Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2011
Mean arterial pressures bracketing prolonged monitoring interruptions have negligible systematic differences from matched controls without such gaps.
Comparing intraoperative hemodynamic data from anesthesia information management systems (AIMS) among hospitals involves handling missing or edited values. There routinely are periods >5 minutes ("gaps") in recorded blood pressure in AIMS records. Previous studies showed the importance of monitoring the incidences of unexplained gaps, because providers interpolate when charting vital signs in gaps. We studied whether ignoring missing vital signs during gaps systematically biases monitoring results. ⋯ Our results show that when comparing hospitals using mean MAP data from hundreds of AIMS cases, statistical issues related to gaps are of minor importance. The more important issues when comparing hospitals are the incidences of gaps themselves and/or the manual editing of automatically recorded vital signs. Nevertheless, when quantifying hemodynamic variability (e.g., brief periods with rapid changes in MAP), gaps cannot be ignored. Furthermore, none of our results apply to individual patients (i.e., it is best not to have gaps in blood pressure during anesthesia).
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Anesthesia and analgesia · Aug 2011
Zaltoprofen inhibits bradykinin-mediated enhancement of glutamate receptor activity in substantia gelatinosa neurons.
Zaltoprofen, a propionic acid derivative of nonsteroidal anti-inflammatory drugs, has been proposed to inhibit the nociception mediated by bradykinin. Here, I attempted to clarify the molecular mechanisms underlying the blocking effect of zaltoprofen on bradykinin-mediated enhancement of excitatory glutamatergic transmission in the superficial dorsal horn of the spinal cord. ⋯ These findings suggest that the antinociceptive effect of zaltoprofen may block the augmenting effect of bradykinin on AMPA currents through inhibition of protein kinase C activation, without affecting COX in the superficial dorsal horn.
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After submission of a manuscript to a peer-reviewed anesthesia journal, several authors were asked to cite additional references from the journal to which they submitted. We hypothesized that there were differences among the anesthesiology journals in both the total number of self-citations and the proportion of self-citations to the total number of references in each manuscript for the years 2005 and 2010. ⋯ Although the number and rate of self-citations differed among anesthesia journals, the contribution of self-citation to IF has declined over time for most anesthesia journals. These results suggest periodic reassessment may be important to ensure that the publication process remains transparent and impartial to bias.
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Anesthesia and analgesia · Aug 2011
Isoflurane posttreatment reduces brain injury after an intracerebral hemorrhagic stroke in mice.
Intracerebral hemorrhage (ICH) is a devastating stroke subtype affecting 120,000 Americans annually. Of those affected, 40%to 50% will die within the first 30 days, whereas the survivors are left with a lifetime of neurobehavioral disabilities. Recently, it has been shown that volatile anesthetics such as isoflurane can reduce brain injury after an ischemic stroke. As a result, in this study, we investigated the effects of isoflurane as a posttreatment therapeutic modality in ICH-injured mice. Specifically, we investigated whether isoflurane posttreatment can preserve the structural integrity of the brain by reducing apoptotic damage and, in turn, improve functional outcome by amelioration of brain edema and neurobehavioral deficits. ⋯ Our results suggest that isoflurane may be an effective posttreatment therapeutic option for ICH because of its ability to reduce structural damage and subsequently preserve functional integrity.
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It is well established that all drugs of abuse converge onto common circuitry and induce chronic addiction by modulating the addictive signaling molecules such as DeltaFosB in the mesocorticolimbic system. Recent case reports suggest that propofol may have abuse potential. However, there is no direct evidence showing that propofol has an effect on the key addictive signaling molecules in the mesocorticolimbic system. In this study, we determined the effect of propofol on the expression of DeltaFosB in rat nucleus accumbens (NAc) and the potential mechanism involved. ⋯ In the current study, we have identified, for the first time, that propofol is able to induce the addictive signaling molecule DeltaFosB in NAc via dopamine receptor D1. This new evidence at the molecular level suggests that propofol may have abuse potential.