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

The effects of hydration status on cerebral blood flow (CBF) and development of cerebrospinal fluid (CSF) lactic acidosis were evaluated in rabbits with experimental pneumococcal meningitis. As loss of cerebrovascular autoregulation has been previously demonstrated in this model, we reasoned that compromise of intravascular volume might severely affect cerebral perfusion. Furthermore, as acute exacerbation of the inflammatory response in the subarachnoid space has been observed after antibiotic therapy, animals were studied not only while meningitis evolved, but also 4-6 h after treatment with antibiotics to determine whether there would also be an effect on CBF. To produce different levels of hydration, animals were given either 50 ml/kg per 24 h of normal saline ("low fluid") or 150 ml/kg 24 h ("high fluid"). After 16 h of infection, rabbits that were given the lower fluid regimen had lower mean arterial blood pressure (MABP), lower CBF, and higher CSF lactate compared with animals that received the higher fluid regimen. In the first 4-6 h after antibiotic administration, low fluid rabbits had a significant decrease in MABP and CBF compared with, and a significantly greater increase in CSF lactate concentration than, high fluid rabbits. This study suggests that intravascular volume status may be a critical variable in determining CBF and therefore the degree of cerebral ischemia in meningitis.
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PMID:Effect of hydration status on cerebral blood flow and cerebrospinal fluid lactic acidosis in rabbits with experimental meningitis. 154 82

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.
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PMID:Intracranial pressure and cerebral perfusion pressure in experimental streptococcus pneumoniae meningitis. 157 Apr 13

Meningeal penetration of bacteria induces an inflammatory response which affects mainly the endothelium of cerebral vessels. This inflammatory reaction is directly responsible for thrombosis and indirectly creates cerebral oedema and reduced cerebral blood flow. Cerebral ischemia is the result of all these phenomenons. Nowadays, control of cerebral oedema is the main goal of intensive care treatment of meningitis that needs invasive monitoring of intracranial pressure. We may hope that in a next future new therapeutic agents will be able to control inflammatory reaction and vascular process.
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PMID:[Resuscitation of severe meningitis in infants and children]. 318 20

The concentration of cyclic adenosine 3',5'-monophosphate (cAMP) in cerebrospinal fluid was measured in 45 samples from 45 subjects, one sample per subject. 12 of the studied persons were (control group) neurologically normal, 11 were suffering from acute cerebral ischemia with deep coma, and 22 from meningitis of different types. The mean value obtained in the control group was 21.4 +/- (SEM) 3.3 nmol/l, in the group of acute cerebral ischemic attack with deep coma it was 7.00 +/- 0.81 nmol/l and in the group of meningitis 5.5 +/- 0.4 nmol/l. These values are significantly lower than the control group (p less than 0.001). These low levels, observed in the two groups of patients, may be attributed to the altered cAMP metabolism in the central nervous system because of deep coma and bacterial infections.
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PMID:Cerebrospinal fluid cyclic adenosine 3',5'-monophosphate in cases of severe cerebral ischemia and meningitis. 630 42

An association between hyperglycemia and mortality from cerebral ischemia has been reported in both animals and man. Recently, a similar observation has been made in animals with bacterial meningitis. The present study of 83 patients with bacterial meningitis showed no association between initial serum glucose concentration and subsequent mortality. Therefore, no therapeutic recommendations regarding optimal blood glucose levels in patients with meningitis can be made at this time.
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PMID:Hyperglycemia is not associated with mortality in bacterial meningitis. 661 75

Central nervous system infections may be complicated by development of severe brain edema, which can be a significant factor in mortality and morbidity. Increased intracranial pressure can cause additional damage to the central nervous system by impairment of cerebral blood flow, which is dependent on cerebral perfusion pressure. A reduction of cerebral perfusion pressure, caused by elevation of intracranial pressure, may cause cerebral ischemia. We studied cerebral perfusion pressure in 17 patients, ages 45 days to 11 years, with severe central nervous system infections and who were in deep coma. Meningitis was diagnosed in 64.7%, and encephalitis in 29.4%. The patients who survived (64.7%) did not differ significantly from those who died (36.5%) in severity of disease and maximal intracranial pressure during the course of the illness. A striking difference in minimal cerebral perfusion pressure recorded was found between survivors and nonsurvivors: all patients with minimal cerebral perfusion pressure greater than 30 mm Hg survived, whereas those with lower pressure died. In survivors, cerebral perfusion pressure could be maintained adequately by reduction of intracranial pressure, but nonsurvivors developed noncompliance of brain tissue, and cerebral perfusion pressure could not be maintained at levels that ensure adequate cerebral blood flow, resulting in cerebral ischemia and death. Continuous monitoring of mean arterial blood pressure and intracranial pressure in children with severe central nervous system infections will enable rapid diagnosis and initiation of treatment when cerebral perfusion pressure is reduced to critical levels. Such treatment might improve the prognosis.
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PMID:Cerebral perfusion pressure in central nervous system infections of infancy and childhood. 686 94

