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

The authors studied the effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) (study 1) and on cerebral oxygenation (study 2) during mechanical ventilation in 8 patients, 4 with hepatic (HE) and 4 with septic encephalopathy (SE). In study 1, a positive linear relationship between CBF(y) and PaCO2 (x) was observed (y = 2.44x - 55.5, r = 0.6276, P less than 0.01, n = 18). In the study 2, hypocapnic-hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 8 patients. A good linear relationship was observed between CBF/CMRO2 (CMRO2 = cerebral oxygen consumption, y) and jugular venous PO2 (PjVO2, x) (y = 0.99x - 15.53, r = 0.8962, P less than 0.01, n = 18). It is concluded that cerebrovascular reactivity to CO2 was preserved in these patients, therefore, intentional or inadvertant hyperventilation may produce cerebral ischemia. Moreover, JPVO2 may be useful in monitoring cerebral oxygenation in such patients.
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PMID:Cerebrovascular reactivity to CO2 in patients with hepatic or septic encephalopathy. 216 Jul 9

The effect of cerebral ischemia on the activity of pyruvate dehydrogenase (PDH) enzyme complex (PDHC) was investigated in homogenates of frozen rat cerebral cortex following 15 min of bilateral common carotid occlusion ischemia and following 15 min, 60 min, and 6 h of recirculation after 15 min of ischemia. In frozen cortical tissue from the same animals, the levels of labile phosphate compounds, glucose, glycogen, lactate, and pyruvate was determined. In cortex from control animals, the rate of [1(-14)C]pyruvate decarboxylation was 9.6 +/- 0.5 nmol CO2/(min-mg protein) or 40% of the total PDHC activity. This fraction increased to 89% at the end of 15 min of ischemia. At 15 min of recirculation following 15 min of ischemia, the PDHC activity decreased to 50% of control levels and was depressed for up to 6 h post ischemia. This decrease in activity was not due to a decrease in total PDHC activity. Apart from a reduction in ATP levels, the acute changes in the levels of energy metabolites were essentially normalized at 6 h of recovery. Dichloroacetate (DCA), an inhibitor of PDH kinase, given to rats at 250 mg/kg i.p. four times over 2 h, significantly decreased blood glucose levels from 7.4 +/- 0.6 to 5.1 +/- 0.3 mmol/L and fully activated PDHC. In animals in which the plasma glucose level was maintained at control levels of 8.3 +/- 0.5 mumol/g by intravenous infusion of glucose, the active portion of PDHC increased to 95 +/- 4%. In contrast, the depressed PDHC activity at 15 min following ischemia was not affected by the DCA treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pyruvate dehydrogenase activity in the rat cerebral cortex following cerebral ischemia. 271 7

The activity of electroencephalogram (EEG) and cortical somatosensory evoked potential (SEP) was suppressed during cerebral ischemia in rats subjected to the 4-vessel occlusion. Considerable variations were demonstrated in the decrease of phosphocreatine and ATP concentration during ischemia among the rats measured with 31P-NMR, accompanied with cerebral acidification. Hypercapnia, induced in the rats studied by the inhalation of a gas mixture of 30-40% CO2, suppressed the activity of EEG and cortical SEP. The cerebral acidification observed during the ischemia was more severe than that under the hypercapnia, implying that cerebral acidification is one of the possible causes for the decrease in the electrical activity of the brain during ischemia.
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PMID:Effect of cerebral ischemia and hypercapnia on cerebral pH studied with 31P-NMR and electrical activity in rat brain. 272 63

The effects of cerebral ischemia on cerebral microvascular reactivity and prostanoid synthesis were examined in chloralose-anesthetized newborn pigs. Microvascular responses and periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were determined between 10 and 140 min after a 20-min period of total cerebral ischemia, as well as in sham-control piglets without cerebral ischemia. After cerebral ischemia, the decrease in pial arteriolar diameter in response to topical norepinephrine (10(-4) M) was similar in sham (-27 +/- 6%) and postischemic (-25 +/- 5%) piglets. However, the increase in pial arteriolar diameter in response to hypercapnia (10% CO2 ventilation) that was observed in sham piglets (+21 +/- 5%) was absent after ischemia (-2 +/- 3%). In contrast, dilations of pial arterioles in response to topical prostaglandin (PG)E2 (at 100 ng PGE2/ml: sham, +13 +/- 3%; postischemia, +21 +/- 4%) and topical isoproterenol (10(-6) M) (sham, +29 +/- 4%; postischemia, +23 +/- 3%) were not decreased by prior cerebral ischemia. In sham piglets, norepinephrine and hypercapnia produced increases in cortical periarachnoid prostanoid concentrations, whereas after cerebral ischemia, neither stimulus increased cortical periarachnoid prostanoid concentrations. The results are consistent with the hypothesis that failure of hypercapnia to dilate pial arterioles after cerebral ischemia results from the inability of this stimulus to increase cerebral vasodilator prostanoid synthesis.
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PMID:Cerebral ischemia alters cerebral microvascular reactivity in newborn pigs. 275 Sep 42

