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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 cerebral hypoperfusion supposedly due to constriction of cerebral vessels is considered to be one of the most important factors limiting the recovery of the brain after cerebral ischemia. An experimental study on dogs was carried out to determine the changes in the responsiveness of cerebral vessel to the dilating effects of increase of arterial pressure (AP) and of CO2 inhalation after 3-6 min of cardiac arrest. Responsiveness was measured by the ratio of change in intracranial pressure (ICP) to change in AP (delta ICP/delta AP) and to change in PCO2 (delta ICP/delta PCO2), since in a bony cranium the changes in cerebral vessel diameter are reflected by instantaneous ICP change. delta ICP/delta AP following the administration of intravenous epinephrine was 33%, 43%, 36%, 37% and 16% of pre-ischemic value 1 h, 2 h, 3 h, 4 h and 5 h after cerebral ischemia, respectively. delta ICP/delta PCO2 following 10% CO2 inhalation was 13%, 32%, 55%, 50%, 70% and 75% of pre-ischemic value 1/2 h, 1 h, 2 h, 3 h, 4 h and 5 h after cerebral ischemia, respectively. Normal delta ICP/central venous pressure (delta CVP) was observed during the post-ischemic period, although statistical analysis was not done. From this we concluded: After 3-6 min of cardiac arrest, cerebral arteries constricted for more than 5 h during post-ischemic period. These arteries did not respond well to the dilating effects of increased arterial pressure or CO2 inhalation, but after 3 h their responses to CO2 inhalation returned to their pre-ischemic levels. The intracranial pressure became more or less dependent on CVP during post-ischemic period.
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PMID:Responsiveness of cerebral vessels to changes of blood pressure and partial pressure of carbon dioxide after a transient period of cardiac arrest in dogs. 298 92

Regional cerebral blood flow (rCBF) during hypertension and hypercapnia was studied in 33 patients with putaminal hemorrhage, using a single photon emission CT by means of Xenon 133 inhalation method. The results obtained were as follows: 1) A significant relationship was obtained between the impairment of autoregulation, CO2 reactivity and the degree of cerebral ischemia, i. e., in most cases, these vascular responses were impaired in cases of ischemia showing the rCBF decrease over 30 to 40% of normal values. However, there were particular cases with cerebral ischemia of over 30 to 40% in which autoregulation seemed to be preserved in the acute stage, which was considered to be the similar phenomenon as so called "false autoregulation". 2) The cerebrovascular responses such as autoregulation and CO2 reactivity were preserved in cases of less than 50 ml of hematoma volume. In cases with 50 to 74 ml of hematoma volume however, autoregulation and CO2 reactivity were mostly impaired, especially in the affected hemisphere rather than the non-affected, in the period of 1 to 2 months from the onset. Furthermore, the impairment was also involved in both hemispheres if the hematoma was over 75 ml in volume. 3) The cerebrovascular responses were markedly impaired in the region of basal ganglia of the affected hemisphere which corresponded well to the hematoma site. 4) There was a close correlation between the cerebrovascular responses and the activity of daily life (ADL), i. e, the prognosis might be poor in cases with global impairment, but which seemed to be rather good in cases with local impairment. It might be concluded, from the results mentioned above, that the study of autoregulation and CO2 reactivity is probably significant in estimating the pathogenesis and the treatment of cerebral ischemia following hypertensive putaminal hemorrhage.
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PMID:[A study of cerebrovascular autoregulation and CO2 reactivity in putaminal hemorrhage]. 310 23

Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.
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PMID:Effect of hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebrovascular disorders. 311 60

A model of cerebral ischemia was implemented by means of bilateral occlusion of carotid arteries in rabbits. A reduction of the blood flow was observed during first 3 days after the occlusion in the cortex and white matter, followed by a slow restoration up to 80 per cent of initial level. The responses of the blood flow to CO2 were reduced and often inverted during the 1st week, had a phasic character and returned to near normal by the 14th day. The responsiveness of vessels to CO2 and head-down tilt were sharply reduced and inverted during the 1st week and did not return to normal. Simultaneous recording of the blood flow parameters and of the responsiveness of cerebral vessels provides a better insight into the dynamics of postischemic restoration of functional state of various parts of the brain vascular system.
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PMID:[Dynamics of the cerebral blood flow and reactivity of the cerebral vessels after bilateral occlusion of the carotid arteries]. 314 Dec 22

