Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
When to release allocated operating room time to increase operating room efficiency.
We studied when allocated, but unfilled, operating room (OR) time of surgical services should be released to maximize OR efficiency. OR time was allocated for two surgical suites based on OR efficiency. Then, we analyzed real OR schedules. We added new hypothetical cases lasting 1, 2, or 3 h into OR time of the service that had the largest difference between allocated and scheduled cases (i.e., the most unfilled OR time) 5 days before the day of surgery. The process was repeated using the updated OR schedule available the day before surgery. The pair-wise difference in resulting overutilized OR time was calculated for n = 754 days of data from each of the two surgical suites. We found that postponing the decision of which service gets the new case until early the day before surgery reduces overutilized OR time by <15 min per OR per day as compared to releasing the allocated OR time 5 days before surgery. These results show that when OR time is released has a negligible effect on OR efficiency. This is especially true for ambulatory surgery centers with brief cases or large surgical suites with specialty-specific OR teams. What matters much more is having the correct OR allocations and, if OR time needs to be released, making that decision based on the scheduled workload. ⋯ Provided operating room (OR) time is allocated and cases are scheduled based on maximizing OR efficiency, then whether OR time is released five days or one day before the day of surgery has a negligible effect on OR efficiency.
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Anesthesia and analgesia · Mar 2004
Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.
Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. ⋯ The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.
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Anesthesia and analgesia · Mar 2004
The effects of hydroxyethyl starch on lung capillary permeability in endotoxic rats and possible mechanisms.
In this study we examined the effects of hydroxyethyl starch (HES 200/0.5) on lung capillary permeability in endotoxic rats and explored the possible mechanisms. Male Wistar rats were randomly divided into seven groups treated with saline, lipopolysaccharide (LPS; 6 mg/kg), LPS plus HES (3.75, 7.5, 15, or 30 mL/kg), or HES (30 mL/kg) alone for 4 or 2 h. Lung capillary permeability, lung neutrophil accumulation, expression of CD11b on the blood neutrophil cell surface, lung cytokine-induced neutrophil chemoattractant protein level, and nuclear factor kappa B (NF-kappaB) activation in blood neutrophils and lungs were measured. HES at doses of 3.75 and 7.5 mL/kg significantly reduced LPS-induced increases of lung capillary permeability. HES was found to inhibit lung neutrophil accumulation, cytokine-induced neutrophil chemoattractant protein, and NF-kappaB activation in parallel and to inhibit CD11b expression in a dose-dependent manner. These findings demonstrate that HES has beneficial effects on capillary leak in acute lung injury and that the mechanisms underlying this action involve an antiinflammatory effect of HES, including inhibition of NF-kappaB activation. ⋯ A randomized, controlled laboratory experiment indicated that hydroxyethyl starch (HES) could reduce increased lung capillary permeability in endotoxemia. This effect may be due to an antiinflammatory effect of HES.