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Query: UMLS:C0917798 (
cerebral ischemia
)
17,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Total starvation is effective for acute weight reduction in obesity. However, in 200 patients, most of whom also had internal diseases, 8% exhibited sometimes severe complications, i.e. reversible
cerebral ischemia
in 3 hypertensive patients when the blood pressure was lowered to the normal range by natriuresis of fasting; breakdown of water and electrolyte homeostasis with circulatory
collapse
, vomiting and vertigo; acute crises of paroxysmal nocturnal hemoglobinuria and porphyria respectively and increase of transaminases up to 200 mu/ml, or cardiac arrhythmias. Relative (?) contraindications for total fasting appear to be clinical sings of arteriosclerosis such as vascular bruits, angina pectoris and intermittent claudication. In case of doubt, the method should only be used in hospital.
...
PMID:[Complications in null-diet]. 91 86
Clinical studies have demonstrated the prognostic importance of increased intracranial pressure in central nervous system infections. To delineate development of intracranial pressure in meningitis experiments were carried out in rabbits. Meningitis was induced by injecting streptococcus pneumoniae bacteria into the cisterna magna and blood, and intracranial pressures were continuously recorded. In the experimental model, three stages were seen: incubation period (0-8 h)--in which CSF becomes positive for the infecting organism and biochemical changes occur, but there are no hemodynamic or intracranial pressure changes; stage of slowly increasing intracranial pressure - because blood pressure remains normal, cerebral perfusion pressure is maintained adequate for cerebral metabolic need (9-24 h); terminal stage (greater than 25 h)--with hemodynamic
collapse
, critical reduction of cerebral perfusion pressure,
cerebral ischemia
, and death of the experimental animals. It is suggested that a similar sequence occurs in human disease. The clinical implication stresses the need for early recognition and treatment of intracranial hypertension as an important adjunct to antibiotic treatment of the infecting organism.
...
PMID:Intracranial pressure and cerebral perfusion pressure in experimental streptococcus pneumoniae meningitis. 157 Apr 13
Despite recent advances in the treatment of status epilepticus (SE), the mortality and morbidity associated with this condition remains high. Although the reasons for this excessive mortality are not known, several factors are suspected, including
cerebral ischemia
, cardiovascular
collapse
, toxic stimulation by neurotransmitters and hormones, or toxic products of intermediary metabolism. Cerebral lactic acidosis can cause cortical injury and has been shown to occur with seizures in experimental animals and in a limited number of human studies. We determined cerebrospinal fluid (CSF) and plasma lactate in 29 patients with generalized SE of diverse etiology. CSF was obtained within 12 h of termination of clinical seizure activity. The mean CSF lactate for all SE patients was elevated (3.74 +/- 0.31 mM) as compared with that of normal controls (1.60 +/- 0.10 mM) from non-neurologic patients undergoing spinal anesthesia. In patients who died or had a poor neurologic recovery, CSF lactate level was 5.36 +/- 0.58 mM (9 patients), whereas in 20 patients who showed good recovery CSF lactate level was 3.01 +/- 0.22 mM (p less than 0.005). The results demonstrate that SE causes a significant increase in CSF lactate and suggest that the magnitude of lactate elevation may serve as a predictive indicator of morbidity and mortality.
...
PMID:Cerebrospinal fluid lactate levels and prognosis in status epilepticus. 174 53
A review of 15 cases of pancreas transplantation at the Presbyterian University Hospital in Pittsburgh showed that all of the neurologic complications occurred outside of the pancreas transplantation surgery itself. Major CNS complications included hypoxic encephalopathy (20 per cent), cerebral and spinal-cord infarction (7 per cent), and seizures (13 per cent). These appeared to be closely associated with cardiovascular
collapse
or cardiac arrest that often occurred following septic, hemorrhagic, or additional surgical-anesthetic stresses, removed in time from the transplantation. When patients who died of sudden cardiorespiratory arrest were included, the overall frequency of global
cerebral ischemia
was 33 per cent. The occurrence of herpes zoster neuritis (13 per cent) was contrasted with the lack of CNS infections. The possible associations of visual hallucinations with cyclosporine therapy (7 per cent), CSF pleocytosis with OKT3 therapy (7 per cent), and compressive neuropathy with operative-anesthetic monitoring (7 per cent) were discussed in relation to previous reports in the literature. Randomized controlled clinical studies were suggested to distinguish more clearly the complications due to pancreas transplantation from those due to the natural history of the underlying diabetes and to distinguish the beneficial and adverse effects of pancreas transplants from those of coexisting renal transplants.
