Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study tested the protective activity of antibodies to the LPS core of Haemophilus influenzae (Borrelli et al., Infect. Immun. 1995;63: 3683-92) in a hematogenous meningitis model. Meningitis was established by intraperitoneal inoculation of infant rats with H. influenzae type b (Hib). The severity of infection was determined by daily assessment of mortality, symptoms of disease and weight changes. Mortality occurred rapidly after infection with 10(5)cfu/rat and most animals died within 24 h. At a lower infection dose (10(4)cfu/rat) the rats survived, but developed symptoms of disease such as tremor, hypothermia, lethargy and anorexia within 12-72 h post challenge. Surviving animals showed decreased weight gain. Bacteremia was detected by daily blood-cultures in 10/10 rats and cleared 6 days after inoculation. The monoclonal anti-LPS antibody MAHI 3 was used in passive protection studies. MAHI 3 increased the survival in the high inoculum group (10(5)cfu/rat) from 10-17% in control animals to 60-90%. At the lower inoculum concentration (10(4)cfu/rat) MAHI 3 treatment reduced the symptoms and blood counts. Intraperitoneal injection of MAHI 3 was more effective than intranasal injection as shown by the effect on bacteremia. We conclude that anti-LPS antibodies can protect against mortality caused by hematogenous Hib infections in infant rats.
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PMID:Monoclonal anti-LPS inner core antibodies protect against experimental hematogenous Haemophilus influenzae type b meningitis. 1062 58

Pneumococcal meningitis resulting from Streptococcus pneumoniae has a death rate of 28% in adults. In severe head injury and stroke, inflammatory changes and intracranial hypertension are improved by induced hypothermia, which also is neuroprotective. We hypothesized that moderate hypothermia ameliorates inflammatory changes in experimental pneumococcal meningitis. Wistar rats were cooled systemically, and meningitis was induced by pneumococcal cell wall components. The increase of regional cerebral blood flow in the meningitis animals was blocked by hypothermia at 6 hours. The reduction of intracranial pressure correlated with temperature. The influx of leukocytes into the cerebrospinal fluid and levels of tumor necrosis factor alpha in the cerebrospinal fluid were decreased. Cooling the animals 2 hours after meningitis induction to 30.5 degrees C was also protective. We conclude that hypothermia is a new adjuvant approach to reduce meningitis-induced changes, in particular intracranial pressure, in the early phase of the disease.
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PMID:Induced hypothermia in experimental pneumococcal meningitis. 1082 34

Brain injury due to bacterial meningitis results in a high mortality rate and significant neurologic sequelae in survivors. The objective of this study was to determine if the application of moderate hypothermia shortly after the administration of antibiotics would attenuate the inflammatory response and increase in intracranial pressure that occurs in meningitis. For this study we used a rabbit model of severe Group B streptococcal meningitis. The first component of this study evaluated the effects of hypothermia on blood-brain barrier function and markers of inflammation in meningitic animals. The second part of the study evaluated the effects of hypothermia on intracranial pressure, cerebral perfusion pressure and brain edema. This study demonstrates that the use of hypothermia preserves CSF/serum glucose ratio, decreases CSF protein and nitric oxide and attenuates myeloperoxidase activity in brain tissue. In the second part of this study we show a decrease in intracranial pressure, an improvement in cerebral perfusion pressure and a decrease in cerebral edema in hypothermic meningitic animals. We conclude that in the treatment of severe bacterial meningitis, the application of moderate hypothermia initiated shortly after antibiotic therapy improves short-term physiologic measures associated with brain injury.
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PMID:Hypothermia as an adjunctive treatment for severe bacterial meningitis. 1103 98

Therapeutic hypothermia may improve outcome after severe head injury, but its efficacy has not been established in children with a severe head injury. The authors evaluated the effects of hypothemia (33-34 degrees C) in 9 severely closed head-injured children (under 16 years old). The cooling period was 3 to 21 days (mean 9.3). Hypothermia significantly reduced ICP when it reached 33-34 degrees C. From 3 to 6 months after injury, 6 (67%) of the 9 patients had good outcome (good recovery in 2 and moderate disability in 4), but 3 (33%) had poor outcome (severe disability in 2 and vegetative state in one). Complications, including infectious disorders (pneumonia, meningitis, sepsis), cardio-vascular system dysfunction (cardiac arrhythmia, hypotension), decreased platelet counts, hypokalemia, diabetes insipidus, acute pancreatitis occurred during hypothermia in 7 patients (78%). The results of this study suggest that treatment with hypothermia in children with severe head injury is often accompanied complications, but it is an effective method to control intracranial hypertension and may have improved the outcome.
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PMID:[Clinical analysis of hypothermia in children with severe head injury]. 1112 94

