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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A digital model study has been developed for quantitative assessment of experimental errors in the analysis of 133Xe clearance curve from the brain. A small computer synthesized a model of the clearance curve, varying combinations of fast and slow components. The curves were convoluted with Poisson random digits to simulate statistical fluctuations. Identical curves were overlapped with varying intervals to study the influence of remaining activity. The height over area method to ten minutes was confirmed to overestimate CBF by 10% to 15% with a slow component of 20 ml/100 gm per minute, and the overstimation was increased with a lower slow flow component. The initial slope value was shown to have a close relationship with the fast flow component when the latter was less than 100 ml/100 gm per minute. Errors due to statistical fluctuations were determined only by the initial height (Ho cps), as the percent standard deviation was deltaHo/Ho in the height over area method and 2 deltaHo/HologHo in the initial slope method, where deltaHo equals square rootHo. Remaining activity caused errors of 1% to 3% in the initial slope method with an injection interval of 15 minutes. The influence of remaining activity can be eliminated with an injection interval of more than 25 to 30 minutes in the initial slope method and more than 40 minutes in the height over area method.
Stroke
PMID:Some experimental errors in calculating regional cerebral blood flow from the intracarotid 133Xe clearance curve. A quantitative evaluation employing a digital model. 115 73

Hydralazine is shown to have a very complex cerebral hemodynamic effect. It raises the intracranial pressure which, together with its effect upon systemic blood pressure, reduces the cerebral perfusion pressure. In spite of this and a concomitantly induced hyperventilation by hydralazine, CBF increases with some delay. The conclusion is that hydralazine is a cerebral vasodilator acting immediately upon cerebral capacitance vessels but later upon the resistance vessels as well.
Stroke
PMID:A paradoxical cerebral hemodynamic effect of hydralazine. 115 77

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.
Stroke
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Continuous measurements of systemic blood pressure (BP), cerebral perfusion pressure and CBF were accomplished in the cat during transient hypertension, hypercapnia and bilateral carotid artery occlusion. From these measurements resistance values in the circle of Willis and in the cerebral arteries distal to the circle were calculated. The results indicate that the arteries of the circle of Willis and the arteries distal to the circle of Willis dilate and contract independently.
Stroke
PMID:Cerebral blood flow regulation: vascular resistance adjustments in the circle of Willis. 126 7

The cerebrovascular response to hypercapnia and hyperventilation was studied in normal and jaundiced baboons by the intracarotid 133Xe injection technique. The baboons with bile duct ligation were found to have decreased CBF at all levels of PaCO2. This difference between normal and jaundiced baboons was 13% at normocapnia rising to 33% with hypercapnia and 37% with hypocapnia. The CBF values all were increased toward normal by use of an alpha-adrenoreceptor blockade (phentolamine). It is suggested that the obstructive jaundice potentiated an inherent vasoconstrictor alpha-adrenergic mechanism to oppose the effects of CO2. Also, alteration of the PaCO2 may have produced its effects on the cerebral vessels by altering this adrenergic mechanism.
Stroke
PMID:Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice. 126 12

We used a multitracer positron emission tomography (PET) approach to assess metabolic changes in infarcted and periinfarct tissue in acute ischaemic stroke. 16 patients were studied within 6-48 hours (mean, 23 h) after onset of symptoms from a first hemispheric stroke and again 13-25 days later (mean, 15.6 days). Regional cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGlc), blood flow (CBF) and blood volume (CBV) were measured and oxygen extraction (OEF) as well as glucose extraction (GEF) and microvascular transit time were calculated. PET images were three-dimensionally aligned using serial CT or MRI scans. Regions of interest on the side of the infarction were individually compared to contralateral mirror regions. In the infarction core CBF, CMRO2 and CMRGlc were significantly lower than on the contralateral side and did not change during time. In the periinfarct regions there was a decreased CMRO2 with progressive deterioration over time while CBF slightly increased. Only in a few ischaemic regions with initially increased OEF oxygen metabolism was preserved during the course of time.
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PMID:Metabolic derangement in viable periinfarct tissue in the course of acute ischaemic infarction: a multitracer positron emission tomography (PET) study. 135 84

Twenty-four patients presenting an acute stroke with watershed cerebral infarct on CT scan or MRI were included in this retrospective study. Age was 63 +/- 14 years (mean +/- SD), and sex ratio was 2 men for 1 woman. Main clinical features were: in anterior location, lower limb weakness and frontal syndrome with transcortical motor aphasia in left lesions or spatial dyscalculia in right ones; in posterior location, brachiofacial weakness with constant quadranopsia and hypoesthesia, and Gerstmann syndrome in left lesion. There was no distinctive feature for subcortical and multiple infarcts. In bilateral infarcts, there were one pseudobulbar syndrome, and 2 pseudo brainstem syndromes with neuropsychological signs. Aetiologies were severe carotid artery disease in 14 cases, severe cardiopathy in 6, isolated cerebral angiitis in 1, essential thrombocythemia in 1, protein C deficiency with sickle cell disease in 1, and cholesterol emboli in 1 anatomical case. CBF performed in carotid artery occlusions or tight stenoses showed evidence of haemodynamic changes. Microembolic process can be proposed in the case with cholesterol emboli. Preventive treatment is discussed.
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PMID:Watershed cerebral infarcts: retrospective study of 24 cases. 135

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.
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PMID:Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs. 140 68

Stimulation of the cerebellar fastigial nucleus (FN) increases CBF but not metabolism and reduces the tissue damage resulting from focal cerebral ischemia. This effect may result from enhancing CBF in the ischemic tissue without increasing local metabolic demands. To test this hypothesis, we studied whether the reduction in tissue damage is restricted to the neocortex, a region in which the CBF increase is independent of metabolism, and whether stimulation of the dorsal medullary reticular formation (DMRF), a treatment that increases both cerebral metabolism and CBF, also protects the brain from ischemia. In halothane-anesthetized Sprague-Dawley rats, the middle cerebral artery (MCA) was occluded either proximally or distally to the lenticulostriate branches. The FN or DMRF were then stimulated for 1 h (50-100 microA; 50 Hz; 1 s on/l s off). Twenty-four hours later, the infarct volume was determined. FN stimulation substantially reduced the size of the infarct, an effect that was greater with distal (-69 +/- 8%; n = 6; p < 0.001; mean +/- SD) than with proximal (-38 +/- 8%; n = 8; p < 0.001) MCA occlusion. The reduction occurred only in neocortex (-43 +/- 9%; p < 0.001) and not in striatum (-16 +/- 21%; p > 0.05). Stimulation of the FN also enhanced recovery of EEG amplitude in the ischemic cortex (+48%; p < 0.003). DMRF stimulation (n = 7) did not affect the stroke size or EEG recovery (p > 0.05). Thus, stimulation of the FN, but not the DMRF, attenuates the damage resulting from focal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of the fastigial nucleus enhances EEG recovery and reduces tissue damage after focal cerebral ischemia. 140 Jun 50

Measurements of CBF and CMR in human ischemia and infarction have provided valuable insight into the pathophysiology of stroke and important guidance to the development of therapeutic strategies. Further research combing therapeutic manipulation with CBF and CMR will be important for developing optimal methods to treat ischemic cerebrovascular disease. At this time, no value has been demonstrated for these techniques in individual patient care decisions. Although now widely available, CBF and CMR measurements should still be considered clinical research tools until they can be shown to provide benefit in reducing morbidity and mortality or reducing medical expenses in clinical practice.
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PMID:Hemodynamics and metabolism in ischemic cerebrovascular disease. 155 9


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