There are subtle kinematic differences in patellar tracking between the natural knee and a TKR presumably due to differences in the shape and position of the patellar groove. There are no kinematic differences in patellar movement between the FB- and MB-TKR.
Digital templating in hip replacement is commonly performed with radiological markers to determine the magnification. The latter can also be determined by measuring the distance from the x-ray focal spot to the object and the distance from the x-ray focal spot to the radiological cassette or image receptor. We used post-operative radiographs of total hip replacements and hemiarthroplasties from 22 patients to calculate the magnification using both methods. The accuracy of each method was ascertained by measuring the size of the head of the implant projected on to the radiographs and comparing the result with the known size recorded in the medical records. The accuracy was found to be similar with a mean absolute measurement error of 2.6% (SD 1.4; 0.0% to 5.2%) for the radiological marker and 2.8% (sd 2.2; 0.4% to 10.1%) for the distance method (p = 0.75). The mean radiation dose for templating radiographs (pelvis and lateral of the hip) was similar when taken using a radiological marker (328 mSv SD 142) (n = 51) or using the distance measurement method (324 mSv SD 39) (n = 39) (p = 0.90). We conclude that the distance measuring method is as accurate as the radiological marker method, but may avoid some of the disadvantages such as misplacement of the marker or placement outside the radiological field. It may also be more acceptable to the patient and radiographer.
To test whether nitric oxide and prostaglandin pathways interact in hypercapnic cerebral vasodilatation, cerebral blood flow (CBF) was measured in enflurane anaesthetized Sprague-Dawley rats using the hydrogen clearance method. Isometric tension was measured in rat middle cerebral arteries in vitro. The neuronal NO synthase inhibitor 7-nitroindazole (7-NI 60 mg kg-1 i.p.) reduced the hypercapnic CBF response by 62 +/- 7% (but not the hypoxic response) and indomethacin (IMC 6 mg kg-1 i.v.) reduced the hypercapnic CBF response by 60 +/- 5%. Combined application caused only an 80 +/- 1% reduction. The attenuation of hypercapnic CBF by IMC was diminished by 7-NI and similarly 7-NI had less effect in the presence of IMC. Spermine-NO (50 microM 0.5 microL min-1 intracortically) increased eucapnic and hypercapnic CBF in the presence of IMC. In isolated middle cerebral arteries, combined application of sodium nitroprusside (SNP 3 nM) and prostacyclin (30 nM) had a synergistic vasodilatory effect. Milrinone (PDE-III inhibitor) also potentiated prostacyclin-mediated vasodilatation. Our results suggest that the NO- and IMC-sensitive pathways involved in the hypercapnic response are distinct, however, both may interact synergistically. A similar synergism was observed between the effects of SNP and prostacyclin.
Hypercapnic cerebral blood flow was not impaired in SHR. The contribution of nitric oxide- and prostaglandin-dependent vasodilation appeared to be intact Our results are consistent with the hypothesis that neuronal rather than endothelial production of nitric oxide may be responsible for maintaining hypercapnic cerebral vasodilation in SHR.
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