Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oligoclonal Ig bands were found in serum and CSF of 13 of 83 patients (16%) with verified subarachnoid hemorrhage (SAH). Serum Ig bands were more common in patients with SAH than in those with cerebral ischemia. The reverse was true with oligoclonal Ig bands in CSF. These patterns suggest that there are two different mechanisms and sites of IgG synthesis: an inflammatory process after acute stage of vascular damage and a latent immunologic process--ie, polyclonal B-cell activation by injury to the brain.
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PMID:Oligoclonal immunoglobulin G in acute subarachnoid hemorrhage and stroke. 395 7

In order to study the effects of various degrees of cerebral ischemia on the auditory nerve-brain stem evoked potentials (BAEP), the cerebral perfusion pressure (CPP), defined as the difference between mean arterial blood pressure (MAP) and intracranial pressure (ICP), was systemically manipulated in anesthetized, paralyzed and ventilated cats. The CPP was varied by decreasing MAP, either by hemorrhage or by the infusion of a vasodilating drug, and elevating ICP by infusion of mock CSF into the cisterna magna, or by MAP depression and ICP elevation simultaneously. Even though the lower limit of adequate CPP is considered to be 40 mm Hg, the EEG became isoelectric at an average CPP of 24 mm Hg and the BAEP became isoelectric at an average CPP of 7 mm Hg. These extremely low CPP values of 7-24 mm Hg are far below the range of autoregulation of cerebral blood flow (CBF) so that the brain stem auditory pathway is still capable of generating its electrical response (BAEP) at very low CBF. This is paradoxical since these same regions of the brain have been shown to have the highest levels or regional metabolism as shown by their very high local cerebral blood flow and local glucose utilization.
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PMID:Auditory nerve-brain stem evoked potentials in cats during manipulation of the cerebral perfusion pressure. 618 18

In this study we examined the reactions of cerebral vessels to hypercapnia and hypoxia during the recovery period following cerebral ischemia. We used ventilated, lightly anesthetized rats and induced complete ischemia by CSF compression, incomplete ischemia by bilateral carotid occlusion combined with hypotension. After 15 min of ischemia and 60 min of recirculation the animals were rendered hypercapnic or hypoxic for 2-3 min and local CBF was then measured autoradiographically with 14C-iodoantipyrine. Following complete ischemia vascular CO2 responsiveness was abolished or attenuated in most structures analysed. However, there was a considerable interstructural heterogeneity. For example, in the cerebellum and the red nucleus flow rates were observed which approached values obtained in hypercapnic control animals, whereas CO2 responsiveness was abolished in several cortical areas and hippocampus. The response to CO2 following incomplete ("forebrain") ischemia varied considerably. In the cerebral cortices areas with low flow rates were often mixed with hyperemic zones, and in most structures that had very low flow rates during ischemia, CO2 responsiveness was lost or grossly attenuated. Structures that had suffered moderate or only mild ischemia had better retained or completely preserved CO2 response. The cerebrovascular reaction to hypoxia was found to be attenuated in most, but not abolished in any of the structures examined. In general, the vascular response to hypoxia was better preserved than that to hypercapnia. Reactivity was similar following complete and incomplete ischemia. As observed during hypercapnia, there were pronounced interstructural variations with considerable increases in flow rates e.g. in the substantia nigra and the cerebellum.
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PMID:Cerebral circulatory responses to hypercapnia and hypoxia in the recovery period following complete and incomplete cerebral ischemia in the rat. 641 51

In 17 patients with cough syncope, electroencephalograms showed normal interictal recordings in 12 patients, minimally abnormal recordings in 4, and a moderately abnormal recording in 1. Fourteen episodes of cough syncope (six patients) were recorded, with the EEGs showing diffuse theta and delta slowing during the episodes. These findings were similar to those seen during other types of syncope. Although eight patients had rhythmic or clonic-like movements during the episodes, no epileptiform activity was seen. The exact mechanism of cough syncope is not known, but the vigorous coughing probably increases CSF pressure enough to impair intracranial circulation, causing syncope due to cerebral ischemia.
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PMID:EEG in cough syncope. 653 80

Using a HPLC method the concentrations of oxypurines were simultaneously measured in CSF of patients with acute cerebrovascular lesions (CVL) and global cerebral ischemia (GCI) in an attempt to study disturbed brain metabolism during cerebral oxygen deprivation. In cerebral infarction both hypoxanthine and xanthine gradually increased from normal levels at admission to pathologically increased on the fourth day from onset of symptoms. There was no correlation between these substances and the clinical score but the maximum CSF-hypoxanthine concentration was significantly correlated to the maximum lesion volume determined by computerized tomography. In GCI the hypoxanthine-xanthine concentrations were considerably increased less than 20 hours from onset of unconsciousness but the initial levels did not predict the final outcome. These findings suggest that the end products of nucleotide degradation accumulate rapidly in acute cerebral hypoxia but more gradually in CVL probably due to growing local edema with subsequent local hypoxia. In controls and patients with CVL the CSF-urate concentrations were positively correlated to those of CSF-albumin. However, in CVL the increase of urate was relatively much more pronounced than the increase of albumin indicating that urate is a sensitive marker of dysfunction of blood-brain barrier.
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PMID:Oxypurines in cerebrospinal fluid as indices of disturbed brain metabolism. A clinical study of ischemic brain diseases. 665 6

