen, but to a lesser degree than the astrocytes. No endothelial cell damage was observed. Even 18 h of occlusion did not change the plasma membranes. The intercellular spaces were free of HRP from the first luminal to the first abluminal tight junction. The cytoplasm exhibited HRP-containing vesicles of various types and shapes. Some were freely situated; others were connected to the plasma membrane and then open to the vessel lumen or to the basement membrane. Since no cell damage was demonstrated, and since no HRP was diffusely dispersed in the cytoplasm it is assumed that vesicles are responsible for the enhancement of the vesicular transport that normally occurs after intravenous injection of HRP.
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PMID:Increased permeability of cerebral vessels to horseradish peroxidase induced by ischemia in Mongolian Gerbils. 96 82

Rats were subjected to total cerebral ischemia by occluding outflow from the heart. In control experiments and following different periods of ischemia, potassium concentration was measured in cisternal cerebrospinal fluid (CSF). It rose to 19.4 mEq/liter following 16 minutes of ischemia. Changes in cerebrovascular resistance (CVR) were also assessed by measuring the cerebral perfusion rate (CPR). Following two minutes of ischemia, CVR was decreased to half control value. After 8 and 16 minutes of ischemia, CVR was markedly increased, and "no-flow" state was approached after 16 minutes of ischemia. The CVR increased concomitantly with increase in potassium concentration in cisternal CSF. We suggest that the increase in CVR following cerebral ischemia is due to increase in potassium concentration in brain extracellular fluid and is part of a vicious circle that leads to brain death.
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PMID:No-flow state following cerebral ischemia. Role of increase in potassium concentration in brain interstitial fluid. 113 Oct 72

Cerebral ischemia was induced in gerbils by bilateral carotid ligation for periods of 10 to 40 minutes. Cerebral blood flow (CBF) was measured by hydrogen clearance. Following ischemia, ultimate clinical and electroencephalogram recovery could be predicted in every case within the first five minutes by recovery could be predicted in every case within the first five minutes by recovery of CBF to at least 100% of the control level. In animals without EEC recovery, the postischemic CBF was always less than 80% of control and progressively declined to zero. Residual flow during ischemia appeared to minimize the likelihood of brain death. The determination of ultimate brain death appeared to coincide with a major circulatory abnormality that is probably microvascular.
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PMID:Cerebral blood flow. A predictor of recovery from ischemia in the gerbil. 113 11

Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 +/- 4.2 ml/100 gm/min to 26.3 +/- 4.4 (p less than .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.
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PMID:Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function. 115 66

The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.
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PMID:Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 2: Brain morphology. 115 67

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69


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