Plasma from donor dogs, pretreated with DDAVP, transfused into a German shorthair pointer with type II von Willebrand's disease.
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Publications and source records attributed to K H Kraus.
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The buccal mucosa bleeding time (BMBT; duration of hemorrhage from standardized cuts made with a spring-loaded disposable device in the mucosal surface of the upper lip) was used to evaluate the hemostatic competence of dogs. The mean (+/- SD) BMBT for 34 healthy dogs was 2.62 +/- 0.49 minutes. The BMBT of healthy dogs anesthetized with halothane or tranquilized with xylazine were not significantly different from the BMBT of healthy dogs evaluated without chemical restraint. The BMBT was significantly (P less than 0.01) prolonged 21 hours after aspirin (10 mg/kg of body weight) was administered orally to 10 healthy dogs; however, the mean aspirin-induced increase in BMBT was only 0.40 minutes. The BMBT of 28 of 30 dogs with various diseases not traditionally associated with hemostatic deficiencies were near or within the range of BMBT for healthy dogs; however, 2 dogs had BMBT of greater than 8 minutes. In contrast, BMBT were prolonged in most dogs with diseases known to induce deficient primary hemostasis; the 3 dogs with thrombocytopenia (less than or equal to 20,000 platelets/microliter), the 7 Doberman Pinschers with von Willebrand's disease (von Willebrand factor antigen; less than or equal to 18 U/dl), and 5 of the 6 dogs with severe azotemia (serum urea nitrogen; greater than or equal to 124 mg/dl) had prolonged BMBT. The BMBT of 16 dogs were determined immediately before they were subjected to various surgical procedures, and the severity of the hemorrhage encountered during these procedures was subjectively evaluated; the amount of hemorrhage from 12 of the 16 dogs was considered to be appropriate for the corresponding surgical procedures, but the remaining 4 dogs bled excessively during surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Eight adult male Beagles were given 1 microgram of 1-deamino-8-D-arginine vasopressin (DDAVP)/kg of body weight, SC or by slow IV infusion on separate occasions. Both routes of administration induced highly significant increases (P less than 0.0001) in plasma concentrations of von Willebrand factor (vWf) antigen (Ag) and botrocetin cofactor (BCf) activity, an indication of platelet-associated vWf activity. In most instances, increases in plasma vWf:Ag and BCf values induced by SC injection were as large as or larger than those induced by slow IV infusion. With both routes of administration, BCf activity increased more than the vWf:Ag concentration, so that high BCf-to-vWf:Ag ratios were found in plasma after DDAVP administration. In plasma samples obtained before DDAVP administration, sodium dodecyl sulfate-electrophoresis resolved the vWf into a series of multimeric proteins with molecular weights similar to those of human vWf. Sodium dodecyl sulfate-electrophoresis of plasma samples obtained after DDAVP administration revealed mainly the larger molecules of vWf that were increased by DDAVP administration.
Infusion of the vasopressin analogue DDAVP into five normal dogs at doses of 0.1-2.0 micrograms DDAVP per kg body weight induced dose-dependent increases in the plasma content of coagulation factor VIII and von Willebrand factor. Plasma concentrations of von Willebrand factor (determined antigenically as factor VIII-related antigen and functionally as coagglutinin cofactor activity) and coagulation factor VIII were measured immediately before and at 10, 30, and 120 min after 10-min intravenous infusions of DDAVP. The greatest increases in coagulation factor VIII were produced with the 2.0 micrograms/kg dose. Ten minutes after infusion the mean increase in coagulation factor VIII was 32 units/dl (concentrations of all indices were reported relative to concentrations in a standard canine plasma pool, arbitrarily assigned a concentration of 100 units/dl) and this increase did not change significantly throughout the duration of the experiment. At 10 min post-infusion, the mean factor VIII-related antigen concentration increased 81 units/dl (dose = 2.0 micrograms/kg) and did not change significantly for the duration of the experiment. The maximum mean increase in coagglutinin cofactor activity, 141 units/dl, occurred 10 min after infusion (dose = 1.0 microgram/kg). Coagglutinin cofactor activity decreased significantly from peak activity by 120 min post-infusion.