We present an analysis of the neurologic manifestations of Staphylococcus aureus infections in 43 patients. Half of the infections whose source could be identified were nosocomial. The spectrum of neurological sequelae included meningitis, solitary and multiple intracerebral and epidural abscesses, cerebral ischemia and hemorrhage, acute encephalopathies, subdural empyemas, spinal abscesses, and radicular compression syndromes. In the majority of patients the course was severe and protracted and relapses were frequent. Mortality was high (28%), even with early diagnosis and treatment; diabetes mellitus, alcohol abuse, and chronic renal failure were unfavorable prognostic factors. In patients with abscess formation early surgical drainage improved the outcome. However, often treatment was complicated by sequestration at inaccessible foci and secondary dissemination. Combined antibiotic therapy with flucloxacillin and chloramphenicol may be the most successful antibiotic regimen.
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PMID:Neurologic manifestations of Staphylococcus aureus infections. Analysis of 43 patients. 752 54

Excessive extracellular fluid concentrations of the amino acids glutamate and aspartate play an important role in the pathogenesis of neuronal cell damage during hypoxia, hypoglycemia, and seizure. The purpose of these investigations was to test the hypothesis that bacterial meningitis causes progressive increase in excessive extracellular fluid concentrations of excitatory and inhibitory neurotransmitters. To test this hypothesis, Escherichia coli was injected intracisternally in juvenile rabbits after which neurotransmitter concentrations were measured with in vivo microdialysis. The data showed significant elevation of the excitatory amino acids aspartate and glutamate, as well as of the inhibitory neurotransmitters gamma-amino butyric acid and taurine in the excessive extracellular fluid of animals injected with E. coli compared with control animals injected with saline. However, concentrations of these excitatory and inhibitory amino acids rose late in the course of meningitis, at a time when the animals were hypotensive (mean blood pressure < or = 40 mm Hg). These data show that the major increase in excitatory neurotransmitters during experimental meningitis occurs in association with the cerebral ischemia produced by septic shock rather than being produced by the meningitis itself.
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PMID:Effect of experimental Escherichia coli meningitis on concentrations of excitatory and inhibitory amino acids in the rabbit brain: in vivo microdialysis study. 790 33

Neutrophils (PMN) accumulate and are associated with cerebrovascular disturbances after experimental traumatic or ischemic brain injury, and meningitis. We hypothesized that posttraumatic PMN accumulation in brain is mediated by the PMN adhesion receptor Mac-1 (CD11b/CD18). Anesthetized rats were randomized to receive 2 mg/kg intravenously of murine monoclonal antibody to rat Mac-1 (1-B6) or anti-Mac-1 F(ab)2' [1-B6F(ab)2'] fragment (Repligen Corp., Cambridge, MA). Control rats were treated with isotype matched control antibody. Rats were subjected to percussive trauma to the right parietal cortex 30 min after treatment. Rats were killed 24 h posttrauma, and PMN accumulation was assessed by myeloperoxidase (MPO) activity. The presence of 1-B6F(ab)2' bound to PMN in brain after trauma was assessed by immunohistochemistry. Complete blood cell counts were obtained before treatment and 24 h after trauma. Brain MPO activity was reduced by 43% in the 1-B6-treated rats vs. controls (0.31 +/- 0.09 vs 0.55 +/- 0.10 U/g, n = 6/group, p = 0.013) and by 34% in the 1-B6F(ab)2'-treated rats vs. controls (0.43 +/- 0.10 vs. 0.65 +/- 0.09 U/g, n = 6/group, p = 0.006). Systemic neutropenia developed in the 1-B6-treated rats (absolute PMN count decreased by 73% vs. baseline) but not in rats treated with 1-B6F(ab)2' (absolute PMN count increased by 26 and 25% vs. baseline in treated and controls, respectively). Immunohistochemical staining showed 1-B6F(ab)2' on the surface of infiltrated PMN 24 h after trauma. Mac-1 mediates posttraumatic PMN accumulation in brain. This accumulation can be attenuated by 34%, without reducing circulating PMN, using an anti-Mac-1 F(ab)2' fragment; however, some PMN coated with 1-B6F(ab)2' still infiltrate into traumatized tissue. These results are similar to those reported in models of cerebral ischemia, and suggest the participation of multiple PMN adhesion pathways after ischemic and traumatic brain injury.
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PMID:Antibodies against Mac-1 attenuate neutrophil accumulation after traumatic brain injury in rats. 883 1

Reactive oxygen intermediates (ROI) contribute to neuronal injury in cerebral ischemia and trauma. In this study we explored the role of ROI in bacterial meningitis. Meningitis caused by group B streptococci in infant rats led to two distinct forms of neuronal injury, areas of necrosis in the cortex and neuronal loss in the dentate gyrus of the hippocampus, the latter showing evidence for apoptosis. Staining of brain sections with diaminobenzidine after perfusion with manganese buffer and measurement of lipid peroxidation products in brain homogenates both provided evidence that meningitis led to the generation of ROI. Treatment with the radical scavenger alpha-phenyl-tert-butyl nitrone (PBN) (100 mg/kg q8h i.p.) beginning at the time of infection completely abolished ROI detection and the increase in lipidperoxidation. Cerebral cortical perfusion was reduced in animals with meningitis to 37.5+/-21.0% of uninfected controls (P < 0.05), and PBN restored cortical perfusion to 72.0+/-8.1% of controls (P < 0.05 vs meningitis). PBN also completely prevented neuronal injury in the cortex and hippocampus, when started at the time of infection (P < 0.02), and significantly reduced both forms of injury, when started 18 h after infection together with antibiotics (P < 0.004 for cortex and P < 0.001 for hippocampus). These data indicate that the generation of ROI is a major contributor to cerebral ischemia and necrotic and apoptotic neuronal injury in this model of neonatal meningitis.
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PMID:Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci. 895 28


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