Brain injury in meningitis occurs in part as a consequence of leukocyte migration and activation. Leukocyte integrins are pivotal in the inflammatory response by mediating adhesion to vascular endothelium and extracellular matrix proteins. We have demonstrated that moderate hypothermia early in the course of meningitis decreases leukocyte sequestration within the brain parenchyma. This study examines whether hypothermia alters neutrophil integrin expression in a rabbit model of bacterial meningitis. Prior to the induction of meningitis, peripheral blood samples were obtained and the neutrophils isolated. Sixteen hours after inducing group B streptococcal meningitis, animals were treated with antibiotics, i.v. fluids, and mechanically ventilated. Animals were randomized to hypothermia (32-33 degrees C) or normothermia conditions. After 10 hours of hypothermia or normothermia, neutrophils were isolated from the blood and cerebral spinal fluid (CSF), stained for beta1 and beta2 integrins, and analyzed using flow cytometry. Cerebral spinal fluid neutrophil beta1 integrin expression was significantly decreased in hypothermic animals. Beta-1 integrins can assume a higher affinity or "activated" state following inflammatory stimulation. Expression of "activated" beta1 integrins was also significantly decreased in hypothermic animals. Beta2 CSF neutrophil integrin expression was decreased in hypothermic animals, but failed to reach significance. These data suggest hypothermia may attenuate extravasated leukocyte expression of both total and "activated" beta1 integrins.
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PMID:Hypothermia attenuates beta1 integrin expression on extravasated neutrophils in an animal model of meningitis. 1140 4

We evaluated the anti-inflammatory and neuroprotective effects of hypothermia during the early phase of experimental Escherichia coli meningitis in the newborn piglet. Hypothermia significantly attenuated the meningitis-induced acute inflammatory responses such as increased intracranial pressure, decreased glucose level, increased lactate concentration, increased tumor necrosis factor-alpha level and leukocytosis in the cerebrospinal fluid. Decreased cerebral cortical cell membrane Na+,K+-ATPase activity and increased lipid peroxidation products, indicative of meningitis-induced brain damage, were significantly improved with hypothermia. Hypothermia also significantly improved the meningitis-induced reduction in brain ATP and phosphocreatine levels. In summary, hypothermia significantly attenuated the acute inflammatory responses and the ensuing brain injury in experimental neonatal bacterial meningitis.
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PMID:Effect of hypothermia on brain cell membrane function and energy metabolism in experimental Escherichia coli meningitis in the newborn piglet. 1149 47

Nitric oxide (NO) plays a central role in the pathogenesis of bacterial meningitis. However, the role of NO produced by endothelial NO synthase (eNOS) in meningitis is still unclear. We investigated the influence of eNOS depletion on the inflammatory host response, intracranial complications, and outcome in experimental pneumococcal meningitis. Leukocyte accumulation in the cerebrospinal fluid was more pronounced in infected eNOS-deficient mice than in infected wild type mice. This effect could be attributed to an increased expression of P-selectin, macrophage inflammatory protein-2, keratinocyte-derived cytokine, and interleukin (IL)-1beta in the brain of infected eNOS-deficient mice. However, no differences in the cerebral expression of intercellular adhesion molecule-1, tumor necrosis factor-alpha, and IL-6 as well as of neuronal NOS and inducible NOS could be detected between infected wild type and mutant mice. In addition to enhanced leukocyte infiltration into the CSF, meningitis-associated intracranial complications including blood-brain barrier disruption and the rise in intracranial pressure were significantly augmented in infected eNOS-deficient mice. The aggravation of intracranial complications was paralleled by a worsening of the disease, as evidenced by a more pronounced hypothermia, an enhanced weight reduction, and an increased death rate. The current data indicate that eNOS deficiency is detrimental in bacterial meningitis. This effect seems to be related to an increased expression of (certain) cytokines/chemokines and adhesion molecules; thus leading to increased meningeal inflammation and, subsequently, to aggravated intracranial complications.
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PMID:Lack of endothelial nitric oxide synthase aggravates murine pneumococcal meningitis. 1170 34