A 21-mm defect was created in 1 femoral diaphysis each of 15 dogs. Periosteum as well as a cylinder of bone was removed, and the defect was stabilized with a bone plate. Twelve of the defects were filled with an equal volume of autogenous cancellous bone harvested from the ipsilateral ilium. Three defects were left untreated. Cranial to caudal radiographs were taken postoperatively and every 4 weeks for 16 weeks. The radiographs were evaluated for healing using two ordinal scales. At 16 weeks, the dogs were euthanized and the femurs harvested for biomechanical testing and histologic evaluation. Both operated and contralateral not operated femurs were mechanically tested to failure in torsion, and load at failure and stiffness were calculated. All dogs tolerated the procedure well, and were using the operated limb within 1 or 2 days postoperatively. There were no complications noted during the 16 weeks of the study. Unfilled defects did not heal and became atrophic nonunions. The defects filled with autogenous cancellous bone healed in a consistent pattern of consolidation, incorporation, and remodeling, with uniform increases of both ordinal scales used. The femoral cortex opposite the bone plate demonstrated most mature remodeling, evident both radiographically as well as histologically. Unoperated femurs failed at 13.61 +/- 3.88 N-m and grafted femurs failed at 2.96 +/- 1.3 N-m, which was 23% of the measurement of the unoperated femur. Relative stiffness of the unoperated femurs was 5974 +/- 4316 N-m2/radian, and grafted femurs had a relative stiffness of 642 +/- 561 N-m2/radian, which was 10.4% of the measurement of unoperated femur. This model proved to be a critically sized defect, which when left unfilled resulted in an atrophic nonunion, and when filled with cancellous bone resulted in a consistent healing pattern.
Effects of desmopressin acetate (1-desamino-8-D-arginine vasopressin [DDAVP]) on plasma von Willebrand factor (vWf) were studied in 12 purebred Doberman pinschers confirmed to have von Willebrand's disease (vWd) (plasma vWf antigen [vWf:Ag] concentrations, less than 30 U/dl). Twelve dogs had subnormal plasma botrocetin cofactor (BCf) activity and 11 dogs had prolonged buccal mucosa bleeding times. Tranquilization of three dogs with lenperone and three dogs with xylazine did not induce significant changes in mean plasma vWf:Ag concentrations or mean BCf activities. Thirty and 120 minutes after administration of DDAVP (1 micrograms/kg subcutaneously), there was significant shortening of the mean buccal mucosa bleeding time. Ten dogs responded to DDAVP with increases in BCf activity which exceeded 10 U/dl at 30 or 120 minutes, or both, after the drug was administered. At the same time, increases in plasma vWf:Ag concentrations were smaller than the increases in BCf activity. It was shown by multimeric analysis that primarily the higher molecular weight forms of vWf increased in plasma in response to DDAVP.
Evoked potentials were produced by anodal stimulation over the motor cortex in six dogs. Potentials were recovered from the cranial thoracic and caudal lumbar portions of the spinal cord, and the radial and sciatic nerves. Evoked potential averages were recorded every 1.5 minutes during 40 minutes of aortic occlusion and during 40 minutes of reperfusion. Mean amplitudes of evoked potentials recovered from the caudal lumbar spinal cord decreased to 50% of original values at minute 12.2. Upon release of occlusion, the evoked potentials returned to baseline levels and remained there throughout the period of reperfusion. Sciatic nerve amplitudes decreased to 50% of original values at minute 4.5. In no subject could wave forms be recovered after minute 9.0. Upon release of occlusion, the evoked potentials returned to baseline levels and above, then deteriorated to 29 +/- 12% after 40 minutes of reperfusion. We concluded that transcranially induced evoked potentials were highly sensitive to spinal cord ischemia. Evoked potentials recovered from the sciatic nerve were consistent with functional grey matter immediately upon reperfusion, but deteriorated during reperfusion.
