The objective of this study was to evaluate the initial fixation strength of a biodegradable interference screw compared with press-fit fixation and a titanium interference screw in anterior cruciate ligament reconstruction using a bone-patellar tendon-bone graft. Porcine lower limbs were used. The specimens underwent 500 loading cycles between 60 and 250 N. This corresponds to loads in the graft during aggressive rehabilitation. Thereafter, intact specimens were loaded to failure. Failure mode was defined by visual analysis. Under cyclic loads none of the interference screw fixations failed. In the press-fit group (angle between load axis and tunnel axis 80 degrees), five specimens failed. The mean maximal load to failure was 945 N (+/- 87) for the titanium screw, 797 N (+/- 60) for the biodegradable screw, and 708 N (+/- 211) for the five press-fit specimens that did not fail during cyclic loading. With respect to primary fixation strength, biodegradable screws are a reasonable alternative to titanium interference screws. The press-fit fixation did not provide a secure fixation in all cases. Five press-fit specimens failed under cyclic loads comparable with those seen under conditions of accelerated rehabilitation.

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To assess the possible role of nicotinergic control in nociception and pain, experiments were carried out on rats under urethane anesthesia in which nociceptive activity was elicited by electrical stimulation of afferent C fibers in the sural nerve and recorded from single neurones in the thalamus and from ascending axons in the spinal cord. Intravenous administration of nicotine (0.01-0.5 mg/kg) depressed the nociceptive activity evoked in the thalamus and the spinal cord in a dose-dependent way. The maximum depression in thalamus and spinal cord was 40% of control activity and obtained at a dose of 0.025 mg/kg. Likewise, local administration of nicotine to the spinal cord by intrathecal injection (5, 10, and 30 micrograms) reduced the nociceptive activity evoked in neurones of the thalamus and in ascending axons of the spinal cord, the maximum of the depression being 40% of control activity. The depressant effect of nicotine (0.05 mg/kg) was reduced by mecamylamine (1 mg/kg) but not by atropine (0.5 mg/kg). It is concluded that the antinociceptive effect of nicotine is due to a specific action of the alcaloid at the spinal level.