Loss of cerebrovascular autoregulation in experimental meningitis in rabbits.

Tureen, Jay H.; Dworkin, Ronald J.; Kennedy, Stephen L.; Sachdeva, Meena; Sande, Merle A.

doi:10.1172/jci114475

Cited by 114 publications

(46 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast to results obtained with previous models [66], the rate of cerebral blood flow measured in these rabbits with the microsphere technique was increased 18 hours after intracerebral Hib challenge. Pretreatment of the animals with monoclonal antibody (IB 4 , 1.5 mg/kg) decreased CSF pleocytosis (consistent with previous observations [32]) but was associated with an increase in bacterial concentrations in the CSF.…”

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitiscontrasting

confidence: 99%

“…Hippocampal blood flow in the same animal is reduced to --50% of control values. Whereas autoregulation of cerebral blood flow is maintained in normal animals, this ability is generally lost during experimental pneumococcal meningitis [66]. ICP remains stable despite marked alterations in cerebral blood flow in normal animals but rises progressively with changes in cerebral blood flow in animals infected with pneumococci.…”

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitismentioning

confidence: 98%

See 1 more Smart Citation

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

View full text Add to dashboard Cite

Morbidity and mortality associated with bacterial meningitis remain high, although antibiotic therapy has improved during recent decades. The major intracranial complications of bacterial meningitis are cerebrovascular arterial and venous involvement, brain edema, and hydrocephalus with a subsequent increase of intracranial pressure. Experiments in animal models and cell culture systems have focused on the pathogenesis and pathophysiology of bacterial meningitis in an attempt to identify the bacterial and/or host factors responsible for brain injury during the course of infection. An international workshop entitled "Bacterial Meningitis: Mechanisms of Brain Injury" was organized by the Department of Neurology at the University of Munich and was held in Eibsee, Germany, in June 1993. This conference provided a forum for the exchange of current information on bacterial meningitis, including data on the clinical spectrum of complications, the associated morphological alterations, the role of soluble inflammatory mediators (in particular cytokines) and of leukocyte-endothelial cell interactions in tissue injury, and the molecular mechanisms of neuronal injury, with potential mediators such as reactive oxygen species, reactive nitrogen species, and excitatory amino acids. It is hoped that a better understanding of the pathophysiological events that take place during bacterial meningitis will lead to the development of new therapeutic regimens.Although the recent licensure of Haeniophilus influenzae type b (Hib) polysaccharide conjugate protein vaccines has had a marked impact on the incidence of invasive Hib disease in the United States and Western Europe. bacterial meningitis overall remains a significant problem worldwide. In addition, despite the introduction of new antimicrobial agents and improved diagnostic techniques, the mortality and morbidity associated with bacterial meningitis remain unacceptably high. This discrepancy between a rapid bacteriologic response at the site of infection (i.e .. eradication of viable bacteria from the CSF due to treatment with potent bactericidal agents) and the persistence of the associated neurological sequelae and mortality has prompted intense investigation over the past two decades into the pathophysiology of this disease. Indeed. recent clinical studies have employed adjunctive agents (e.g .. dexamethasone) in an attempt to reduce mortality and alleviate neurological sequelae [1][2][3][4]. These studies and the resulting recommendations regarding the use of adjunctive dexamethasone have recently been reviewed [5.6].In line with the current emphasis on the pathogenesis and pathophysiology of bacterial meningitis. two workshops were held in California in the 1980s [7]. Recognizing that many advances have been made in this field in the several years since those meetings. the Department of Neurology at the University of Munich organized a similar workshop, which was held in Eibsce. Germanv. on 25 and 26 June 1993. As IS evident from its title-"Bacterial Meningitis: Mechanisms...

show abstract

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitiscontrasting

confidence: 99%

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitismentioning

confidence: 98%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

View full text Add to dashboard Cite

show abstract

“…In bacterial meningitis, inflammation in subarachnoid space surrounds blood vessels, and the resulting vasculitis causes temporary vasospasm (31)(32)(33). Brain edema, increased ICP, systemic hypotension, and impaired cerebral blood flow autoregulation can lead to a decrease in cerebral blood flow (34). These changes result in local ischemic damage with subsequent glutamate release and development of excitotoxic injury like hypoxic ischemic encephalopathy.…”

Section: Discussionmentioning

confidence: 99%

Effects of MK-801 (dizocilpine) on Brain Cell Membrane Function and Energy Metabolism in Experimental Escherichia coli Meningitis in the Newborn Piglet

Shim

Kim

et al. 2003

J Korean Med Sci

View full text Add to dashboard Cite

We evaluated the efficacy of non-competitive N-methyl-D-aspartate receptor antagonist MK-801 (dizocilpine) as an adjuvant therapy in experimental neonal bacterial meningitis. Meningitis was induced by injecting 10(6) colony forming units of Escherichia coli into the cisterna magna. MK-801 3 mg/kg was given as a bolus intravenous injection, 30 min before the induction of meningitis. MK-801 did not down-modulate the inflammatory parameters, such as increased intracranial pressure, cerebrospinal fluid (CSF) leukocytosis, increased lactate and TNF-alpha levels in the CSF, and hypoglycorrhachia observed in the meningitis group. MK-801 did not significantly attenuate the elevated glutamate concentration in the CSF. However, MK-801 showed some neuroprotective effects as evidenced by significant attenuation of cerebral lipid peroxidation products (conjugated dienes) and increase of brain high-energy phosphate compounds (ATP and PCr). Improvement in cerebral cortical cell membrane Na+, K+ -ATPase activity did not reach a statistical significance. These results suggest that MK-801 was effective in ameliorating brain injury in neonatal bacterial meningitis, although it failed to attenuate the inflammatory responses.

show abstract

“…alterations in CBF. Studies of human infants and monkeys and rabbits show reductions in CBF or cerebral blood velocity during bacterial meningitis ( 19). Cerebral perfusion may be impaired during bacterial meningitis as a consequence of vasculitis.…”

mentioning

confidence: 99%

“…Cerebral perfusion may be impaired during bacterial meningitis as a consequence of vasculitis. impaired autoregulation ( 19). or hypotension.…”

mentioning

confidence: 99%