Three-dimensional movements of the pelvis and the lumbar intervertebral joints in walking and trotting dogs.

Current knowledge of the physiological range of motion (ROM) in the canine axial system during locomotion is relatively limited. This is particularly problematic because dogs with back-related dysfunction frequently present for routine consultations. To collect detailed kinematic information and describe the three-dimensional motions of the pelvis and the lumbar spine (i.e. intervertebral joints S1/L7-L2/L1), we recorded ventro-dorsal and latero-lateral X-ray videos of three walking and trotting dogs and reconstructed their pelvic and intervertebral motions using X-ray reconstruction of moving morphology and scientific rotoscoping. Pelvic roll displayed a monophasic motion pattern and the largest ROM with on average 13° and 11° during walking and trotting, respectively. Pelvic yaw had the smallest ROM with on average 5° (walk) and 6° (trot). A biphasic pattern was observed for pelvic pitch with a mean ROM of 8°. At both gaits, the greatest intervertebral motions occurred either in S1/L7 or L7/L6. The intervertebral motions were mono- or biphasic in the horizontal and the transverse body planes and biphasic in the sagittal plane. Cranial to L6/5, the ROM tended to decrease from 3° to <1.5° in all three planes. Our results confirm that pelvic displacement and intervertebral joint movements are tightly linked with pelvic limb action at symmetrical gaits. The overall small movements, particularly cranial to L5, are consistent with the epaxial musculature globally stabilising the spine against the external and internal limb forces acting on the pelvis and the trunk during walking and trotting.

Immunologic monitoring of OKT3 induction therapy in cardiac allograft recipients.

OKT3 induction therapy was monitored in 31 cardiac allograft recipients during the 1st year posttransplant. Serum level of OKT3, anti-OKT3 antibodies, and interleukin-2 (IL-2) were monitored during the first 2 months posttransplant. These values were retrospectively correlated with allograft rejection episodes which occurred during the 1st year posttransplant and allograft survival rates over a 3-year observation period. We found that OKT3 induction therapy (10-14 days) was not associated with the development of anti-OKT3 antibodies manifest by dropping OKT3 levels during OKT3 therapy, and is not associated with the development of vascular rejection in our patient population. Patients with high titer ant-OKT3 antibodies, erratic serum OKT3 levels, and/or high serum IL-2 levels (> or = 5 ng/ml) during the first 2 months posttransplant showed a higher incidence of allograft rejection (predominantly cellular rejection) during the 1st year posttransplant and showed lower allograft survival rates. We also showed that a concomitant elevation of serum IL-2 levels was found in patients who developed anti-OKT3 antibodies. CD3+ T-cell levels were not predictive of inefficacy of OKT3 therapy. We conclude that immunologic monitoring of serum OKT3, anti-OKT3 antibody, and possibly serum IL-2 levels is critical for identification of patients who develop early, OKT3-resistant rejection episodes and for the identification of patients who may be more susceptible to allograft rejection and decreased allograft survival long after completion of OKT3 therapy.

First successful transfer of cryopreserved feline (Felis catus) embryos resulting in live offspring.

Sexually mature domestic cats were hormonally stimulated to induce superovulation; embryo recovery was accomplished by laparotomy. Embryos were frozen by conventional embryo freezing methods used in the domestic cattle embryo transfer industry. Thawing was achieved in a 28 degrees C or 37 degrees C waterbath or in ambient air. Overnight culture of the frozen-thawed embryos in a supplemented Nutrient Mixture F-10 (Ham's) or Earle's Balanced Salt Solution with 20% heat-treated newborn calf serum resulted in five successful term litters from recipient queens. Embryo recipients who became pregnant had been treated with a subcutaneous injection of follicle-stimulating hormone (FSH-P) once every 24 hr for 6 days in the amount of 0.2 mg/day for the first 5 days and 0.1 mg on the sixth day, followed by two intramuscular 750 IU injections of human chorionic gonadotropin 24 hr apart, beginning on the same day as the sixth injection of FSH-P.

Naloxone and experimental spinal cord injury: Part 1. High dose administration in a static load compression model.

