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3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statins) is one of the most commonly prescribed agents for controlling hyperlipidemia. Apart from their lipid-lowering property, statins are well known for their pleiotropic effects, such as improvement of vascular endothelial dysfunction, attenuation of inflammatory responses, stabilization of atherosclerotic plaques, inhibition of vascular smooth muscle proliferation, and modulation of procoagulant activity and platelet function. The vasculo-protective effect of statins is mainly mediated by inhibition of the mevalonate pathway and oxidized low-density lipoprotein generation, thereby enhancing the biosynthesis of endothelium-derived nitric oxide. Accumulating clinical evidence strongly suggests that administration of statins reduces overall mortality, the development myocardial infarction and atrial fibrillation, and length of hospital stay after a major cardiac/noncardiac surgery. This review updates the clinical pharmacology and therapeutic applications of statins during major operations, and highlights the anesthesia considerations for perioperative statin therapy.

Objectives Both overproduction of nitric oxide and oxidative injury to the cardiovascular and pulmonary systems contribute to fatal pathophysiology during endotoxemia. We investigated the effect of propofol on oxidative stress-related enzymes in lung (L2), heart (H9C2) and macrophage (NR8383) cells during endotoxemia. Methods Experimental endotoxemia was induced by co-culture of Escherichia coli lipopolysaccharide (15 μg/mL) in the abovementioned three types of cells that were under the effect of propofol (15 or 30 μM for 1 or 4 hours). Cellular expression of induced nitric oxide synthase (iNOS), superoxide dismutase (SOD) 1 and 2, and p47phox (representing NADPH oxidase) were determined by immunoblotting. The cellular oxidative burst activity was determined using a dihydroethidium method via flow cytometry to represent the level of reactive oxygen species. The in vivo endotoxemia model was also employed for comparison using a systemic injection of lipopolysaccharide (15 mg/kg) under propofol maintenance (15 or 30 mg/kg/h). The Student t test (two groups) was used for statistical evaluation among the means, and the Newman–Keuls test was used for analysis of variance in the statistical analysis. Results In lung L2 cells, propofol significantly reduced the expression of iNOS, SOD1, SOD2, and p47phox under LPS-induced endotoxemia. However, in H9C2 cardiac cells and NR8383 macrophages, only the expression of iNOS was significantly suppressed, but not that of SOD1, SOD2, or p47phox. The level of reactive oxygen species was suppressed in all three kinds of cell. In in vivo animal tissue, except for the suppression of iNOS expression in lung and heart cells, propofol in lung cells produced only SOD1 suppression, but in rat heart the expression of both SOD1 and SOD2 was suppressed. Conclusion These results suggest that propofol may have a protective role for lung cells. This effect is associated with its suppression of oxidative-related enzymes, including iNOS, SOD1, SOD2, and p47phox. In cardiac myocytes and macrophages, propofol also provides an antioxidative effect, probably via its inhibition of iNOS. The overall effect of propofol in the organs may be a combination of its effects on various cells. In addition, a reduction in reactive oxygen species plays a major role in the beneficial effect of propofol on experimental endotoxemia.

Objectives Patients suffering from neuropathic pain are difficult to treat and many methods are used to resolve this issue. In this study, we used a model of neuropathic pain comprising rats with chronic constriction injury (CCI) on the left sciatic nerve to investigate the chronic effect of gabapentin via intrathecal administration. We also observed the expression of dorsal spinal protein kinase C gamma subunit (PKCγ) and other pain-related molecules in the spinal area which included cyclooxygenase 2 (COX2), c-Fos and cyclic AMP-dependent transcription factor (ATF3) in the neuropathic pain animals. Methods Male Sprague-Dawley (SD) rats (250–380g) were randomly assigned to four groups, i.e., control, gabapentin (Gaba), MK801, and gabapentin plus MK801 (Gaba+M) groups. A PE-5 catheter was inserted into the lumbar spine area via the cervical spine area. CCI was performed the following day after the intrathecal catheter implant surgery. Gabapentin (1.05μmol/day) was then given the following day after CCI surgery. Intrathecal gabapentin was administrated for 14 consecutive days. Pain-related behavior was assessed every 2 days thereafter by measuring the latency of foot withdrawal elicited by noxious radiant heat or Von Frey microfilament applied to the hind-paw plantar surface. MK801 (30μg/day), an N -methyl-D-aspartate (NMDA) receptor blocker, was also added for potential effect. The tissue of dorsal horn of the lumbar spine was harvested on the 14 th day for the expression of COX2, c-Fos, ATF3 and PKCγ with Western blotting, and positive finding protein was then checked on 7 th day for further evaluation. Results The beneficial effect of intrathecal gabapentin of statistic significance on thermal duration and mechanical microfilament appeared after 7-day and 11-day consecutive treatment, respectively. Furthermore, the NMDA receptor blocker also potentiated the effect on the behavior of thermal and mechanical stimulations. Gabapentin had no effect on the expression of COX2, c-Fos and ATF3. Interestingly, the expression of PKCγ in the spinal cord was initially inhibited by gabapentin on the 7 th day but was potentiated on the 14 th day. Conclusions Our results indicate that chronic intrathecal gabapentin has beneficial effects on the behaviors of both thermal and mechanical stimulations in the neuropathic pain animals and the NMDA blocker can potentiate this effect. Furthermore, gabapentin has biphasic effect on the expression of PKCγ in the spinal cord on Day 7 and Day 14 for the model rats with CCI.

Objective In developed countries, the societies of anesthesiologists have published reports of anesthesia quality. However, there are still no publications on anesthesia quality in Taiwan, even though the Taiwan Society of Anesthesiologists (TSA) was founded in 1956. This study was designed to evaluate the quality of anesthesia in Taiwan using databases maintained by the TSA and the Bureau of National Health Insurance-Taiwan (BNHI-T). Methods The TSA published annual reports in 1995–1998 and 2002–2008 (with a 3-year interval), which included a survey on anesthesia-related mortality and morbidity, the manpower and composition of anesthesia teams, and the causes of anesthesia-related complications. Since 2002, the BNHI-T has collaborated with the National Health Research Institute-Taiwan to establish a database of health care service. To understand anesthesia quality in Taiwan, we collected data from the annual TSA surveys and the BNHI-T, and analyzed trends in anesthesia-related mortality, causes of anesthesia complications, and relative manpower composition. Results The rate of anesthesia-related mortality was 11.9 deaths/100,000 cases. More than 50% of all anesthesia-related complications were preventable. About 1500 anesthetic procedures were performed annually by each anesthesiologist in Taiwan. The ratio of anesthesiologists to nurse anesthetists was 1:3–5. Conclusion Anesthesia-related mortality was about 10-fold higher in Taiwan than in the United States, Japan and the United Kingdom. Mortality related to quality of anesthesia in Taiwan must be reduced. To achieve this target, we have recommended the following six approaches: (1) decrease the workload of anesthesiologists; (2) increase reimbursement by the BNHI-T for anesthesia; (3) improve the training quality of anesthetist residents; (4) strengthen the quality of board examinations; (5) improve the training quality of nurse anesthetists; and (6) standardize monitoring procedures and equipment. Only once these measures are introduced, in combination with effective quality assurance and subjective improvement systems, can we expect an improvement in the quality of anesthesia in Taiwan.