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11. |
Ultrastructural morphometry of anterior cruciate and medial collateral ligaments: An experimental study in rabbits |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 96-103
R. A. Hart,
S. L‐Y. Woo,
P. O. Newton,
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摘要:
AbstractThis study presents morphometric analyses of collagen subfascicle area fraction and collagen fibril diameter distributions for the anterior cruciate (ACL) and medial collateral (MCL) knee ligaments from transmission electron micrographs of ligament cross sections of five mature, female New Zealand White rabbits. Statistically significant differences in subfascicular area fractions were found between the ACL and MCL (0.89 ± 0.02, 0.97 ± 0.01, respectively; p<0.001). Mean fibril diameters for the ACL and MCL were also significantly different (0.059 ± 0.005, 0.085 ± 0.011 μm, respectively; p0.1). The relative amount of variation in the pooled fibril diameter data due to variation between animals, ligaments, locations within ligaments, and among fibrils at individual locations are reported. The variation of fibril diameter distributions between the ACL and MCL was substantially greater than the variation between different locations within each ligament cross section as well as between different animals. The structural differences reported may help explain known differences in the biomechanical properties of the ACL a
ISSN:0736-0266
DOI:10.1002/jor.1100100112
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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12. |
Antagonist drugs and bone vascular smooth muscle |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 104-111
Michael T. Dean,
Michael B. Wood,
Paul M. Vanhoutte,
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摘要:
AbstractAn ex vivo canine tibia model was used to quantitate the specific adrenergic subtype contribution in bone vasculature. Tibiae were obtained from mongrel dogs, the nutrient artery was catheterized, and the bone was placed in an ex vivo perfusion apparatus at constant flow. Perfusion was accomplished using oxygenated Krebs‐Ringer solution. A norepinephrine dose‐response curve was obtained by using incremental single bolus doses. Each bone was perfused with a vasoactive drug at a standard physiologic dosage. After 30 min of perfusion, a second norepinephrine dose‐response curve was generated. The degree of attenuation of the norepinephrine dose‐response curve, as determined by the total area under the curve, was interpreted as the relaxation effect of the drug on the smooth muscle of the vascular bed. Prazosin (α1‐receptor antagonist), rauwolszin (α2‐receptor antagonist), propranolol (β‐receptor antagonist), and diltiazem (calcium‐entry inhibitor) were evaluated. Our data suggest that α1and α2adrenergic receptor antagonism results in a quantitatively similar attenuation of norepinephrine‐induced vascular smooth muscle contraction. Calcium‐entry antagonism produced less, but significant, attenuation of smooth muscle contractility. Beta‐adrenergic receptor blockade yielded only a slight, although consistent, reduction in reactivity. Simple perfusion with Krebs‐R
ISSN:0736-0266
DOI:10.1002/jor.1100100113
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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13. |
Combined effect of acute denervation and ischemia on the microcirculation of skeletal muscle |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 112-120
Long‐En Chen,
Anthony V. Seaber,
James R. Urbaniak,
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摘要:
AbstractUsing direct in vivo videomicroscopy and a fluorescein dye technique, reperfusion injury after 3 h of ischemia was studied in the acutely denervated cremaster muscle of the rat. Compared with normally innervated controls, ischemia‐induced reperfusion injury was more severe in the denervated group and included a delay of blood flow recovery, vortex formation, edema, hemorrhage, and vessel spasm. Vessel size was reduced at the arteriole and small artery level, and there was a decrease of reactive hyperemia. The injury mechanism may be related to a loss of active vasomotion and vascular response to vasoactive substances after denervation. The results suggest that shortening the ischemia time of denervated tissues may reduce ischemia‐induced reperfusion injury. Similarly, given the same ischemia time, improved tissue reperfusion may be expected if the nerve supply is maintai
ISSN:0736-0266
DOI:10.1002/jor.1100100114
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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14. |
Angular deformities and forearm function |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 121-133
Augusto Sarmiento,
Edward Ebramzadeh,
David Brys,
Richard Tarr,
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摘要:
