Biomedical subjects
Publications and source records attributed to J J Scott.
The initial burst has been re-examined following conditioning of the muscle to investigate its intrafusal origins. The burst was present in the response to stretch of spindle afferents that innervated the bag1 fibre and those that did not. There was, however, a difference in amplitude of the burst. These findings are discussed in terms of intrafusal mechanisms.
The use of fluorescence spectroscopy to discriminate atherosclerotic from normal tissue is limited by a lower sensitivity for calcified than noncalcified atherosclerotic plaque (65% vs. 93%, respectively). To evaluate plasma emission as a means to detect calcified plaque, 325 normal and atherosclerotic cadaveric aortic sites were irradiated through a 100-micron silica fiber in blood by a pulsed holmium laser (lambda = 2.1 microns, fluence = 4 J/mm2). A photodiode positioned near the proximal end of the fiber detected plasma emission during a laser pulse. Plasma emission was detected at 0% (0/110) of normal, 0% (0/107) of noncalcified atherosclerotic tissue, and 91% (98/108) of calcified atherosclerotic sites. Spectroscopic analysis confirmed the presence of calcium lines in the plasma emission from calcified atherosclerotic plaque. Although ablative fluences (greater than 3 J/mm2) were required for plasma generation, a single laser pulse ablated only to a depth of 67 +/- 16 microns in normal tissue. In an additional 10 calcified atherosclerotic sites, laser ablation was continued as long as plasma emission was detected. In all cases, plaque ablation was terminated before arterial perforation. Furthermore, the adjunctive use of plasma detection improved the accuracy of fluorescence spectroscopic classification of normal and atherosclerotic tissue. In conclusion, plasma detection has a high sensitivity (91%) and specificity (100%) for calcified atherosclerotic plaque and may be a useful adjunct for laser angioplasty guidance. Furthermore, plasma detection can be implemented both simply and inexpensively.
1. We have used the glycogen-depletion technique, combined with myofibrillar ATPase (mATPase) staining for muscle fibre type, to study the fibre-type composition of four skeleto-fusimotor (beta) units in cat peroneus tertius, namely, one beta dynamic (beta d) unit and three beta static (beta s) units. 2. Depletion of glycogen was observed in serial cross-sections of thirty-four beta-unit extrafusal muscle fibres of various types traced from origin to insertion. No fibre was depleted of glycogen throughout its length; depletion was restricted to a number of zones, usually about five. Oxidative (type I) and oxidative-glycolytic (type IIA) fibres were depleted for a significantly greater proportion of their total length than glycolytic IIB fibres. 3. The fibre-type composition of the beta d unit was determined by tracing its fibres from end to end. The muscle unit consisted of one intrafusal bag1 fibre and ninety-three extrafusal muscle fibres comprising seventy-six type I fibres, eleven IIC fibres, and six fibres that changed from IIC to I during the course of their length (IIC/I fibres). The extrafusal fibre-type composition was thus 81.7% I plus 18.3% IIC and IIC/I. 4. The three beta s units (beta s1, beta s2, beta s3) were all fast-contracting and fatigued rapidly. Identification of their extrafusal fibre types, made in 1 mm2 areas sampled from different parts of each unit, gave mixed compositions as follows: beta s1, IIB + 6.7% IIA; beta s2, IIB + 5.8% IIA; beta s3, IIB + 29.9% IIA. The intrafusal component of each unit included either one or two long chain fibres. 5. In a discussion of the results, the fact that the continuous stimulation of extrafusal muscle fibres does not deplete them of glycogen throughout their length is examined in relation to the work of others who have assumed that it did. With regard to the finding of mixed extrafusal fibre types in the beta units, a distinction is drawn between minimal (around 5%) and moderate mixing. It is suggested that minimal mixing may occur in any motor unit as the outcome of endplate degeneration with foreign replacement, but that moderate mixing indicates an on-going process of conversion from one fibre type to another which in the adult may prove to occur only among beta units.
Nerve regeneration promoters offer the possibility of enhancing recovery following nerve injury by increasing the numbers of regenerating axons and decreasing the period of tissue denervation. To date, recent studies have concentrated on evaluating the action of such promoters on the nerve itself and on the restoration of motor function. This study examines afferent regeneration by evaluating the recovery of muscle spindles and tendon organs after nerve injury and treatment with alpha-melanocyte stimulating hormone or nerve stimulation. Treatment was found to be effective in enhancing short-term recovery after nerve-crush injury in terms of increasing the rate of functional and morphological recovery. Following nerve section, there was an increase in the number of reinnervating axons compared with control values.
