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

Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 +/- 6.2 and 58.9 +/- 4.6 ml/100 g/min (mean +/- SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 +/- 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74% and further to 58% of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 +/- 4.9 and CeBF to 53.9 +/- 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral and cerebellar blood flow autoregulations in acutely induced cerebral ischemia in spontaneously hypertensive rats--transtentorial remote effect. 381 Jul 34

The 4-vessel occlusion rat model of cerebral ischemia was modified to permit the simultaneous measurement of cerebral blood flow (hydrogen clearance), brain edema (specific gravity), cerebrovascular permeability (14C-AIB) and electrocardiogram. Surgery was performed in one stage in the anesthetised, paralysed and ventilated rat and severe hemispheric ischemia was produced in all animals. Electrode implantation did not alter cortical specific gravity or Ki for 14C-AIB. During 4-vessel occlusion mean cortical CBF was 5.8 +/- 1.4 ml-1 100 g-1 min. and this was associated with an isoelectric ECoG; 15 min of ischemia produced a significant reduction in mean cortical specific gravity (increase in brain edema). Following 15 min ischemia, 180 min of recirculation were permitted. Post-ischemic blood flow showed an immediate hyperemia (CBF = 202 +/- 12 ml-1 100 g-1 min.) followed by hypoperfusion (CBF = 58 +/- 8 ml-1 100 g-1 min). There was an early further decrease in cortical specific gravity. Further recirculation led to a significant increase in cortical specific gravity (resolution of brain edema). The transfer constant (Ki) for 14C-AIB was not altered at any stage in recirculation. This appears to be a model of pure cytotoxic edema until 180 min recirculation after 15 min cerebral ischemia. Recirculation permitted return of cortical electrical activity.
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PMID:Recirculation after cerebral ischemia. Simultaneous measurement of cerebral bloodflow, brain edema, cerebrovascular permeability and cortical EEG in the rat. 381 32

This study was undertaken to determine the minimum CBF and CMRO2 required by the human brain to maintain normal function and viability for more than a few hours. Positron emission tomography (PET) was used to perform regional measurements in 50 subjects with varying degrees of cerebral ischemia but no evidence of infarction. There were 24 normal subjects, 24 subjects with arteriographic evidence of vascular disease of the carotid system, and two subjects with reversible ischemic neurological deficits due to cerebral vasospasm. Minimum values found in the 48 subjects with normal neurological function were 19 ml/100 g-min for regional cerebral blood flow (rCBF) and 1.3 ml/100 g-min for regional cerebral metabolic rate of oxygen (rCMRO2). Minimum values for all 50 subjects with viable cerebral tissue were 15 ml/100 g-min for rCBF and 1.3 ml/100 g-min for rCMRO2. Comparison of these measurements with values from 20 areas of established cerebral infarction in 10 subjects demonstrated that 80% (16/20) of infarcted regions had rCMRO2 values below the lower normal limit of 1.3 ml/100 g-min. Measurements of rCBF, regional cerebral blood volume, and oxygen extraction fraction were less useful for distinguishing viable from infarcted tissue. These data indicate that quantitative regional measurements of rCMRO2 with PET accurately distinguish viable from nonviable cerebral tissue and may be useful in the prospective identification of patients with reversible ischemia.
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PMID:Cerebral blood flow and cerebral metabolic rate of oxygen requirements for cerebral function and viability in humans. 387 67

Complete 20-min lasting cerebral ischemia was induced in 12 rabbits. They received PGI2 3 min before, during, and for 15 min after ischemia. Control animals with complete cerebral ischemia over the same period of time were not given PGI2 medication. The ECoG changes of the animals receiving PGI2 recovered twice as fast as those of the controls. PGI2 had no noticeable effect on the loosening of the CNS white matter after ischemia; however, the perivascular swelling was much less conspicuous. PGI2 reduced the spectrum of neuronal changes and decreased the number of pathologically changed neurons in the cerebral hemispheres. Sporadically, the Purkinje cells underwent homogenisation without shrinkage of cytoplasm. The bulbar motoneurons were morphologically normal in all animals treated with PGI2. The results indicate a cytoprotective action of PGI2 on cerebral neurons during ischemia, and/or the prevention of CBF disturbances by this compound.
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PMID:Influence of prostacyclin on early morphological changes in the rabbit brain after complete 20-min ischemia. 390 57