Perturbations in cerebral hemodynamics at the time of ablation of an arteriovenous shunt have been regarded as important in the pathogenesis of swelling and hemorrhage complicating resection of arteriovenous malformations (AVMs). A carotid-jugular fistula model in the rat had previously been investigated and found to simulate in part the nonhemorrhagic pathophysiology of a large cerebral arteriovenous fistula. Utilizing this model and measuring cerebral blood flow in 14 regions with a [14C]iodoantipyrine autoradiographic technique, the effects of hypocapnea on the cerebral circulation in opened and closed fistulas were investigated. Regional cerebral blood flow (rCBF) in control animals ranged from a median of 53 to 64 ml/100 g/min at a partial arterial carbon dioxide pressure (PaCO2) of 28 +/- 2 mm Hg and 85 to 112 ml/100 g/min at a PaCO2 of 40 +/- 5 mm Hg. In animals with an open carotid-jugular fistula created 12 weeks before the study, these median rCBF values at comparable PaCO2 levels ranged, respectively, from 15 to 39 ml/100 g/min and 50 to 68 ml/100 g/min (the 25th percentile for the open fistula in the hypocapneic group was 15 ml/100 g/min in 5 of the 14 regions studied). In contrast, median rCBF in the closed fistula group ranged from 73 to 100 ml/100 g/min in hypocapneic animals and from 118 to 187 ml/100 g/min in normocapneic animals. These results demonstrate the preservation of CO2 reactivity; hypoperfusion in the presence of a carotid-jugular fistula, hyperemia on fistula occlusion, and the potential to induce cerebral ischemia with hyperventilation in this model of a cerebral arteriovenous fistula.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of hyperventilation on cerebral blood flow in the rat with an open and closed carotid-jugular fistula. 279 97

The clinical value of noninvasive continuous monitoring of conjunctival oxygen tension for assessment of cerebral perfusion during carotid endarterectomy performed under general anaesthesia has been evaluated. The patients (n = 17; mean age 62.5 +/- 1.7 years) were monitored as follows: conjunctival oxygen tension (PcjO2); internal jugular venous oxygen tension at the skull base level (PcijvO2); arterial blood pressure; arterial and internal jugular venous blood gases; acid-base data and lactate, pyruvate levels; end-tidal CO2 concentration. The mean preanaesthetic PcjO2 level of 4.86 +/- 0.40 kPa was significantly lower than PaO2(PcjO2)/PaO2 ratio of 0.48). Following anaesthesia, a larger PcjO2-PaO2 gradient (ratio 0.32) was seen in spite of the hyperoxic situation (FiO2 = 0.40) due to vasoconstriction induced by slight hypocapnia (reduction of PaCO2 from 5.13 +/- 0.08 to 4.64 +/- 0.10 kPa). The carotid artery crossclamping resulted in a rapid and pronounced decrease of PcjO2, while PcijvO2 remained unchanged. No relationship between PcjO2 and stump pressure was found, while a significant correlation (P less than 0.02) between PcjO2 and lactate in effluent venous blood from the brain was demonstrable. It is concluded that PcjO2 monitoring seems a clinically useful trend indicator of cerebral perfusion in the individual patient. Due to large interindividual variations in basal PcjO2 readings and in PcjO2 changes during carotid artery clamping, however, transconjunctival oxygen tension monitoring does not seem to allow early and accurate recognition of impending cerebral ischaemia during carotid endarterectomy, and its routine use therefore seems of limited value.
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PMID:Continuous conjunctival oxygen tension (PcjO2) monitoring for assessment of cerebral oxygenation and metabolism during carotid artery surgery. 281 41