The Ia afferent axon innervating the muscle spindle is characterised by the dynamic nature of its response to stretch. Traditionally this response has been attributed to the properties of the bag1 intrafusal muscle fibre, a view supported recently by reports of stretch-activation of the bag1 fibre. Some spindle capsules lack a bag1 fibre and the Ia afferent axon terminates on the bag2 and chain fibres only. Such axons may be identified by their lack of an enhanced dynamic response to infusions of succinylcholine. In these experiments the responses to passive stretch of these axons have been investigated and found to be indistinguishable from those of the main Ia population. This implies that the bag1 fibre is not essential to the generation of the dynamic response of primary endings.
The tibial functional index has been employed to assess functional recovery in rats following nerve repair by direct coaptation under tension or by grafting. Recovery after direct repair of small to moderate gap sizes was better than that after grafting.
Muscle-spindle afferents are commonly classified according to their conduction velocity. Under certain conditions such classifications may not be feasible and another form of identification is required. In this study 5 tests, comprising either quantitative or qualitative criteria, have been evaluated as a means of classifying spindle afferents. The choice of these tests was made on the basis of predicted physiological differences arising from the structural variations in the endings. Prior conditioning of the spindles was found to enhance the distinction between the two types of afferent. All the tests generated similar identifications with a maximum of 10% of afferents being classified differently by any two tests.
An experiment has been performed on adult cats to investigate the sensory reinnervation of muscle spindles and tendon organs in peroneus brevis following immediate and delayed repair of the divided muscle nerve. The results demonstrate that delaying nerve repair for up to 6 weeks does not give rise to any significant detrimental effect on such reinnervation.
1. We have assessed the sensory reinnervation and recovery of regenerated muscle spindles in extensor digitorum longus (EDL) 6, 8 and 13 weeks after the muscle, with its nerve left intact, had been devascularized. Recordings were made from the dorsal roots of the responses of single afferent fibres to ramp-and-hold stretch of the regenerated spindles whose sensory reinnervation was subsequently examined in teased, silver preparations. 2. The spindle population in four normal EDL muscles ranged from 53 to 83 (mean 69); analysis of the afferent innervation of 166 normal b1b2c spindles showed that 23% had primary endings supplied by two Ia afferents. Regenerated spindles were identified as belonging to one of four groups in which afferents establish sensory endings on intrafusal muscle fibres in groups 1-3, but not in group 4. Sensory reinnervation was complete after 6 weeks recovery and similar proportions of group 1-3 spindles occurred after each recovery period, i.e. 58% after 6 weeks, 65% after 8 weeks and 62% after 13 weeks. We estimate that about half the original spindle population was lost owing to persistent ischaemic necrosis; that 30% regenerated and acquired functional afferent connections (group 1-3 spindles); and that the total loss of spindle afferents was over 60%. 3. The conduction velocities of the regenerated spindle afferents were very similar to those of normal EDL spindle afferents. The proportions that responded normally to ramp-and-hold stretch at the end of each recovery period increased from 58% after 6 weeks to 61% after 8 and 88% after 13. Other responsive spindle afferents were either predominantly phasic or only responded to supramaximal stretch. The proportions of these decreased as recovery progressed reducing from 19% after 6 weeks to 9% after 13 weeks in the case of those giving predominantly phasic responses and from 23% after 6 weeks to 3% after 13 weeks in the case of those unresponsive to physiological stretch. 4. The mean peak and held firing rates of regenerated spindle afferents responsive to 10 mms-1 ramp-and-hold stretches were all significantly lower than normal. There was no marked trend towards higher firing rates after longer periods of recovery through, considered separately, the mean peak firing rates of the normally responding afferents did show a distinct improvement. The mean dynamic and velocity indexes were not significantly different from normal. 5. The ratio of Ia:spindle II afferents, as identified by their responses to stretch, was 1:1.22 in the control animals and 1:1.26 in the experimental series.(ABSTRACT TRUNCATED AT 400 WORDS)
The functional recovery of cat muscle spindles has been examined following short periods of denervation and reinnervation. The restoration of function was more rapid than after longer periods of denervation though the firing rates showed a similar reduction except after the shortest recovery periods when a number of highly dynamic afferents were recorded.
Tests were made to ascertain the numbers of skeletofusimotor axons reinnervating muscle spindles following crush or section of the nerve to peroneus tertius in adult cats. After short periods of recovery there was no change in the proportion of skeletofusimotor axons compared with normal animals.
