Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Comparative StudyA comparison of the neurotoxic effects on the spinal cord of tetracaine, lidocaine, bupivacaine, and ropivacaine administered intrathecally in rabbits.
We have reported that increased glutamate concentrations in microdialysate of the cerebrospinal fluid (CSF) may be clue phenomena to elucidate mechanisms of neurotoxicity of intrathecal tetracaine. However, little is known about whether this is true for other local anesthetics. In this study, we compared the effects of local anesthetics on glutamate concentrations in CSF microdialysate and neurologic and histopathologic outcome. Rabbits were assigned into 5 groups (n = 6 in each) and intrathecally received 0.3 mL of NaCl solution (control), 2% tetracaine, 10% lidocaine, 2% bupivacaine, or 2% ropivacaine. Neurologic and histopathologic assessments were performed 1 wk after the administration. Intrathecal local anesthetics significantly increased glutamate concentrations with no significant differences among the four local anesthetics. The sensory and motor functions in the lidocaine group were significantly worse than in the other groups. Characteristic histopathologic changes were vacuolation in the dorsal funiculus and chromatolytic damage of motor neurons. The extent of vacuolation of the dorsal funiculus was in the order of lidocaine = tetracaine > bupivacaine > ropivacaine. Although the differences among the local anesthetics cannot be explained by glutamate concentrations, the results suggest that the margin of safety may be smallest with lidocaine. ⋯ Large concentrations of local anesthetics administered intrathecally increased glutamate concentrations in the cerebrospinal fluid. The margin of safety may be smallest with lidocaine.
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Anesthesia and analgesia · Aug 2003
Postoperative pain experience: results from a national survey suggest postoperative pain continues to be undermanaged.
Postoperative pain can have a significant effect on patient recovery. An understanding of patient attitudes and concerns about postoperative pain is important for identifying ways health care professionals can improve postoperative care. To assess patients' postoperative pain experience and the status of acute pain management, we conducted a national study by using telephone questionnaires. A random sample of 250 adults who had undergone surgical procedures recently in the United States was obtained from National Family Opinion. Patients were asked about the severity of postsurgical pain, treatment, satisfaction with pain medication, patient education, and perceptions about postoperative pain and pain medications. Approximately 80% of patients experienced acute pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain, with more patients experiencing pain after discharge than before discharge. Experiencing postoperative pain was the most common concern (59%) of patients. Almost 25% of patients who received pain medications experienced adverse effects; however, almost 90% of them were satisfied with their pain medications. Approximately two thirds of patients reported that a health care professional talked with them about their pain. Despite an increased focus on pain management programs and the development of new standards for pain management, many patients continue to experience intense pain after surgery. Additional efforts are required to improve patients' postoperative pain experience. ⋯ A survey of 250 US adults who had undergone a recent surgical procedure asked about their postoperative pain experience. Approximately 80% of patients experienced pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain. Additional efforts are required to improve patients' postoperative pain experience.
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Anesthesia and analgesia · Aug 2003
Lidocaine attenuates cytokine-induced cell injury in endothelial and vascular smooth muscle cells.
Local anesthetics have been reported to attenuate the inflammatory response and ischemia/reperfusion injury. Therefore, we hypothesized that pretreatment with local anesthetics may protect endothelial and vascular smooth muscle (VSM) cells from cytokine-induced injury. Human microvascular endothelial cells and rat VSM cells were pretreated with lidocaine or tetracaine (5-100 microM for 30 min) and then exposed to the cytokines tumor necrosis factor-alpha, interferon-gamma, and interleukin-1beta for 72 h. Cell survival and integrity were evaluated by trypan blue exclusion and lactate dehydrogenase release. The role of adenosine triphosphate-sensitive potassium (KATP) channels, protein kinase C, or both in modulating local anesthetic-induced protection was evaluated with the mitochondrial KATP antagonist 5-hydroxydecanoate, the cell-surface KATP antagonist 1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenyl]sulfonyl-3-methylthiourea (HMR-1098), and the protein kinase C inhibitor staurosporine. Lidocaine attenuated cytokine-induced cell injury in a dose-dependent manner. Lidocaine (5 microM) increased cell survival by approximately 10%, whereas lidocaine (100 microM) increased cell survival by approximately 60% and induced a threefold decrease in lactate dehydrogenase release in both cell types. In contrast, tetracaine did not attenuate cytokine-induced cell injury. 5-hydroxydecanoate abolished the protective effects of lidocaine, but staurosporine and HMR-1098 had no effect on the lidocaine-induced protection. This study showed that lidocaine, but not tetracaine, attenuates cytokine-induced injury in endothelial and VSM cells. Lidocaine-induced protection appears to be modulated by mitochondrial KATP channels. ⋯ This study demonstrates that lidocaine attenuates cytokine-induced injury of endothelial and vascular smooth muscle cells via mechanisms involving adenosine triphosphate-sensitive potassium channels. Protection of the vasculature from cytokine-induced inflammation may preserve important physiological endothelial and vascular smooth muscle functions.
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Anesthesia and analgesia · Aug 2003
Clinical TrialThe effects of large-dose propofol on cerebrovascular pressure autoregulation in head-injured patients.
In healthy individuals, cerebrovascular pressure autoregulation is preserved or even improved when propofol is infused. We examined the effect of an increase in propofol plasma concentration on pressure autoregulation in 10 head-injured patients. Using target-controlled infusions, the static rate of autoregulation was determined at a moderate (2.3 +/- 0.4 microg/mL) and a large (4.3 +/- 0.04 microg/mL) plasma target concentration of propofol. Using norepinephrine to control cerebral perfusion pressure, transcranial Doppler measurements from the middle cerebral artery were made at a cerebral perfusion pressure of 70 and 85 mm Hg at each propofol concentration. Middle cerebral artery flow velocities at the large propofol concentration were significantly lower than at the moderate concentration, without any concurrent increase in arterio-jugular difference in oxygen content, a finding compatible with maintained flow-metabolism coupling. Despite this, static rate of autoregulation decreased significantly from 54% +/- 36% to 28% +/- 35% (P = 0.029). Our data suggest that after head injury, the cerebrovascular effects of propofol are different from those observed in healthy individuals. We propose that large doses of propofol should be used cautiously in head-injured patients, because there is the potential to increase the injured brain's vulnerability to secondary insults. ⋯ Propofol is used for sedation and control of intracranial pressure in head-injured patients. In contrast to previous data from healthy individuals, we show a deterioration of cerebrovascular pressure autoregulation with fast propofol infusion rates after head injury. Large propofol doses may increase the injured brain's vulnerability to secondary insults.