...
PMID:Neurologic complications of pancreas transplants. 304 46
The effect of transient
cerebral ischaemia
connected with acute orthostatic hypotension on plasma adrenaline and noradrenaline levels was studied in seven healthy male volunteers during tilt. Sublingual administration of 1 mg nitroglycerin was used to block peripheral vascular reflexes and thus to provoke orthostatic intolerance. A consistent increase in plasma adrenaline concentrations (from 19.2 to 104.3 pg/ml on average, P less than 0.01) was found in six subjects who developed clinical signs of
collapse
after tilting. Plasma adrenaline never changed after tilting without
collapse
. Posturally stimulated plasma noradrenaline increases were similar yet irrespective of the presence of
collapse
.
...
PMID:Venous plasma adrenaline response to orthostatic syncope during tilting in healthy men. 308 88
Cerebral ischaemia
, in which the brain-stem components of the ABP were isoelectric, was accompanied by the paradoxical persistence of the compound action potential of the auditory nerve (wave 1). This ischaemia was induced in cats by reducing mean arterial blood pressure and elevating intracranial pressure, resulting in decreased cerebral perfusion pressure (CPP). This is unexpected since the inner ear is supplied by a branch of an intracranial artery. To study this phenomenon, CPP was manipulated and when average CPP was 13.5 mm Hg, only wave 1 remained. In 7 of 9 experiments, clamping of both common carotid arteries did not abolish wave 1. Experiments with radioactive tracers demonstrated a remaining residual blood flow through the inner ear. This remaining auditory nerve response is probably not due to a very low metabolism of the inner ear or to the cochlea being supplied by anastomoses from the middle ear, supplied by the external carotid artery. The residual cochlear blood flow and the persistent wave 1 can probably be explained in the following way: at low CPPs the smaller intracranial blood vessels
collapse
so that the brain tissue is not perfused, leading to loss of the brain-stem components of the ABP. However, flow still persists in the larger intracranial arteries. This blood preferentially flows to the cochlea since the intracochlear pressure is slightly below the intracranial pressure due to the presence of the oval and round windows. Thus a sufficient blood flow to the cochlea is maintained, with sparing of wave 1.
...
PMID:Persistence of auditory nerve response and absence of brain-stem response in severe cerebral ischaemia. 620 4
Middle cerebral artery occlusion was performed in rats while the animals were inside the nuclear magnetic resonance (NMR) tomograph. Successful occlusion was confirmed by the
collapse
of amplitude on an electrocorticogram. The ultrafast NMR imaging technique UFLARE was used to measure the apparent diffusion coefficient (ADC) immediately after the induction of
cerebral ischemia
. ADC values of normal cortex and caudate-putamen were 726 +/- 22 x 10(-6) mm2/s and 659 +/- 17 x 10(-6) mm2/s, respectively. Within minutes of occlusion, a large territory with reduced ADC became visible in the ipsilateral hemisphere. Over the 2 h observation period, this area grew continuously. Quantitative analysis of the ADC reduction in this region showed a gradual ADC decrease from the periphery to the core, the lowest ADC value amounting to about 60% of control. Two hours after the onset of occlusion, the regional distribution of ATP and tissue pH were determined with bioluminescence and fluorescence techniques, respectively. There was a depletion of ATP in the core of the ischemic territory (32 +/- 20% of the hemisphere) and an area of tissue acidosis (57 +/- 19% of the hemisphere) spreading beyond that of ATP depletion. Regional CBF (rCBF) was measured autoradiographically with the iodo[14C]antipyrine method. CBF gradually decreased from the periphery to the ischemic core, where it declined to values as low as 5 ml 100 g-1. When reductions in CBF and in ADC were matched to the corresponding areas of energy breakdown and of tissue acidosis, the region of energy depletion corresponded to a threshold in rCBF of 18 +/- 14 ml 100 g-1 min-1 and to an ADC reduction to 77 +/- 3% of control. Tissue acidosis corresponded to a flow value below 31 +/- 11 ml 100 g-1 min-1 and to an ADC value below 90 +/- 4% of control. Thus, the quantification of ADC in the ischemic territory allows the distinction between a core region with total breakdown of energy metabolism and a corona with normal energy balance but severe tissue acidosis.
