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

Post-ischemic delayed cerebral hypoperfusion (PDH) is considered to be one of the most critical factors limiting brain recovery after cerebral ischemia. This experiment was designed to determine the characteristics of PDH and the effects of nicardipine on the PDH. Twenty-four dogs underwent complete cerebral ischemia for 15 min using aortic clamping method with aorto-atrial bypass formation, and cerebral cortical blood flow (c-CBF), brain stem blood flow (s-CBF), intracranial pressure (ICP), and perfusion pressure (PP) were measured for 48h. Eight dogs (1 microgram group) received nicardipine 1 microgram.kg-1.min-1 for 4 h following 10 micrograms bolus iv injection 5 min after declamping of aorta. Another 8 dogs (2 micrograms group) received 10 micrograms + 2 micrograms.kg-1.min-1 nicardipine in the same manner as in group 1. The remaining 8 served as controls. In the control group c-CBF and s-CBF decreased to 60% and 55% of pre-ischemic values, respectively 1 hour after declamping of aorta, and returned to pre-ischemic values 10 and 6 h later, respectively, in spite of no significant changes in PP's. 1 microgram group and 2 micrograms group maintained pre-ischemic CBF value throughout the experimental period, and the values were significantly higher than in control group between 1st and 5th h post-ischemia. There were no significant differences in ICP's among the 3 groups throughout the experiment. In conclusion, PDH appears to be a phenomenon always accompanying transient complete cerebral ischemia, and it is assumed to be caused by constriction of cerebral vessels. Nicardipine improved PDH, indicating that the underlying mechanism of PDH must be related to a disorder in Ca2+ metabolism of cerebral vessels after ischemia.
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PMID:[Cerebral hemodynamics of post-ischemic delayed hypoperfusion (PDH) and the effects of nicardipine on the PDH]. 234 97

The effect of reversible cerebral ischemia on brain edema development was studied with a gravimetric method. CBF changes after ischemia were correlated with alterations in brain SG. Forebrain ischemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The SG of different brain structures was determined in a Percoll column up to 24 hr after ischemia. In addition, rCBF was measured by [14C]iodoantipyrine autoradiography. Cerebral ischemia resulted in reduction of CBF to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischemia, blood flows were still reduced to 30% to 50% of the control level indicative of DPH. SG in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischemia and was still significantly reduced at 1 hr, although it was normal again 6 hr later. Regression analysis revealed a significant correlation between CBF obtained during ischemia and the corresponding SG found at 10-min recirculation, which could also be established at 1-hr recirculation. Therefore, a causal relation between the development of the DPH and the formation of ischemia might be considered.
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PMID:Is postischemic hypoperfusion related to brain edema? 239 11

In 43 patients suffering from unilateral supratentorial ischaemia the changes over an interval of 3 years in clinical score, quantified EEG (using the neurometric method) and CBF (Xenon inhalation method) were studied. The patients were examined 3 times: shortly after the onset of ischaemia and respectively 3 and 36 months after this first measurement. Three patients died from causes not related to cerebral ischaemia. In the surviving patients the EEG and clinical score improved, often dramatically; the CBF values did not change significantly. Most of the changes occurred in the first 3 months after the stroke. For the evaluation of the prognostic value of the various parameters, 2 sub-groups of patients with different outcome but comparable initial clinical scores were studied. A persistent neurological deficit was predicted by a low CBF at the first measurement. The neurometric parameters obtained from the initial EEG had no value in this respect.
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PMID:Recovery from cerebral ischaemia. EEG, cerebral blood flow and clinical symptomatology in the first three years after a stroke. 245 26

Cerebral ischaemia in the region of an internal carotid artery (ICA) stenosis may be caused by embolism or cerebral hypoperfusion. A severe ICA stenosis may be well compensated by collateral blood supply, however, in some patients the capacity of the collateral blood supply is insufficient. Studies evaluating therapeutic modalities or natural history of carotid artery disease should therefore include a test capable of assessing cerebral haemodynamics. However, most studies, invasive as well as non-invasive, have focused on the ability of the test to diagnose the ICA lesions itself, rather than the haemodynamic changes induced by the stenosis. This paper reviews non-invasive methods for haemodynamic evaluation of carotid artery disease. Haemodynamic evaluation of ICA stenoses may be performed accurately by different techniques. Analysis of Doppler waveforms obtained distal to the ICA lesion and CBF reactivity tests may identify patients with severe reduction in ICA perfusion pressure. Periorbital Doppler examination and OPG identifies ICA lesions causing minor pressure gradients, however, they are unable to discriminate between minor and moderate to severe pressure reduction. Transcranial Doppler examination may prove to be useful in haemodynamic assessment of ICA stenoses, but, this remains to be evaluated. Presently, in addition to direct evaluation of the carotid arteries, we use a combination of periorbital Doppler examination and analysis of distal ICA waveforms. In cases of an ICA stenosis and orthograde flow any severe pressure reduction may be ruled out. In cases of inverted flow, analysis of distal ICA waveforms may identify patients with severe reduction in ICA perfusion pressure.
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PMID:Haemodynamic evaluation of carotid artery disease. 265 4

