Effect of hydration status on cerebral blood flow and cerebrospinal fluid lactic acidosis in rabbits with experimental meningitis.

Tureen, Jay H.; Täuber, Martin G.; Sande, Merle A.

doi:10.1172/jci115676

Cited by 53 publications

(37 citation statements)

References 28 publications

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“…Therefore, artificial increases in blood pressure lead to increases in cerebral blood flow, which in turn lead to increases in ICP in animals with meningitis. Fluid-restricted rabbits have further decreases in mean arterial pressures and cerebral blood flow, with the accumulation of CSF lactate after treatment with ceftriaxone, whereas these changes do not occur in euvolemic rabbits [67]. The implications for the policy of fluid restriction, which may be adhered to rigidly during the early phase of meningitis because of concerns about the syndrome of inappropriate secretion of an tidiuretic hormone, were not lost on the participants during the discussion period.…”

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitismentioning

confidence: 99%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

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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...

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Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitismentioning

confidence: 99%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

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“…Ischemia is associated with a marked release of EEA and other amino acids from injured neurons (7,26). We have previously shown that global cerebral blood flow is not markedly reduced in our model of meningitis, as long as animals do not develop hypotension (15,16), and, early in the disease, blood flow is actually increased (1 3). Shock and global cerebral hypoperfusion were therefore probably not responsible for the changes in amino acid concentrations in this study.…”

Section: Discussionmentioning

confidence: 77%

“…Blood samples for arterial lactate concentrations and for blood gases were sampled at 0, 16, and 22 h and CSF samples (0.2 mL) were obtained for amino acid concentrations, lactate concentrations, bacterial titers, and white blood cell counts at 0 and 22 h. Blood pressure was measured at 22 h before killing the animals. The 22-h time point was chosen as end point in this study because, in our model, meningitis is fully developed by 20 to 24 h with maximal CSF bacterial titers and leukocytosis, but animals are not yet agonal and do not have seizures (15,16). Fractions of microdialysate (sampled during 1-to 2-h intervals) were collected in polypropylene tubes for analysis throughout the experiment and are reported as baseline and peak values derived from the first and last two samples.…”

Section: Methodsmentioning

confidence: 99%

“…Cerebral blood flow studies in humans and experimental animals with bacterial meningitis suggest that, after an initial hyperemic phase (13), ischemia occurs under certain circumstances and may contribute to the development of neuronal injury (14)(15)(16). As with other forms of ischemia-induced CNS injury it is conceivable that the harmful effects of ischemia could be potentiated by EAA during meningitis.…”

Section: The Infectious Diseases Laboratories [Lg-r Jh T Mamentioning

confidence: 99%

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Amino Acids in Cerebrospinal and Brain Interstitial Fluid in Experimental Pneumococcal Meningitis

et al. 1993

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ABSTRACT. Excitatory amino acids are increasingly implicated in the pathogenesis of neuronal injury induced by a variety of CNS insults, such as ischemia, trauma, hypoglycemia, and epilepsy. Little is known about the role of amino acids in causing CNS injury in bacterial meningitis. Several amino acids were measured in cerebrospinal fluid and in microdialysis samples from the interstitial fluid of the frontal cortex in a rabbit model of pneumoccocal meningitis. Cerbrospinal fluid concentrations of glutamate, aspartate, glycine, taurine, and alanine increased significantly in infected animals. Among the amino acids with known excitatory or inhibitory function, interstitial fluid concentrations of glutamate were significantly elevated (by 470%).Alanine, a marker for anaerobic glycolysis, also increased in the cortex of infected rabbits. The elevated glutamate concentrations in the brain extracellular space suggest that excitotoxic neuronal injury may play a role in bacterial meningitis. (Pediatr Res 33: 510-513, 1993) Abbreviations CSF, cerebrospinal fluid EAA, excitatory amino acid cfu, colony-forming unit poorly understood. Cerebral blood flow studies in humans and experimental animals with bacterial meningitis suggest that, after an initial hyperemic phase (13), ischemia occurs under certain circumstances and may contribute to the development of neuronal injury (14-16). As with other forms of ischemia-induced CNS injury it is conceivable that the harmful effects of ischemia could be potentiated by EAA during meningitis.A few studies have examined concentrations of amino acids in CSF in bacterial meningitis. A first report in 1975 found increased levels of glutamic acid, glutamine, and y-aminobutyric acid in the CSF of patients with bacterial meningitis (1 7). Other authors have also reported abnormal CSF concentrations of amino acids, but the importance of these changes has not been explored in detail (18)(19)(20). Importantly, it is not known whether amino acid concentrations in the CSF reflect changes occurring in the brain interstitial fluid, the medium relevant for the potential neurotoxicity of EAA. To test the hypothesis that changes in amino acids may play a role in CNS injury during meningitis, we measured in the present study brain interstitial fluid concentrations of several amino acids in a rabbit model of pneumoccoca1 meningitis and determined whether changes similar to those observed in the CSF during meningitis occur in the brain. Interstitial fluid concentrations of amino acids were measured in the cortex because of its proximity to the inflammation in the subarachnoid space and because pathologic changes were primarily found in the cortex in a recent histopathologic study in rats with experimental pneumococcal meningitis (2 1).EAA, physiologic neurotransmitters in the mammalian CNS, are increasingly implicated in the pathogenesis of neuronal injury induced by a variety of CNS insults, such as global and focal ischemia, brain and spinal cord trauma, hypoglycemia, and epilepsy (1-7). There is good...