Previous studies by other investigators using a dynamic weight drop injury model in cats or rats have demonstrated a beneficial effect of naloxone in promoting motor recovery after experimental spinal cord injury. The effective doses ranged from 0.8 mg (total dose) in rats to a high dose of 10 mg/kg in cats. We report here an evaluation of high dose naloxone (10 mg/kg) in a model of cord injury in rats using a static load compression technique. After induction of injury at T-12, naloxone (10 mg/kg) was administered by the intraperitoneal route, followed by five additional bolus injections over the course of the next 2 days. Animals were randomly assigned to this treatment regimen (n = 10) or to a saline control group (n = 10). The animals were observed for 4 weeks, with testing of recovery of hind limb motor function (Tarlov score and on an inclined plane). Although there were slight differences in recovery, the overall evaluation showed no statistically significant difference between the naloxone-treated and control groups. The spinal cords of the sacrificed animals were studied morphometrically; there was no statistically significant difference between the residual gray and white matter at the site of cord injury between the treated and control groups. Naloxone did not seem to promote recovery of motor function in this model of spinal cord injury.

Naloxone and experimental spinal cord injury: Part 2. Megadose treatment in a dynamic load injury model.

We previously reported that high dose naloxone (10 mg/kg) failed to promote recovery of motor function after a static load injury of the spinal cord in rats. In the present experiments, using the more traditional dynamic weight drop model, we tested megadose naloxone administered by the intraperitoneal route in 23 rats, including saline controls (Experiment 1). Thirty minutes after a cord injury at T-12, naloxone was given i.p. in a bolus of 100 mg/kg, followed by a continuous i.p. infusion of 50 mg/kg/hour for 23 hours. Again, no benefit was observed; this raised a question regarding naloxone and its absorption and serum levels. In another study, reported separately, we found that naloxone administered by the subcutaneous route affords higher and more sustained serum levels than by i.p. administration. Consequently, in 20 rats (Experiment 2), we repeated the protocol, using subcutaneous naloxone in a bolus dose of 150 mg/kg, followed by continuous infusion of 75 mg/kg/hour for 23 hours; the result was again negative. Morphometric determination of the residual (normal) cross sectional areas of gray and white matter at the epicenter of the cord lesion showed no statistically significant difference between treated and control animals in either Experiment 1 or Experiment 2. In view of the negative findings at high dose (10 mg/kg) and megadose naloxone, it seems that a reasonable next step would be an evaluation of lower doses using a factorial research design, incorporating a range of doses of naloxone in relation to a variety of intensities of cord injury. This question will be addressed in future experiments.

Models of spinal cord injury: Part 1. Static load technique.

Testing of potential therapies for spinal cord injury has been significantly hampered by the unavailability of a standardized, reproducible animal model with predictable outcome at a given force of injury (dose-response). The rat was selected in the development of this model in preference to larger animals for economy and availability; this permits use of large numbers of animals to increase statistical validity. In the experiments reported in this article, a static load method (weight placed gently on cord) of inducing cord injury was evaluated. A total of 198 Sprague-Dawley rats were used. Under general anesthesia, a one-level laminectomy was carried out at T-12 with the dura mater intact. Weights varying from 80 to 150 g were lowered onto the dorsal surface of the intact dura mater for durations of 0 to 300 seconds. Recovery of motor function was assessed for up to 8 weeks using two behavioral tests, a modified Tarlov scale and an inclined plane test of hind limb motor function. A statistically significant relationship was found between force of injury and motor recovery as measured by the Tarlov scale, but this did not correlate with inclined plane performance; the duration that the weight rested on the cord did not influence outcome. Pathologically, there was variation in the extent of damage for a given injury load. A semiquantitative pathological assessment of cord injury showed a statistically significant correlation between pathological score and behavioral deficit as measured by the Tarlov scale, but this did not correlate with inclined plane performance. In view of these deficiencies, the static load technique does not seem to be an ideal model for spinal cord injury research.

Spontaneous spinal cord "injury potential" in the rat.

A marked ionic change in both the intra- and the extracellular space at the site of an acute spinal cord lesion has been reported in the literature. The present study was undertaken to measure spontaneous electrical potentials that might be associated with the previously observed ionic shifts. With the use of an impact (weight drop) model of cord injury in rats, lesions were induced at T-8. DC potentials were measured simultaneously both rostrally and caudally with respect to site of injury over a time course of 4 hours after injury. The potentials were positive with respect to lesion site, and the intensity decreased with time during 4 hours of observation. These results seem to support reported ionic shifts and migrations in injured cords and represent, to our knowledge, the first reported measurement of spontaneous injury potential in the cord of a mammal.