The effects on regional cerebral blood flow (rCBF) of raised intracranial pressure (ICP) and of naloxone and thyrotropin releasing hormone (TRH) during this condition were studied in anaesthetized rabbits. The ICP was elevated until a central ischaemic response was observed. The regional blood flow was determined with the microsphere technique before and during elevation of the ICP (ICPe) and after drug treatment. Total CBF was reduced by about 70% during ICPe while the uveal blood flow increased slightly and some other peripheral tissue blood flows remained unaffected. The administration of TRH caused an increase in mean arterial blood pressure (MAP) from 11.9 +/- 0.6 to 14.6 +/- 0.7 kPa and a normalization of the rCBF. In some peripheral tissues, e.g. gastric mucosa and spleen, TRH reduced the blood flow by 53% and 76%, respectively. In blood pressure stabilized animals no effect on rCBF was seen after TRH. Naloxone had no consistent effect on MAP or local blood flow. It was concluded that in the range of cerebral perfusion pressure studied there was a passive relationship between cerebral blood flow and perfusion pressure. The lack of effect of naloxone and the marked effect of TRH during cerebral ischaemia are consistent with a mechanism of action of TRH not related to a 'physiological' antagonism of opioids.
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PMID:Effects of raised intracranial pressure on regional cerebral blood flow: a comparison of effects of naloxone and TRH on the microcirculation in partial cerebral ischaemia. 392 9

This study examines the effect of fibrinogen and consequent blood viscosity reduction on cerebral blood flow and cellular injury following severe cerebral ischemia for 30 minutes in 78 Wistar rats. In half of these rats 10 to 15 cc's of blood was removed and replaced with a mixture of 5% albumin and autologous red blood cells maintaining a constant hematocrit but resulting in a 30% decrease in fibrinogen and corresponding reduction in viscosity. Fibrinogen reduction in a slight increase in baseline CBF and the elimination of post-ischemic hyperemia at 24 hours. Both study and control animals showed a similar decrease in CBF at 30 minutes and 2 hours. There was no significant difference in the severity of ischemic cellular change between the fibrinogen reduction group and controls, although there was a significant inverse relationship between the amount of viscosity change and severity of cellular injury within the treatment group. Fibrinogen reduction alone cannot significantly ameliorate ischemic injury in this model. Viscosity reduction therapy should include reduction of hematocrit and alteration of red cell deformability.
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PMID:Fibrinogen, blood viscosity, and cerebral ischemia. 397 56

The energy state of the brain during and after transient cerebral ischemia was examined in rats by in vivo measurement of 31P-nuclear magnetic resonance (NMR) spectra using a topical magnetic resonance spectrometer. EEGs and regional CBF (rCBF) were monitored on the same ischemic models. Immediately after the induction of ischemia, the height of the ATP and phosphocreatine peaks in the spectrum began to decrease with a concurrent increase of the inorganic phosphate (Pi) peak. The calculated pH from the chemical shift of Pi decreased during ischemia. The EEG pattern became flat immediately after ischemic induction. The rCBF decreased below the sensitivity level of the measuring instrument. With 30-min ischemia, the 31P-NMR spectrum returned to a normal pattern rapidly after recirculation. However, recovery of the EEG was delayed. The rCBF after recirculation showed postischemic hyperemia followed by hypoperfusion. In cases of 120-min ischemia, none of the spectra showed recovery. Thus, we could investigate the dynamic process of pathophysiological changes occurring in the ischemic brain in vivo.
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PMID:In vivo studies of energy metabolism in experimental cerebral ischemia using topical magnetic resonance. Changes in 31P-nuclear magnetic resonance spectra compared with electroencephalograms and regional cerebral blood flow. 398 22