...
PMID:Evolution of regional changes in apparent diffusion coefficient during focal ischemia of rat brain: the relationship of quantitative diffusion NMR imaging to reduction in cerebral blood flow and metabolic disturbances. 759 32
One of the most prominent phenomena that occurs during the early phase of
cerebral ischemia
has been shown to be the immunohistochemical
collapse
of cytoskeletal proteins. Among these, microtubule-associated protein 2 (MAP 2) has been shown to be vulnerable to ischemic injuries. In order to select a suitable volatile anaesthetic from the standpoint of cytoskeletal protein breakdown during
cerebral ischemia
, we compared the effect of isoflurane, halothane and sevoflurane on MAP 2 degradation during 20 min of forebrain ischemia in the rat. Under 1 MAC of three volatile anesthetics, forebrain ischemia was induced by the occlusion of the bilateral common carotid artery combined with a lowering of mean arterial pressure to 50 mmHg. Immediately after
cerebral ischemia
, four regions of the brain, the frontoparietal cortex, brainstem, hippocampus and cerebellum, were removed separately and homogenized. Subsequently, MAP 2 from each region was quantitatively measured using an enzyme-linked immunosorbent assay. MAP 2 in the frontoparietal cortex and hippocampus was significantly protected from degradation with isoflurane anaesthesia more than with halothane and sevoflurane anaesthesia.
...
PMID:[Effects of volatile anesthetics on microtubule-associated protein 2 degradation during forebrain ischemia in the rat]. 783 96
One of the most prominent features of the early phase of
cerebral ischaemia
is the immunohistochemical
collapse
of cytoskeletal proteins. Among these proteins, microtubule-associated protein 2 (MtP2) has been shown to be vulnerable to ischaemic injuries. In order to identify a suitable volatile anaesthetic on the basis of cytoskeletal protein breakdown during
cerebral ischaemia
, we have compared the effects of isoflurane and halothane on MtP2 degradation in rats. Under equipotent isoflurane or halothane anaesthesia, forebrain ischaemia was induced by occlusion of the bilateral common carotid artery, combined with a decrease in mean arterial pressure to 50 mm Hg. After 20 min of ischaemia, the frontoparietal cortex, brainstem, hippocampus and cerebellum were removed separately and homogenized. MtP2 from each region was measured using an enzyme-linked immunosorbent assay. MtP2 degradation in the frontoparietal cortex and hippocampus was significantly (P < 0.05 and P < 0.01) less with isoflurane anaesthesia (75.6 (SD 10.7)% and 72.3 (12.8)%, respectively) than with halothane (65.0 (13.1)% and 54.7 (13.9)%, respectively).
...
PMID:Isoflurane reduces microtubule-associated protein 2 degradation compared with halothane during forebrain ischaemia in the rat. 812 1
Recently, attention has been focused on the degradation of cytoskeletal proteins in animal models of
cerebral ischemia
, as the
collapse
of cytoskeletal proteins may be closely related to cytoskeletal disintegration and ultimate neuronal cell death. Among these proteins, microtubule-associated protein 2 (MAP2) has been shown to be highly vulnerable to ischemic injuries. To determine the degree of anesthetic effect on the
collapse
of cytoskeletal proteins, we compared the effect of three inhalation anesthetics; isoflurane, halothane, and nitrous oxide (N2O), on MAP2 degradation during 20 min of forebrain ischemia in the rat. Under equipotent anesthesia, forebrain ischemia was induced by the occlusion of the bilateral common carotid artery (CCA) combined with a lowering of mean arterial pressure (mAP) to 50 mmHg. After 20 min of ischemia, three regions of the brain, the frontoparietal cortex, brainstem, and hippocampus, were removed and separately homogenized. Subsequently, MAP2 of each region was measured using an enzyme-linked immunosorbent assay (ELISA). In the frontoparietal cortex and hippocampus, MAP2 was significantly protected from degradation when isoflurane was used combined with nitrogen (N2). However, the protective effects of isoflurane were drastically reduced when N2O was given instead of N2. These results suggest that the use of N2O should be discontinued when severe
cerebral ischemia
is accidentally incurred during anesthetic management.
...
PMID:Nitrous oxide attenuates the protective effect of isoflurane on microtubule-associated protein2 degradation during forebrain ischemia in the rat. 932 46
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