Reversibly and irreversibly disturbed brain cell metabolism may be monitored in an indirect way by the analyses of enzymes in the CSF according to the hypothesis of cell swelling induced by energy shortage. Adenylate kinase fulfils the criteria for an ideal CSF marker with the exception that it is not organspecific, which necessitates precautions to avoid influence of AK in erythrocytes and serum. When taking such limitating factors into account, AK determinations may be diagnostically useful in combination with radiological and clinical observations. Besides, it is possible that a combination of AK analyses and clinical signs are useful in the prognostication in individual patients suffering from global cerebral ischemia and cerebral infarction.
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PMID:Cerebrospinal fluid markers of disturbed brain cell metabolism. 675 18

Using flat-surface pH electrodes we continuously measured changes in the brain surface pH during respiratory arrest in anesthetized and paralyzed dogs which were previously ventilated with pure oxygen. Respiratory arrest was induced by halting the respirator. The mean arterial PO2 fell from 502.7 +/- 15.9 (1 SD) to 23.7 +/- 18.5, and the mean arterial PCO2 rose from 36.4 +/- 3.5 to 80.4 +/- 7.1 mm Hg, 10 min after asphyxia. The arterial blood pressure increased gradually over several minutes but fell relatively abruptly and profoundly at the end, due to circulatory failure. Initially, and as long as the arterial blood pressure and, therefore, cerebral blood flow were upheld (phase 1), changes in the brain surface pH were small (delta pH/delta t= -0.026 pH unit/min) in spite of severe hypercapnia. When cerebral perfusion pressure fell due to circulatory failure (phase 2), cerebral ischemia occurred and there was an abrupt fall in brain surface pH (delta pH/delta t= -0.067 pH unit/min). Changes in cisternal CSF [H+] grossly underestimated the magnitude of brain surface acidosis during the period of respiratory arrest; the initial difference between the mean brain surface fluid and cisternal CSF [H+] which was 8.9, rose to 15.1 and 47.4 nmol/L, respectively, 5 and 10 min after asphyxia. Changes in sagittal venous blood acid-base variables were more pronounced than those observed in the arterial blood or cisternal CSF; 5 min after respiratory arrest, arterial and sagittal venous blood and cisternal CSF and brain surface pH were 7.20, 7.09, 7.19 and 7.11, respectively. We conclude that (1) in the course of respiratory arrest cerebral outcome can potentially be determined by circulatory failure as evidenced by simultaneous changes in the arterial blood pressure and brain surface pH; (2) cisternal CSF acid-base changes lag behind those on the brain surface and CSF analyses provide unreliable information about the severity of brain acid-base changes during asphyxia; (3) changes in cerebral venous blood acid-base variables best represent the severity of metabolic aberrations in the brain during respiratory arrest.
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PMID:Changes in the brain surface pH and cisternal cerebrospinal fluid acid-base variables in respiratory arrest. 683 98

Our previous experimental and clinical studies yielded the following results: CSF flow around the subarachnoid vessels is often interrupted by subarachnoid clots; anaerobical incubation of CSF-blood mixture led to a marked fall in the pH value; the vasocontractility of anaerobically incubated CSF-blood mixtures was greater than that of aerobically incubated samples; vasocontraction induced by anaerobically incubated samples was inhibited to a far greater extent the prostaglandin synthesis inhibitor meclofenamic acid than by phenoxybenzamine; cases of asymptomatic marked angiographical vasospasm or of cerebral ischemia with relatively slight angiographical vasospasm were not rarely encountered. Those results lead us to a hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobical changes of subarachnoid clots may be factor upsetting the balance of the synthesis of TXA2 and PGI2 from PG endoperoxides on the inner surface of cerebral arteries, in favor of TXA2--which plays a role in arterial contraction and in thrombosing with platelet aggregation. On this basis we have been testing the administrations of trapidil, an antagonist and selective synthesis inhibitor of TXA2, in 20 consecutive suitable cases so far, for the prevention of cerebral vasospasm after aneurysmal rupture. Angiographical vasospasm was seen in 9 of the 20 cases, but no signs of cerebral ischemia were detected in 7 of the 9 cases, either clinically or in CT scan. The importance of thrombus formation by platelet aggregation in symptomatic vasospasm are thus suggested.
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PMID:[Possible role of microthrombus in the pathogenesis of cerebral vasospasm (author's transl)]. 704 95

Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post-hemorrhagic obstructive hydrocephalus in order to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentraions and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in five with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood-CSF barrier can fully explain the observed alterations in ventricular-fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction.
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PMID:Cerebral oxidative metabolism in perinatal post-hemorrhagic hydrocephalus. 739 28

We measured ascorbic acid (reduced and oxidized) in brain, CSF and blood, before, during and after cerebral ischemia in newborn piglets. Bilateral carotid ligation induced a 54% decrease in cerebral blood flow (p < 0.01) and a 43% decrease in the cerebral metabolic rate of oxygen (p < 0.01). After ischemia and reperfusion, we obtained a 60% decrease (p < 0.01) in total brain ascorbic acid content. CSF ascorbic acid increased during reperfusion: +60% at 30 min (p < 0.001) and +160% at 120 min (p < 0.05). Blood ascorbic acid content did not change. These changes and the absence of massive oxidation of ascorbic acid in brain tissue suggest release of ascorbic acid by the brain during ischemia.
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PMID:Ascorbic acid during cerebral ischemia in newborn piglets. 767 Feb 42


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