The authors described methodological improvement and quantitative evaluation in measurement of cerebral blood volume (CBV) by reflectance spectrophotometry. The measurement of blood volume by this method has not been applied to the brain tissue because of the methodological difficulties. In order to obtain the accurate CBV values with this method, it is necessary to keep the proper contact between the sensor for the measurement and the brain tissue to be measured. For this purpose we developed a balance arm. A sensor for CBV measurement was fixed with the one side of the arm and a weight was installed to the other side. The pressure of the sensor to the brain can be adjusted by moving the weight, and the sensor was placed on the brain tissue with the proper pressure. Moreover, the sensor was attached with an acryl-made cap to make the pressure adjustment easier by enlarging the contact surface and to enable to observe the vasculature on the surface of the brain. With this improved method the reasonable changes of CBV could be obtained when the CO2 gas was inhalated and cerebral ischemia was produced in cats. The possibility of the quantitative evaluation was investigated using the homogenized brain tissue of cats. After the elimination of the blood from the brain by the perfusion with the saline, the brain was removed and homogenized. Then, the definite volume of blood, of which hemoglobin volume was already known, was added and measured by this method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Measurement of cerebral blood volume by reflections spectrophotometry: methodological improvement and quantitative evaluation]. 341 68

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

The effect of indomethacin (3mg/kg IA) preloading on the pathophysiology of a model of acute cerebral ischaemia has been tested. Primates anaesthetised with alpha-chloralose were used. Indomethacin reduced basal blood flow by 39% and reduced CO2 reactivity by 71%. Water content changes of the cerebral cortex and relationships between blood flow and extracellular potassium (Ke), and calcium (Cae) activities have been measured. Indomethacin infusion did not effect the water content of the left side but there was more water in all regions of the right hemisphere which were rendered ischaemic. There water increases were significant for blood flows greater than 5ml/100g/min in exposed areas. There was a significant increase in the flow thresholds for change in Ke and Cae. Possible mechanisms for these changes have been discussed.
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PMID:Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin. 706 74

Following severe head injury, derangements of the cerebral vasculature and cerebral blood flow (CBF) often occur, rendering the brain at risk of secondary ischemia. Therefore, monitoring of CBF in head-injured patients is considered useful for understanding the pathophysiology and effects of therapy, although such monitoring has not yet become part of routine patient management in most centers. In this article, we review the current research on CBF in head injury. Understanding of the physiologic relationship between CBF and cerebral oxygen metabolism (CMRO2) is crucial in the interpretation of CBF values obtained in comatose head injured-patients. Although CMRO2 is reduced with coma, there is ample evidence to suggest that vulnerability of the brain to ischemia is in fact enhanced after traumatic injury. It is now well established that cerebral ischemia (CBF < or = 18 mL/100 g/min) is present in approximately 30% of cases within the first 6 hrs postinjury. In addition, early ischemia has been found to correlate with poor outcome and early mortality. Notably, early ischemia was present even with normal or restored blood pressure and arterial oxygenation, which suggests that other, nonsystemic causes of cerebral ischemia after traumatic brain injury exist. Although spasm of the larger cerebral arteries has been postulated as a possible cause of ischemia, recent measurements of cerebral blood volume are more compatible with compromise of the microcirculation, possibly due to perivascular swelling, with endothelial injury and leukocyte stasis. Disturbances of cerebrovascular CO2 reactivity and autoregulation appear to be less frequent than previously assumed. However, when present, such derangements do have consequences for therapy, in particular the management of blood pressure and cerebral perfusion pressure. Potential implications for patient management are discussed.
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PMID:Cerebral blood flow in severe clinical head injury. 749 46

