Reaction time and brake pedal force after total knee replacement: timeframe for return to car driving.

PURPOSE: This prospective cohort study aimed to examine objective and subjective parameters in patients who underwent total knee replacement (TKR) to assess from when on driving a car can be deemed safe again. METHODS: Thirty patients (16 women, 14 men, age 66 ± 11 years) who received TKR of the right knee and 45 healthy controls (26 women, 19 men, age 32 ± 9 years) were asked to perform an emergency braking manoeuvre using a driving simulator. Brake pedal force (BPF), neuronal reaction time (NRT), brake reaction time (BRT), and subjective parameters (pain, subjective driving ability) were measured preoperatively as well as 5 days, 3-4, and 6 weeks after TKR. RESULTS: Preoperative NRT was 506 ± 162 ms, BRT 985 ± 356 ms, and BPF 614 ± 292 N. NRT increased to 561 ± 218 ms, BRT to 1091 ± 404 ms and BPF decreased to 411 ± 191 N 5 days after TKR. Three weeks after surgery, NRT was 581 ± 164 ms and BRT 1013 ± 260 ms, while BPF increased to 555 ± 200 N. Only BPF showed significant differences (p < 0.01). In week 6, all parameters were restored to baseline levels; patients showed significant pain decrease and evaluated their driving ability as "good" again. CONCLUSION: BPF was the only parameter displaying a significant postoperative decrease. However, preoperative patients' baseline levels and subjective confidence in driving ability were only reached 6 weeks after the operation. These results indicate that a minimum waiting period of 6 weeks should be considered before patients can safely participate in road traffic at their individual preoperative safety level again. LEVEL OF EVIDENCE: II.

Inhibition of lectin-like oxidized low-density lipoprotein receptor-1 reduces leukocyte adhesion within the intestinal microcirculation in experimental endotoxemia in rats.

INTRODUCTION: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), the major endothelial receptor for oxidized low-density lipoprotein, is also involved in leukocyte recruitment. Systemic leukocyte activation in sepsis represents a crucial factor in the impairment of the microcirculation of different tissues, causing multiple organ failure and subsequently death. The aim of our experimental study was to evaluate the effects of LOX-1 inhibition on the endotoxin-induced leukocyte adherence and capillary perfusion within the intestinal microcirculation by using intravital microscopy (IVM). METHODS: We used 40 male Lewis rats for the experiments. Ten placebo-treated animals served as a control. Thirty animals received 5 mg/kg lipopolysaccharide (LPS) intravenously. Ten endotoxemic rats remained untreated. In 10 LPS animals, we administered additionally 10 mg/kg LOX-1 antibodies. Ten further LPS animals received a nonspecific immunoglobulin (rat IgG) intravenously. After 2 hours of observation, intestinal microcirculation was evaluated by using IVM; the plasma levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) were determined; and LOX-1 expression was quantified in intestinal tissue with Western blot and reverse-transcription polymerase chain reaction (PCR). RESULTS: LOX-1 inhibition significantly reduced LPS-induced leukocyte adhesion in intestinal submucosal venules (P < 0.05). At the protein and mRNA levels, LOX-1 expression was significantly increased in untreated LPS animals (P < 0.05), whereas in animals treated with LOX-1 antibody, expression of LOX-1 was reduced (P < 0.05). MCP-1 plasma level was reduced after LOX-1 antibody administration. CONCLUSIONS: Inhibition of LOX-1 reduced leukocyte activation in experimental endotoxemia. LOX-1 represents a novel target for the modulation of the inflammatory response within the microcirculation in sepsis.