Controlled tissue expansion using a 100 cc rectangular silicone elastomer expander was performed in the mid-antebrachium and mid-crus of eight adult mixed-breed dogs. Two expander inflation schedules were followed. Group 1 dogs (n = 4) underwent expander inflation using 10 cc sterile saline every other day, and group 2 dogs (n = 4) underwent expander inflation using 15 cc sterile saline every other day until the nominal volume (100 cc) was attained. Significant mean postexpansion increases in skin surface area of 94.1 cm2 (35.9%) and 108.9 cm2 (37.3%) were measured in the antebrachium and crus, respectively (p < .05). In a second procedure, the expanders were removed and skin flaps were developed from the redundant tissue generated during the expansion process. Single pedicle advancement flaps and transposition flaps were used to cover surgically created defects measuring 5 x 10 cm in the antebrachium and crus. Single pedicle advancement flaps consistently measured 10 x 10 cm and could be advanced to cover defects involving one third of the mid-antebrachial or mid-crural circumference. Transposition flaps were rotated up to 170 degrees and the donor site defects were easily closed under minimal or no tension. Complications included an abscess in one dog and seroma formation in four dogs. Differences in success or complication rates between group 1 dogs and group 2 dogs were not observed; an accelerated inflation schedule using 15 cc sterile saline every other day was recommended.
The vascular and microvascular anatomy of the equine deep digital flexor tendon (DDFT) within the digital sheath was studied by injecting the vasculature with either colored latex or barium sulphate for radiographic, microangiographic, histologic, and computed tomographic (CT) evaluation. Consecutive 4-mm thick two-dimensional CT slice data were reconstructed to 3-dimensional volumetric images to enhance spatial evaluation of the blood supply. Gross dissection and angiographic studies identified three major vascular sources. Above the fetlock, the DDFT was supplied by either a branch of the medial palmar artery (Arteriae digitalis palmaris communis II) or a branch of the medial palmar digital artery (A. digitalis [palmaris propria III] medialis). Below the fetlock, the DDFT was supplied by branches from the lateral and medial palmar branches to the proximal phalanx (Ramus palmaris phalangis proximalis). The most distal aspect of the tendon received small branches from the medial and lateral palmar digital arteries. Using histology and microangigraphy we observed an extensive and uniform intratendinous vascular network above and below the fetlock, with a relatively avascular region of tendon palmar to the fetlock. The most distal 2.0 to 2.5 cm of the tendon within the sheath was heavily infiltrated with fibrocartilage along its dorsal aspect.
OBJECTIVE: To compare two external fixation clamp designs for their ability to resist movement of a fixation pin in relation to the connecting rod. STUDY DESIGN: Two designs of external fixator clamps were attached to connecting rods mounted on a jig for mechanical testing. Fixator pins were placed perpendicular to the connecting rod. A mechanical testing machine was used to deflect each 3.2-mm pin at a distance that was 25 mm from the center of the clamp bolt. Both clamp designs were tightened to 4.4, 6.1, and 7.8 newton-meters (N x m) torque, and loads were applied in a position ramp through 4 mm and resisting loads were measured. Two clamp orientations were used during load application, such that the deflection of the pin tended to tighten the clamp bolt or tended to loosen the clamp bolt. The tests were videotaped to determine mode of failure. Comparisons of the load/displacement curves for the two external fixator clamp designs were made using nonlinear equational curve fitting methods. The resultant plateau and rise coefficients were compared using analysis of variance. RESULTS: Slippage of the pin in relation to the clamp occurred with the Kirschner-Ehmer clamp tightened to 4.4, 6.1, and 7.8 N x m, and slipping of the pin in relation to the clamp occurred with the experimental clamp design tightened to 4.4 and 6.1 N x m but not to 7.8 N m. At 7.8 N x m, the 3.2-mm pin deformed plastically with the experimental clamp design. Increasing the torque of the clamp bolt resulted in superior plateau coefficients for both clamp designs. At each level of tightness and in each clamp orientation to applied pin load, the experimental clamp design provided greater plateau coefficients than did the Kirschner-Ehmer clamp design. At 7.8 N x m of tightness, the Kirschner-Ehmer clamp and bolt bent, whereas only slight plastic deformation of the experimental clamp design occurred. CONCLUSIONS: The experimental external fixator clamp was more secure in resisting fixator pin movement at all levels of tightening compared with the Kirschner-Ehmer-type external fixator clamp. At 7.8 N x m of tightening, the new clamp design did not allow slippage of the pin within the clamp. CLINICAL SIGNIFICANCE: The experimental external fixator clamp should result in greater rigidity of fixator configurations, in addition to providing design features that allow addition of a clamp between two installed clamps, sleeved predrilling of pilot holes for all pins, measurement of pin depth, and placement of positive profile pins at all sites.