Kinetically critical sites of femoral head roughening for wear rate acceleration in total hip arthroplasty

Polyethylene wear acceleration from (scratching) damage to the femoral head is a recognized hazard from constructs prone to generate third-body debris, but the phenomenon is nebulous and therefore often is subordinated to more direct and immediate considerations. To help delineate tangible quantitative relationships between counterface roughening and accelerated polyethylene wear, an experimentally validated sliding-distance-coupled finite element model of total hip replacement wear was adapted to incorporate regions of localized femoral head roughening. This computational formulation was used systematically to identify the sites on the femoral head for which a given severity of local roughening (parameterized in terms of roughening patch size and tribologic wear coefficient) was most consequential in terms of elevated polyethylene wear. Two such sites, of nominally comparable kinetic importance, were consistently evident throughout a wide range of roughening severities. These critical sites were located quasi-superiorly near the sagittal midline of the head, one slightly anterior and one slightly posterior of the coronal midline.     

Intragastric nitric oxide is abolished in intubated patients and restored by nitrite

OBJECTIVE: Nitrite in saliva is reduced to nitric oxide (NO) in the acidic stomach, and this NO may serve gastroprotective functions. We studied intragastric NO levels in healthy controls and in intubated intensive care unit patients before and after supplementation with nitrite. DESIGN: Prospective observational study involving patients and controls. SETTING: A mixed intensive care unit and a university laboratory. PATIENTS AND SUBJECTS: Eight healthy volunteers and ten intubated, mechanically ventilated intensive care unit patients. INTERVENTIONS: A tonometric catheter was first evaluated in vitro and then used for all NO measurements. In fasting controls, gastric NO levels were measured repeatedly during periods of saliva depletion and after an intragastric nitrite infusion. In patients, changes in levels of intragastric NO, nitrite in plasma and gastric juice, and S-nitrosothiols in gastric juice were measured in response to an intragastric nitrite infusion. MEASUREMENTS AND MAIN RESULTS: The tonometric catheter had a recovery of 80% with a high intraclass and interclass correlation. Median baseline NO levels in healthy volunteers were 21.6 ppm (interquartile range, 11.4-22.3 ppm) and decreased by 90% to 3.3 ppm (2.0-5.2 ppm) during 25-50 mins of saliva depletion. The NO level was restored by an intragastric nitrite infusion. Baseline NO levels in patients were almost abolished (0.1 ppm [0.07-0.4 ppm]) but increased rapidly to 124 ppm (range, 65-180 ppm) during intragastric nitrite infusion. Nitrite levels in plasma increased from 0.18 +/- 0.03 to 1.3 +/- 0.2 microM (p < .01), and levels of S-nitrosothiols in gastric juice increased from 0.12 +/- 0.09 to 6.7 +/- 1.8 microM. CONCLUSIONS: Intragastric generation of NO requires continuous delivery of nitrite-containing saliva and is almost abolished in critically ill, intubated patients. Enteral supplementation with nitrite could however fully restore gastric NO levels. Future studies will reveal if low NO levels contribute to stress ulcers and gastric overgrowth of bacteria often seen in these patients and in turn if restoring gastric NO with nitrite could be a useful therapeutic approach.