AbstractAngular deformities were created in cadaver forearms at proximal, middle, and distal third levels of the radius and ulna separately, and at middle and distal third levels of both bones, to determine the corresponding limitations of pronation and supination. The ranges of pronation and supination were recorded using a rotational motion measurement apparatus instrumented with a 360° goniometer. These experimental results were compared to data obtained from clinical and radiographic examination of 105 patients with similar residual deformities following treatment of fractures by nonsurgical means, to evaluate the accuracy of the experimental model and to determine if loss of rotational motion could be predicted based on radiographic findings. With cadaver forearms, on the average, angulation of 10° of the radius or ulna in coronal or sagittal planes limited pronation and supination by<24°, whereas angulation of 10° of both the radius and the ulna limited pronation and supination by<18%. Comparison of experimental results with clinical findings showed that, despite the errors involved in measuring forearm deformities in patients using biplanar radiographs, the experimental results predicted the clinical loss of pronation and supination to within 17% for the fractures of the radius, and within 8% accuracy for the fractures of the u
ISSN:0736-0266
DOI:10.1002/jor.1100100115
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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15. |
A finite element study of the initiation of failure of fixation in cemented femoral total hip components |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 134-144
T. P. Harrigan,
J. A. Kareh,
D. O. O'Connor,
D. W. Burke,
W. H. Harris,
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摘要:
AbstractIn order to study initial mechanisms of failure in cemented femoral total hip components, an anatomically accurate three‐dimensional linear finite element model was constructed and verified against experimental strain measurements in the cement mantle. Good agreement was found between predicted and measured strains. The likelihood of failure initiation due to cement‐prosthesis debonding and crack initiation at voids was studied for loading conditions simulating both one‐legged stance and stair climbing. The “out of plane” forces involved in stair climbing appear to be the greatest threat to the fixation of total hip replacements. In stair climbing, cement‐prosthesis debonding and pore crack initiation were probable in the proximal anteromedial region of the cement mantle, and near the distal tip of the implant. The proximal stresses in stair climbing were higher than the distal stresses in either stair climbing or one‐
ISSN:0736-0266
DOI:10.1002/jor.1100100116
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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16. |
Colony‐forming efficiency response of bone marrow stromal cells to acute blood loss |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 145-148
L. Lippiello,
D. Chavda,
J. Connolly,
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摘要:
AbstractColony‐forming efficiency (CFE) was used to monitor the proliferative response of alkaline phosphatase‐positive rabbit bone marrow stromal cells to acute blood loss. The CFE of animals subjected to a 1% blood loss was 0.97 compared with 0.06 (p<0.01) in nonbled animals. Sera obtained from animals 10 days after an initial blood loss stimulated the CFE of marrow cultures from nonbled donors to the same degree as osteogenin. Erythropoietin and control sera (from nonbled animals) had no effect. Hence, acute blood loss and sera from bled animals stimulate proliferation of alkaline phosphatase‐positive marrow stromal cell colonies. The agent(s) responsible is unknown but it is present in serum in response to blood loss. Confirmation of a specific effect on osteoprogenitor cells may warrant the designation “osteop
ISSN:0736-0266
DOI:10.1002/jor.1100100117
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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17. |
The effect of hypothermic ischemia on the α‐adrenergic mechanisms of the canine tibia vascular bed |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 149-155
T. R. C. Davis,
M. B. Wood,
P. M. Vanhoutte,
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摘要:
AbstractThe effect of hypothermic ischemia on α‐1 and ‐2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025–6.4 nmol) on the perfusion pressure was studied. For all bones the first dose‐response curve was produced under control conditions. In one group the second dose‐response curve was generated during a constant infusion of prazosin (α‐1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (α‐2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, α‐1 adrenergic‐mediated vasoconstriction was significantly attenuated (p<0.001). However, α‐2 adrenergic‐mediated vasoconstriction was unaffected by increasing perio
ISSN:0736-0266
DOI:10.1002/jor.1100100118
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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18. |
In memoriam |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page 156-156
Gerald L. Mechanic,
Richard Webber,
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ISSN:0736-0266
DOI:10.1002/jor.1100100119
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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19. |
Masthead |
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Journal of Orthopaedic Research,
Volume 10,
Issue 1,
1992,
Page -
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ISSN:0736-0266
DOI:10.1002/jor.1100100101
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
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