Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of methylprednisolone on pathophysiological alterations in experimental pneumococcal meningitis. Untreated rats injected with pneumococcal cell wall components after hydrolization with M1 muramidase (PCW-M) developed an increase of regional cerebral blood flow (rCBF; 165.0 +/- 12.8%, baseline 100%, mean +/- S.E.M.), brain water content (79.23 +/- 0.10%), intracranial pressure (ICP; 11.9 +/- 1.0 mmHg) and white blood cell (WBC) count in the cerebrospinal fluid (CSF) (2,709 +/- 482 cells/microliters) within 8 h after intracisternal (i.c.) challenge. Pretreatment with methylprednisolone or administration of methylprednisolone 4 h after i.c. challenge significantly attenuated the increase of brain water content (78.88 +/- 0.08% and 78.82 +/- 0.05%, resp.), ICP (7.7 +/- 1.1 mmHg and 4.9 +/- 0.8 mmHg, resp.) and CSF WBC count (1,257 +/- 168 cells/microliters and 976 +/- 105 cells/microliters, resp.). However, methylprednisolone did not inhibit the increase of rCBF (163.5 +/- 13.7% and 160.9 +/- 6.8%, resp.), whereas dexamethasone significantly attenuated microvascular changes. Hypercapnia-induced reactivity of cerebral vessels tested 8 h after i.c. injection was preserved in all groups. In conclusion, we found that methylprednisolone significantly attenuated the increase of brain water content, ICP and CSF WBC count, but had no effect on microvascular changes during the early phase of experimental pneumococcal meningitis.
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PMID:Methylprednisolone attenuates inflammation, increase of brain water content and intracranial pressure, but does not influence cerebral blood flow changes in experimental pneumococcal meningitis. 803 46

The effect of experimental meningitis on regional cerebral blood flow (rCBF), cerebral metabolic rate for oxygen (CMRO2), and cerebrovascular responsiveness to CO2 was determined in pentobarbital-anesthetized rabbits. The animals were inoculated intracisternally with saline (control) or log-phase Haemophilus influenzae type b (Hib). Eighteen hours later rCBF was determined with radiolabeled microspheres at normocapnia, hypocapnia, and hypercapnia. Cerebrovascular responses to hypocapnia and hypercapnia were assessed by calculating the change in cerebrovascular resistance per millimeter mercury change in PaCO2. At all CO2 levels, meningitis (M) was associated with elevated CBF compared with control (C: 47.5 +/- 3.0, M: 60.9 +/- 4.5 ml.100 g-1.min-1 at normocapnia, P < 0.01). Regional differences were present. In forebrain, the hyperemia in meningitis was confined to the superficial cortical grey matter. When compared with control, meningitis was not associated with altered vasoreactivity during hypocapnia (C: -0.026 +/- 0.006, M: -0.026 +/- 0.008 mmHg.ml-1 x 100 g-1.min-1.mmHg PaCO2(-1)) or hypercapnia (C: -0.037 +/- 0.004, M: -0.026 +/- 0.008 mmHg.ml-1 x 100 g.min.mmHg PaCO2(-1)). CMRO2 in meningitis was not significantly different from control (C: 3.53 +/- 0.29, M: 3.51 +/- 0.22 ml O2.100 g-1.min-1). These findings indicate that cerebrovascular responsiveness to CO2 is preserved in experimental Hib meningitis. Furthermore, enhanced CBF together with unchanged CMRO2 indicates that "luxury" cerebral perfusion is present in this model of bacterial meningitis.
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PMID:Cerebrovascular responsiveness to CO2 in Haemophilus influenzae type b meningitis in rabbits. 820 76

We describe a patient with combined meningococcal septicemia and meningitis, cerebral edema and acute respiratory distress syndrome, in whom we balanced the conflicting carbon dioxide strategies for optimal pulmonary and neurological management using jugular oxygen saturation (SjvO2) monitoring to identify the upper limit of "tolerable" hypercapnia. Our observations suggest that significant acidosis was not well tolerated; however, cautious induction of pH down to 7.32 and an arterial carbon dioxide tension (PaCO2) < 5.9 kPa was tolerated acutely without significant cerebral hyperemia. Moreover, with the development of metabolic compensation and normal pH, higher levels of PaCO2 could be permitted. In similar cerebro-pulmonary circumstances we suggest that these findings warrant consideration. Alternatively, invasive monitoring of SjvO2 could be undertaken so that patient-specific criteria for permissive hypercapnia can be determined.
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PMID:Combined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be? 1005 Oct 94