Cerebral blood flow (CBF, by laser Doppler flowmetry) and extracellular cortical concentrations (by microdialysis) of adenosine, inosine, xanthine, hypoxanthine, and lactate were measured together with somatosensory evoked potentials (SEP) in chloralose-anaesthetized spontaneously hypertensive rats (SHR) during relative cerebral ischemia induced by hypotensive hemorrhage. Reduction of mean arterial blood pressure (MABP) to 40-50 mm Hg, which decreased SEP to about 50% of prebleeding control level, decreased CBF only to about 75% of control due to cerebrovascular "autoregulation." A secondary, marked rise in cerebrovascular resistance (CVR) occurred after about 15 min in parallel with a striking increase in heart rate (after initial bradycardia). This late rise in heart rate is probably elicited by relative ischemia in medullary centers. The increase in CVR might indicate increased sympathetic nerve activity to the circle of Willis and large cerebral arteries. Cortical lactate increased initially but started to decline after about 30 min, and after 2 h it was not significantly higher than control. Cortical adenosine, inosine, hypoxanthine, and xanthine increased slowly and were significantly elevated after 50 min of hemorrhage. After 80 min, adenosine and inosine had returned to initial levels, while hypoxanthine and xanthine were further elevated. Despite the apparent partial recovery of metabolic disturbances during late hemorrhage, and with a blood flow maintained at 75% of resting control, SEP did not improve. It is suggested that the depression of SEP is not primarily caused by circulatory-metabolic derangements, but instead by activation of specific inhibitory systems.
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PMID:Relative cerebral ischemia in SHR due to hypotensive hemorrhage: cerebral function, blood flow and extracellular levels of lactate and purine catabolites. 271 8

In a series of patients with unilateral supratentorial ischemia, clinical scores and parameters derived from computer analysis of the EEG and from measurement of the CBF were determined in the first several weeks after the stroke. Seventeen of these patients underwent a carotid-endarterectomy and 15 a STA-MCA bypass operation. Matched control patients were selected from the remaining cases. All patients, including the controls, were eligible for vascular surgery. The measurements were repeated respectively 3 months and 3 years after the first examination. Clinical improvement occurred in all groups. The degree of these clinical changes was similar for operated and non operated cases. EEG changes indicated more improvement in the cases without surgery. Finally, the CBF was remarkably stable in all patients. The overall effects of reconstructive vascular surgery on the recovery after cerebral ischemia appeared to be negligible.
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PMID:Long-term clinical and neurophysiological effects of reconstructive vascular surgery for cerebral ischemia. 272 55

The role of polymorphonuclear leukocytes (PMNLs) in postischemic delayed hypoperfusion in the rat brain was investigated. Cerebral ischemia was accomplished by reversible bilateral occlusion of the common carotid arteries for 15 min combined with bleeding to an MABP of 50 mm Hg. The animals of one group were depleted of their circulating. PMNLs by intraperitoneal injections of an antineutrophil serum (ANS) prior to the experiment. All animals included in this group had fewer than 0.2 x 10(9) circulating PMNLs/L at the start of the experiments. In another group ANS was injected intravenously for 5 min starting 2 min after the ischemic insult. After 4 min of recirculation, the number of circulating PMNLs in this group was below 10% of the normal. Control animals were injected with the same amount of normal sheep serum or were not treated at all. Sixty minutes after termination of ischemia, the local blood flow in previously ischemic cerebral structures was 40-50% of the normal as measured with the [14C]iodoantipyrine technique. In animals treated with ANS prior to the ischemic insult, the postischemic blood flow in the frontal, sensorimotor, and parietal cortex as well as caudoputamen and thalamus was significantly higher than that in non-ANS-treated animals. Treatment with ANS immediately after the ischemic period caused no improvement of the local CBF. It is concluded that PMNLs are involved in the cerebral postischemic flow derangements seen in this model. Their effects seem to be exerted during ischemia or immediately upon reinstitution of blood flow.
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PMID:Delayed hypoperfusion after incomplete forebrain ischemia in the rat. The role of polymorphonuclear leukocytes. 273 15

