PurposeWhen a tourniquet is used during surgery on the extremities, the pressure applied to the muscles, nerves and blood vessels can cause neuromuscular damage that contributes to postoperative weakness. The hypothesis was that the rehabilitation-related results would be improved if total knee arthroplasty (TKA) is performed without the use of a tourniquet.Methods81 patients with osteoarthritis of the knee who underwent TKA surgery were randomized to surgery with or without tourniquet. Active flexion and extension of the knee, pain by visual analog scale (VAS), swelling by knee circumference, quadriceps function by straight leg raise, and timed up and go (TUG) test results were measured before and up to 3 months after surgery.ResultsANCOVA revealed no between-groups effect for flexion of the knee at day 3 postsurgery. Compared with the tourniquet group, the nontourniquet group experienced elevated pain at 24 h, with a mean difference of 16.6 mm, p = 0.005. The effect on mobility (TUG test) at 3 months was better in the nontourniquet group, with a mean difference of -1.1 s, p = 0.029.ConclusionsThe hypothesis that the rehabilitation-related results would be improved without a tourniquet is not supported by the results. When the results in this study for surgery performed with and without tourniquet are compared, no clear benefit for either procedure was observed, as the more pain exhibited by the nontourniquet group was only evident for a short period and the improved mobility in this group was not at a clinically relevant level.Level of evidenceInconsistent results, Level II.

Endogenously produced nitric oxide (NO) induces relaxation in smooth muscle in various organs. The purpose of this study was to investigate whether a NO-mediated relaxation system exists in the human Fallopian tube. To study contractility, the isthmic portion of the tube was obtained from 23 fertile women during operations due to benign non-tubal diseases. Tubal smooth muscle strips were mounted in tissue chambers containing HEPES buffer and connected to a Grass transducer for the isometric registration of contractile activity. By adding L-arginine (the substrate for NO synthesis) or N-nitro-L-arginine methyl ester (L-NAME; an inhibitor of NO synthesis) to the tissue chambers, changes in tubal contractility were monitored. The addition of L-NAME caused increased tubal contractility, while L-arginine, after an initial transient increase in tonus, caused relaxation of the strips. Using immunohistochemistry, NO synthase, the enzyme that catalyses the production of NO from L-arginine, was identified in tubal tissue cells. These results indicate that a NO-dependent relaxation system exists in the Fallopian tube and that NO may play a role as a mediator of tubal contractility.

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The PPAR (peroxisome proliferator activated receptor) transcription factors are ligand-activated nuclear receptors that regulate genes involved in lipid metabolism and homeostasis. PPAR ␣ is preferentially expressed in liver and PPAR ␥ preferentially in adipose tissue. Activation of PPAR ␣ leads to peroxisome proliferation and increased ␤ -oxidation of fatty acids in rodents. PPAR ␥ -activation leads to adipocyte differentiation and improved insulin signaling of mature adipocytes. Both PPAR receptors are believed to be functional targets for treatment of hyperlipidemia in man. We have treated obese diabetic mice ( ob / ob ), which have highly elevated levels of plasma triglycerides, glucose and insulin, for 1 week with WY14,643 (180 mol/kg/day), a selective PPAR ␣ agonist, or rosiglitazone (BRL49653; 2.5 mol/kg/day), a selective PPAR ␥ agonist. The doses used produce a similar therapeutic effect in both treatment groups (lowering of triglycerides and glucose). High resolution two-dimensional gel electrophoresis of livers showed that WY14,643 and rosiglitazone both produced changes in expression pattern of many proteins involved in peroxisomal fatty acid ␤ -oxidation. However, similar experiments performed in lean mice showed significant up-regulation of these proteins only with WY14,643 treatment. Furthermore, the proteins up-regulated by the drugs in obese mice had a higher basal expression in obese controls compared to the lean littermates. Liver PPAR ␥ mRNA levels were determined and we observed that PPAR ␥ 2 mRNA levels were elevated in obese mice compared to lean littermates. As PPAR ␣ and PPAR ␥ recognize similar DNA response elements, it is likely that the effects of rosiglitazone on PPAR ␣ responsive genes in livers of the ob / ob mice are mediated by PPAR ␥ 2. -Edvardsson, U., M. Bergström, M. Alexandersson, K. Bamberg, B. Ljung, and B. Dahllöf. Rosiglitazone (BRL49653), a PPAR ␥ -selective agonist, causes peroxisome proliferator-like liver effects in obese mice.

The PPAR (peroxisome proliferator activated receptor) transcription factors are ligand-activated receptors which regulate genes involved in lipid metabolism and homeostasis. PPARalpha is preferentially expressed in the liver and PPARgamma preferentially in adipose tissue. Activation of PPARalpha leads to peroxisome proliferation in rodents and increased beta-oxidation of fatty acids. PPARgamma-activation leads to adipocyte differentiation and improved insulin signaling of mature adipocytes. Both of these PPAR receptors are potential targets for treatment of dyslipidemia in man. Studies by others using a proteomics approach have characterized the effects of PPARalpha agonists in livers from lean healthy mice. However, we wanted to map the effects of a therapeutic dose of a PPARalpha agonist in a disease model of insulin resistance and diabetes, the obese diabetic ob/ob mouse, by proteomics. Therefore, ob/ob mice, which have highly elevated levels of plasma triglycerides, glucose and insulin, were treated for one week with WY14,643 (180 micromol/kg/day), a well-characterized selective PPARalpha agonist. Plasma triglycerides, glucose and insulin levels were determined and we found significant therapeutic effects on triglycerides and glucose levels. The liver protein compositions were investigated by high-resolution two-dimensional gel electrophoresis which showed that WY14,643 produced up-regulation of at least 16 spots. These were identified by mass spectrometry and 14 spots were found to be components of the peroxisomal fatty acid metabolism. Thus, WY14,643 at a therapeutic dose, caused induction of peroxisomal fatty acid beta-oxidation in obese diabetic mice.

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