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“…This hypotension is frequently exacerbated by hypovolaemia and dehydration, resulting in a decrease in CPP 62 . In addition, exposure to endotoxin can cause significant impairment of cerebral autoregulation leading to a profound reduction in CBF, particularly in the presence of inappropriate CPP 63 .…”

Section: Potential Role For Near-infrared Spectroscopy In Equine Genementioning

confidence: 99%

Use of near‐infrared spectroscopy to identify trends in regional cerebral oxygen saturation in horses

McConnell

Rioja

Bester

et al. 2012

Equine Veterinary Journal

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Summary Reasons for performing study Alterations in cerebral haemodynamics may contribute to perianaesthetic complications in horses. Near‐infrared spectroscopy (NIRS) is frequently used intraoperatively in man to provide information regarding cerebral perfusion. Objectives To determine whether NIRS can identify trends in regional cerebral oxygen saturation (rSO2) in horses and whether there is a correlation between rSO2 and venous oxygen tensions. Methods A cerebral oximeter sensor recorded rSO2 from the dorsal sagittal sinus of 6 healthy horses. Values for rSO2, arterial and venous oxygen and carbon dioxide tensions (PaO2, PvO2, PaCO2 and PvCO2 respectively), along with arteriovenous oxygen saturations (SavO2) were recorded in unsedated (recording period [RP] 1), sedated (RP2) and anaesthetised horses (RP3–5) and during recovery (RP6–8). During anaesthesia, horses were ventilated to achieve states of normo‐ (RP3), hyper‐ (RP4) and hypocapnoea (RP5). Data were evaluated descriptively and analysed using linear mixed‐effects models and Pearson's correlation coefficient. Results Overall mean ± s.d. values for rSO2, PaO2, PvO2, PaCO2, SavO2 and mean arterial pressure varied significantly by RP (P<0.001). Significant decreases in rSO2 were identified between RP1 and the post anaesthetic periods (P<0.001). No significant differences in rSO2 values were identified between RP1 and the intra‐anaesthesia periods or between RP3, RP4 and RP5. Significant correlations were identified between rSO2 and PaO2 (r = 0.448, P<0.001), rSO2 and PvO2 (r = 0.512, P<0.001) and rSO2 and SavO2 (r = 0.469, P<0.001). Conclusions This is the first study to identify trends in rSO2 in horses using NIRS. A positive correlation was identified between rSO2 and PvO2, suggesting that alterations in cerebral oxygenation may be reflected in PvO2. Potential relevance Near‐infrared spectroscopy may be used to monitor trends in rSO2 during equine anaesthesia. Decreasing rSO2 values may act as an early warning signal, alerting clinicians to potential cerebral desaturation events and indicating a need for intervention.

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Effect of hydration status on cerebral blood flow and cerebrospinal fluid lactic acidosis in rabbits with experimental meningitis.

Cited by 53 publications

References 28 publications

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Amino Acids in Cerebrospinal and Brain Interstitial Fluid in Experimental Pneumococcal Meningitis

Use of near‐infrared spectroscopy to identify trends in regional cerebral oxygen saturation in horses

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