CBF and somatosensory evoked potentials (SEPs) were measured in a model of moderate cerebral ischemia in anesthetized spontaneously hypertensive rats. The rats were bled to reduce SEP amplitudes to about 50% of prebleeding control. The consequent blood pressure fall reduced CBF to 77% of control as measured by the laser-Doppler technique. Naloxone (5 mg kg-1 i.v. plus 25 mg kg-1 h-1 i.v. for 30 min) caused a significant increase in SEP amplitudes, while CBF did not change significantly. In addition, the latency of the first SEP component decreased toward prebleeding values. Heart rate (HR) decreased, but MABP was held constant by a pressure-regulating reservoir. In unbled rats, naloxone (5 mg kg-1 i.v.) caused a transient small increase in MABP and SEP amplitudes and decrease in HR. These results indicate that sensory input is regulated by opioid systems. Increased opioid activity may inhibit ascending sensory pathways during relative cerebral ischemia and thereby depress SEP responses. Thus, naloxone can release this inhibition and enhances SEP independently of CBF during relative cerebral ischemia. Similar mechanisms might explain the apparently beneficial effects of naloxone in some stroke models.
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PMID:The effects of naloxone on cerebral blood flow and cerebral function during relative cerebral ischemia. 273 17

Cerebral ischemia and ischemia-reperfusion induced cerebral injury results in the accumulation of free fatty acids and diacylglycerols as a result of increased activity of phospholipases A and C. We have evaluated the incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomes, the effect of cerebral ischemia on 14C incorporation, and the effect of a PAF antagonist (BN 52021) on cerebral blood flow, free fatty acids, diacylglycerols, and polyphosphoinositides. Peak incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomal fractions occurred 30 minutes following intraventricular injection. Peak incorporation into cerebellar synaptoneurosomal fractions was at 60 minutes following intraventricular injection. Turnover in phospholipid pools was similar in the whole brain and synaptoneurosomes (PI greater than PC greater than PE). Considering phosphatidylinositol content in the gerbil brain, the specific activity of 14C arachidonic acid was 22 times greater in PI than PC. Five minutes of bilateral carotid artery ligation resulted in decreased phosphatidylinositol and polyphosphoinositols. Bilateral carotid artery ligation resulted in systemic arterial hypertension, complete forebrain ischemia (CBF less than 7 ml/100 gm/min) and a 20% to 50% reduction in midbrain CBF. Reperfusion resulted in cerebral reactive hyperemia and systemic hypotension. BN 52021 inhibited the maturation of ischemia-reperfusion induced cerebral injury. Cerebral blood flow was improved. Free fatty acids were decreased, suggesting inhibition of phospholipase A activity. Decreased DAG pools with increased PIP2 pools suggest a possible coinhibition of phospholipase C.
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PMID:Arachidonic acid metabolism and cerebral blood flow in the normal, ischemic, and reperfused gerbil brain. Inhibition of ischemia-reperfusion-induced cerebral injury by a platelet-activating factor antagonist (BN 52021). 277 4

The effects of etomidate on focal cerebral ischaemia following transorbital occlusion of the cat middle cerebral artery were investigated. Etomidate had no effect on CBF before or after onset of ischaemia by comparison with controls, but caused a greater fall in CBF in cats with high preocclusion or initial ischaemic CBF than in those in which CBF was lower. There were more sustained rises in Kp on SG. The established flow threshold for water accumulation was lost; more gyri with CBF above and fewer gyri with CBF below the flow threshold accumulated water. The relationship between mean occlusion CBF and in vitro GABA uptake was lost; uptakes from MG were lower and from SG and EG higher than expected. In the ischaemic penumbra there was a trend towards reduction in CBF, disruption of ion homeostasis and cerebral oedema formation, whilst in areas of lower flow there was some recovery of GABA uptake and less cerebral oedema following administration of etomidate.
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PMID:The effects of etomidate in the cat middle cerebral artery occlusion model of brain ischaemia. An experimental study. 288 Mar 10


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