187 babies born elsewhere and referred to the Pediatric Department of the Christian Medical College and Hospital, Ludhiana, for management of prematurity over a period of 6 years were studied. Babies with hypothermia and those below 1200 g were given iv fluids. Preterm babies delivered in the institution and managed in the neonatal special care nursery over 1 year were also studied for comparison. The preterm babies were evenly distributed in the different gestation age groups between 28 and 36 weeks. About half the babies were appropriate for gestational age, while 47% were small for gestational age. The weight ranged from 760 to 2260 g. Males (166) outnumbered females (21) by a ratio of 8:1. There was a high incidence of hypothermia (54%) at the time of admission, more so in babies with gross prematurity. In babies less than 30 weeks old, 80% had become hypothermic during transit to the hospital. A fatal outcome was seen in 69% of babies with hypothermia as compared to 38% of babies admitted without hypothermia. 85% of babies were born in circumstances of potential infection in the form of prolonged rupture of membranes, multiple unsterile vaginal examinations, foul smelling liquor, fever of the mother, or a combination of these. Septicemia, purulent meningitis, bronchopneumonia, and diarrhea were the common infections. Other common morbidities were hyaline membrane disease, necrotizing enterocolitis, and metabolic disturbances. The overall mortality was 54% and it was inversely proportional to the gestational age, increasing from 36% at 35-36 weeks to 82% at 28-30 weeks. On the other hand, there was only a 21% mortality rate among preterm babies delivered at the hospital and managed in the neonatal nursery. Mortality was 9% in babies at 35-36 weeks. Intracranial hemorrhage was the most common cause of death in the study group, accounting for 42% of total deaths (59% of deaths at 28-30 weeks gestation, decreasing to only 4% at 35-36 weeks), followed by septicemia in 31%. On the other hand, septicemia caused about one-third of deaths at 35-36 weeks.
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PMID:Outcome of hospitalised out-born preterm babies. 1228 86

Pneumolysin, the pore-forming toxin produced by Streptococcus pneumoniae, may have an application as an immunogenic carrier protein in future pneumococcal conjugate vaccines. Most of the 90 S. pneumoniae serotypes identified produce pneumolysin; therefore, this protein may confer non-serotype-specific protection against pneumococcal infections such as pneumonia, meningitis, and otitis media. However, as pneumolysin is highly toxic, a nontoxic form of pneumolysin would be a more desirable starting point in terms of vaccine production. Previous pneumolysin mutants have reduced activity but retain residual toxicity. We have found a single amino acid deletion that blocks pore formation, resulting in a form of pneumolysin that is unable to form large oligomeric ring structures. This mutant is nontoxic at concentrations greater than 1,000 times that of the native toxin. We have demonstrated that this mutant is as immunogenic as native pneumolysin without the associated effects such as production of the inflammatory mediators interleukin-6 and cytokine-induced neutrophil chemoattractant KC, damage to lung integrity, and hypothermia in mice. Vaccination with this mutant protects mice from challenge with S. pneumoniae. Incorporation of this mutant pneumolysin into current pneumococcal vaccines may increase their efficacy.
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PMID:Construction and immunological characterization of a novel nontoxic protective pneumolysin mutant for use in future pneumococcal vaccines. 1636 15

Statins exert multiple effects besides lowering the serum cholesterol level, which might be beneficial for patients with sepsis and infections. We designed this study to assess the therapeutic potential of simvastatin in an established animal model of pneumococcal meningitis, a disease characterized by high morbidity and mortality despite effective antibiotic treatment. 24 h after injection of live pneumococci into the cisterna magna of mice, animals were clinically evaluated, cerebrospinal fluid (CSF) leukocyte counts and intracranial pressure were determined, and brains were removed for assessment of bacterial titer and blood-brain barrier breakdown. The following experimental groups were investigated: (I) no infection and treatment with vehicle; (II) infection and treatment with vehicle; infection and treatment with (III) 20 mg/kg or (IV) 40 mg/kg simvastatin s.c. 18 h before and just prior to infection. Treatment with simvastatin dose-dependently decreased CSF leukocyte counts, a marker for CNS inflammation. In addition, hypothermia was completely abolished in the 40 mg/kg simvastatin group. In contrast, a neurological clinical score, and intracranial complications like increase in intracranial pressure and blood-brain barrier breakdown were not altered by the treatment. In conclusion, simvastatin attenuates CNS leukocyte recruitment and systemic complications of experimental pneumococcal meningitis.
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PMID:Simvastatin attenuates leukocyte recruitment in experimental bacterial meningitis. 1913 Sep 4


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