To better understand why neurons accumulate calcium during cerebral ischemia, the influence of specific ion channel inhibitors on the rise in cytosolic free calcium ([Ca2+]c) during hypoxia or ischemia was evaluated in rat cerebrocortical brain slices. [Ca2+]c was measured fluorometrically with the dye fura-2 during hypoxia (95% N2/5% CO2 or 100 microM NaCN), simulated ischemia (100 microM NaCN plus 3.5 mM iodoacetate), or 0.5-1.0 mM glutamate. Hypoxia or ischemia increased [Ca+2]c from 100-250 nM to 1,000-2,500 nM within 3-5 min. Greater than 85% of the calcium accumulation was influx from the extracellular medium. The non-competitive N-methyl-D-aspartate (NMDA) inhibitor MK-801 reduced [Ca2+]c accumulation during hypoxia, but antagonism of alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptors or voltage-gated sodium or calcium channels or Na+/Ca2+ exchangers had no effect. During ischemia, combined antagonism of NMDA, AMPA and voltage-gated sodium channels slowed the rate of calcium accumulation, but not concentration at 5 min. Membrane damage, as indicated by leakage of lactate dehydrogenase into superfusate, occurred coincidentally with calcium influx and ATP loss during both hypoxia and ischemia. We conclude that cytosolic calcium changes during hypoxia or ischemia in cortical brain slices are due to multiple mechanisms, are incompletely inhibited by combined ion channel blockade, and are associated with disruption of cell membrane integrity.
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PMID:Causes of calcium accumulation in rat cortical brain slices during hypoxia and ischemia: role of ion channels and membrane damage. 753 4

Hypoglycemia increases the vulnerability of the perinatal brain to asphyxia, but it is not known if hypoglycemia-induced changes in cerebral hemodynamics and vascular reactivity underlie this vulnerability. This study tested the hypothesis that hypoglycemia exacerbates postischemic hypoperfusion, and impairs postischemic CO2 reactivity. The authors also examined the hypothesis that postischemic hypoperfusion is associated with a reduction in the interstitial concentration of the vasodilator metabolite adenosine. Global cerebral ischemia of 10 minutes duration was induced in newborn pigs anesthetized with isoflurane by occlusion of subclavian and brachiocephalic arteries; cortical cerebral blood flow (CBF) and interstitial adenosine concentration were evaluated simultaneously using the combined hydrogen clearance/microdialysis technique. Hypoglycemia (blood glucose < 25 mg/dl) was induced by regular insulin (25 IU/kg) administered intravenously 2 hours prior to induction of ischemia. In the eight normoglycemic animals, baseline CBF was 38 +/- 4 ml/min/100 gm and baseline adenosine concentration was 1.2 +/- 0.1 microM; in the eight hypoglycemic animals, these values were 39% (p < 0.05) and 62% (p < 0.05) greater, respectively, under baseline conditions. At 1 hour of postischemic reperfusion in normoglycemic animals, CBF was reduced 39% relative to the preischemic baseline (p < 0.01), concomitant with a 27% reduction (p < 0.05) in adenosine concentration, suggesting that this lowered concentration may underlie delayed hypoperfusion. These postischemic reductions in CBF and interstitial adenosine concentration were significantly greater in hypoglycemic animals, with CBF and adenosine concentration reduced 70% (p < 0.001) and 71% (p < 0.01), respectively, relative to baseline. In nine animals preischemic reactivity to hypercapnia was unaffected by hypoglycemia. Postischemic hypercapnic reactivity was retained in the eight normoglycemic animals, but was attenuated 73% (p < 0.05) in hypoglycemic animals. Thus, in the newborn pig, hypoglycemia exacerbates postischemic cortical hypoperfusion and impairs postischemic cerebrovascular reactivity to hypercapnia.
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PMID:Effect of hypoglycemia on postischemic cortical blood flow, hypercapnic reactivity, and interstitial adenosine concentration. 796 18


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