The acute cortical response to surgical brain isolation and subsequent extracorporal normoxic or 30 min hypoxic (PaO2 = 20 mm Hg) perfusions (hypoxic hypoxia with relative ischemia) was evaluated. Cerebral blood flow, arterial pH and CO2 were maintained constant during both perfusions; only the arterial oxygen content was changed. The isolated brain model used in this and previous investigations produces no qualitative ultrastructural changes in the neocortex following brain isolation and normoxic perfusion. However, the acute cortical structural response to 30 min of hypoxic hypoxia with relative ischemia demonstrated a number of important observations. Hypoxic hypoxia produced ultrastructural responses common to cerebral ischemia such as nuclear chromatin clumping, nucleolar condensation and cytoskeletal breakdown. Although neuronal abnormalities seen after 30 min of hypoxic hypoxia were similar to those acute neuronal changes observed following complete cerebral ischemia without recirculation, they differed three ways: (a) mitochondrial swelling and microvacuolation were observed in many cortical pyramidal neurons. (b) Glycogen particles within astroglial processes were observed even after a 30-min period of hypoxic hypoxia. (c) Perivascular astroglial swelling was minimal despite considerable perineuronal swelling. In contrast, incomplete cerebral ischemia produces mitochondrial changes similar to those in hypoxic hypoxia but also causes the depletion of tissue glycogen and perivascular glial swelling. Thus, hypoxic hypoxia with relative ischemia produces a unique acute ultrastructural response compared to either complete or incomplete cerebral ischemia.
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PMID:Acute ultrastructural response of hypoxic hypoxia with relative ischemia in the isolated brain. 281 6

Calcium entry blockers (CEB) have been a major advance in pharmacologic research in the last decade, especially in cardiovascular diseases. In neurology and intensive care, prescription of CEB seems to be more selective. CEB are potent cerebrovascular vasodilating drugs especially after KCL induced vasoconstriction. This property appears less evident when vasoconstriction is achieved by agonist substances. CEB act selectively on cerebral vessels, an effect which prevents the occurrence of systemic arterial hypotension. However they greatly modify the cerebrovascular response to arterial CO2. Concerning the cerebrovascular response to arterial CO2. Concerning their potential benefits in brain ischemia, it is now well admitted that CEB are useful in subarachnoid hemorrhage. Several controlled and uncontrolled human studies have demonstrated the CEB potency in vasospasm prevention and in cerebral ischemic consequences. Nonetheless when the vasospasm is installed, the benefit of the CEB appears less evident. In focal cerebral ischemia, data are few and unclear suggesting a cautious prescription of CEB. Finally CEB seem to increase intracranial pressure in humans, although this effect depends on the underlying neurologic pathology.
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PMID:[Calcium inhibitors: effects on cerebral blood flow and intracranial pressure]. 281 37

This study was conducted to investigate the degree of insult from arrest of cerebral blood flow leading to total brain ischemia, as a model for brain resuscitation studies in rabbits. In normothermic rabbits under light barbiturate anesthesia, cerebral blood flow was completely arrested for 5, 10, 15, 20, 30, 45 and 60 min by intrathoracic occlusion of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries. Arterial blood pressure, arterial pH, arterial blood gases, cerebral blood flow, intracranial pressure, hematocrit and end tidal CO2 were monitored and recorded before, during and for 8 h after reperfusion. Disappearance and return of spontaneous EEG activity, vasomotor and respiratory centers were also recorded. During ischemia, the EEG was suppressed within 15 s and vasomotor and respiratory centers within 3-6 min. In all animals with 5, 10, 15 and 20 min cerebral ischemia bioelectric activity of brain cortex, vasomotor and respiratory centers returned upon recirculation. In about 50% animals with 30, 45 and 60 min ischemia recovery of basic brain function did not occur. After different periods of ischemia, histopathologic lesions were located mostly in the frontal cortex and hippocampus with ischemic neuronal change as the most frequent structural change. Brain cell necrosis was seen after successful resuscitation. This study indicates the feasibility of an ischemic insult in rabbits for use in resuscitation studies.
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PMID:Resuscitation of the rabbit brain after acute complete ischemia lasting up to one hour: pathophysiological and pathomorphological observations. 283 98

Effects of ischemia (20 min) on cerebral cortical prostanoid synthesis and microvascular responses to hypercapnia and topical acetylcholine were examined in anesthetized newborn pigs. Pial arteriolar dilation in response to hypercapnia (10% CO2 ventilation, 10 min) was absent 2 h after ischemia and reversed toward constriction by 24 h postischemia. In sham control piglets, hypercapnia increased cortical periarachnoid fluid prostanoid concentrations. After ischemia, hypercapnia did not affect prostanoid concentrations on the brain surface. Acetylcholine (10(-3) M)-induced pial arteriolar constriction was reversed toward dilation 24 h after cerebral ischemia. Further, acetylcholine-induced prostanoid synthesis was markedly attenuated after ischemia. We conclude that cerebral ischemia-reperfusion alters cerebral prostanoid synthesis and microvascular control in newborn pigs. These abnormalities persist for at least 24 h.
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PMID:Ischemia alters cerebral vascular responses to hypercapnia and acetylcholine in piglets. 291 33


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