1. In adult cats, paired stimulations at short intervals were applied in ventral root filaments to single motor axons innervating the peroneus tertius muscle. Paired impulses were recorded from the muscle nerve simultaneously with the electrical and mechanical responses of the muscle portion of the motor unit (muscle unit). The interstimulus interval was gradually reduced in order to determine the minimum compatible with a full activation of the muscle unit by the second impulse. 2. For motor units of all physiological types, this minimum stimulus interval was the shortest interval allowing initiation and conduction of two impulses in the axon, that is, the absolute refractory period for conduction. Its duration ranged between 0.58 and 0.88 ms, displaying no correlation with the axonal conduction velocity. 3. The amount of tension enhancement produced by paired stimulations at the shortest interval varied with the type of the motor unit: it was largest for fast-fatigable units, intermediate for fast-resistant units and smallest for slow units. 4. Paired impulses elicited by paired stimulations at the shortest possible interval arrived near the muscle at a longer interval because the second impulse was conducted at a slower velocity. The minimum interval between arrival of impulses at the muscle depended on conduction velocity and on conduction distance. 5. In motor axons to peroneus tertius, paired impulses leaving the spinal cord at a mean interval of 0.78 ms arrived near the muscle separated by a mean interval of 1.90 ms. Since such an interval always allowed full activation of the muscle unit by the second impulse, this interval is longer than the refractory period of motor units in this muscle.
An analysis has been made of the numbers and distributions of muscle spindles and tendon organs in the three peroneal muscles of the lower hindlimb of the adult cat. Both peronei brevis and tertius were richly supplied with spindle capsules and tendon organs in comparison with peroneus longus and other muscles of the cat's lower hindlimb. A large number of the capsules in each muscle was involved in tandem linkages, some of these capsules comprising only a bag and some chain fibres. Such capsules were especially prevalent in peroneus tertius. The numbers of extrafusal muscle fibres inserting into each tendon organ indicated that the activity of each motor unit should be monitored by at least one tendon organ. The distributions of the receptors are discussed in relation to the proportion and density of oxidative muscle fibres.
After nerve injury muscles remain denervated until axons return to begin reinnervation and recovery. The delay between injury and recovery in human limb nerves averages 13 weeks after crush, and 16 weeks after transection and suture. In order to assess the effects of such long denervation periods on the recovery of cat muscle receptors, we crushed the common peroneal nerve and denervated peroneus brevis for 10 to 134 days; 39 days were allowed for reinnervation in each experiment. After 50 days denervation, the mean number of terminal bands in the regenerated spindle primary endings was 10.3 compared with a normal mean of 29.0. After 134 days, the mean was 0.6 and spindles were severely atrophied. Despite this most spindle afferent fibers continued to respond normally to ramp-and-hold stretch, abnormal responses being recognized as those that failed to maintain firing during the held phase of the ramp. After 50 days, 21% of spindle afferent fibers responded abnormally and about this proportion did so after all the longer denervation periods. Maximum afferent firing rates were all significantly lower than normal, and many afferent fibers fatigued more rapidly. Tendon organs were atrophied after 113 and 134 days and received fewer terminals, but their afferents fired apparently normally during muscle twitch. These results imply that the consequences of long-term denervation on human muscle spindles would be unlikely to affect the overall pattern of response to stretch of any Ia or II afferent fibers reinnervating them, though the quality of their response might be impaired.
Nerve injury was produced by application of dry ice to the common peroneal nerve. After 20 weeks, muscle-spindle primary endings responded normally to stretch and the spindles were found to have a fully functional fusimotor innervation.
Results are presented of examining the postcrush sensory reinnervation of cat peroneus brevis muscle spindles previously investigated physiologically by Hyde and Scott. It is shown that primary and secondary endings were successfully restored in their final form in the early stages of recovery. The primary endings were shorter than normal and had fewer transverse bands; 12% were judged to be hyperinnervated. Some secondary endings showed signs of growth through the primary region apparently designed to establish secondary terminals in the opposite pole. This is compared with the collateral regeneration of intact motor axons in partially denervated muscle. It is concluded that the defects observed in the regenerated sensory endings had no effect on their functional recovery.
We have studied the effects of chronic slight to moderate lead exposure on the renin-angiotensin-aldosterone system in normotensive man. Plasma renin activity (PRA), blood angiotensin I (AI) concentration, angiotensin converting enzyme (ACE) activity and aldosterone concentration were measured in 33 normotensive men, 25 of whom were occupationally exposed to lead. Positive exponential relationships were found between blood lead and PRA, AI, ACE and aldosterone. Linear relationships were observed between PRA and AI, and between AI and ACE. PRA, AI, and ACE did not significantly correlate with aldosterone. Chronic lead exposure enhanced PRA with a resulting increase in AI levels, which in turn may have produced a substrate-induced increase in ACE. The effects of lead on aldosterone may be mediated in part by an independent pathway. These changes may contribute to the development of hypertension in chronically lead-exposed man.