A model is described in which transient complete cerebral ischemia is induced in rats by intracardiac injection of potassium chloride. The animals were intubated and mechanically ventilated with a nitrous oxide/oxygen (70:30) mixture. Cardiac arrest was achieved following a brief period of ventricular fibrillation. After 5-6 min, the circulation was restored by cardiopulmonary resuscitation and partial exchange transfusion. Local CBF (LCBF) during ischemia and cardiac resuscitation was studied by injection of [14C]iodoantipyrine into the right auricle at various periods during cardiac arrest, and was subsequently analyzed by autoradiography. No radioactive tracer could be visualized in any brain structure, demonstrating the absence of CBF during the cardiac standstill. LCBF was also studied at 5 min and 6.5 h after cardiac resuscitation. Five minutes of recirculation showed an increase in blood flow in all brain structures studied, ranging between 130 and 400% of control values. After 6.5 h of recirculation, the CBF was decreased in 13 of 24 brain structures by 20-50%, concomitantly with the depressed rate of glucose utilization found in 15 brain structures. The neocortical, hippocampal, and striatal concentrations of labile phosphates, lactate, pyruvate, phosphocreatine, glucose, and glycogen were measured 5 min after cardiac arrest. Extensive energy failure and elevation of lactate levels were observed and were similar to earlier reported values. One week following recovery from the ischemic insult, the animals were perfusion-fixed with formaldehyde. The brains were embedded in paraffin, subserially sectioned, and stained with cresyl violet/acid fuchsin. Histopathological changes were assessed by light microscopy as the number of acidophilic or pyknotic neurons. Morphological changes were observed in the hilus of the dentate gyrus, the hippocampal CA1 and subicular regions, the dorsal and lateral septum, the olfactory tubercle, the primary olfactory cortex, the entorhinal cortex, the amygdaloid nuclei, and the reticular nucleus of the thalamus. The distribution of the morphological changes suggests a transsynaptic mechanism, causing neuronal necrosis primarily in the limbic brain areas.
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PMID:Ischemic brain damage in rats following cardiac arrest using a long-term recovery model. 403 Sep 19

A modified collimator and standard gamma camera have been used to measure regional cerebral blood flow following inhalation of radioactive xenon. The collimator and a simplified analysis technique enables excellent statistical accuracy to be achieved with acceptable precision in the measurement of grey matter blood flow. The validity of the analysis was supported by computer modelling and patient measurements. Sixty-one patients with subarachnoid haemorrhage, cerebrovascular disease or dementia were retested to determine the reproducibility of our method. The measured coefficient of variation was 6.5%. Of forty-six patients who had a proven subarachnoid haemorrhage, 15 subsequently developed cerebral ischaemia. These showed a CBF of 42 +/- 6 ml X minute-1 X 100 g brain-1 compared with 49 +/- 11 ml X minute-1 X 100 g brain-1 for the remainder. There is evidence that decreasing blood flow and low initial flow correlate with the subsequent onset of cerebral ischaemia.
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PMID:Regional cerebral blood flow utilizing the gamma camera and xenon inhalation: reproducibility and clinical applications. 408 19

Cerebral ischemia was produced in spontaneously hypertensive rats (SHR) with a range of blood pressures (BP). Measurements were made at 4 hours of the edema produced (% H2O), the damage to the blood brain barrier (BBB) and, the blood flow (CBF) in both hemispheres and the cerebellum and brain stem. There was a statistically significant correlation between CBF and BP and between CBF and % H2O, but the correlation between BP and % H2O was not significant. The BBB is not open to technecium pertechnetate in this model at this time interval. Systemic hypertension is not a significant factor in the early development of ischemic edema in this model because the blood flow in the ischemic area falls with rising blood pressure, probably due to autoregulation in the collateral circulation.
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PMID:The effect of hypertension on ischemic cerebral edema in spontaneously hypertensive rats. 613 66


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