Increase In Passive Force Research Articles

Afferent mechanisms for the reflex response to imposed ankle movement in chronic spinal cord injury.

We have reported earlier that externally imposed ankle movements trigger ankle and hip flexion reflexes in individuals with spinal cord injury (SCI). In order to examine the afferent mechanisms underlying these movement-triggered reflexes, controlled ankle movements were imposed in 17 SCI subjects. In 13 of these subjects, reflex torques were recorded at the hip, knee and ankle in response to 5 ankle movement ranges, and 4 movement speeds. Subjects were tested using both ankle plantarflexion and dorsiflexion movements. The principal outcome measure, peak hip flexion torque of the induced reflexes, was used for comparing the effects of movement range and speed on the reflex response. We found that movement-triggered reflexes were sensitive to the angular range of ankle deflection, but insensitive to the velocity of the movement. Movement amplitudes sufficient to trigger hip and ankle flexion were routinely associated with increases in ankle passive force, suggesting that force-sensitive receptors participated in the reflex response. However, increases in angular range also corresponded to increases in muscle length, making it difficult to distinguish whether the response was triggered by a load-sensitive receptor (e.g., Golgi tendon organ or muscle free nerve ending) or a position-sensitive receptor responsive to absolute ankle angle (e.g., muscle spindle secondary afferent). The absence of velocity dependence of the reflex suggested that spindle Ia afferents were not major contributors. These results suggest movement-triggered reflexes originate in muscle receptors that are sensitive to either absolute muscle length, to muscle force or to both. Although receptors that are sensitive to absolute muscle length cannot be excluded with certainty, the finding that reflex responses require that ankle movements elicit an increase in passive force argues for a prominent role of nonspindle mechanoreceptors, such as group III/IV muscle afferents. These afferents are activated preferentially as muscles are stretched to near maximum length, and they appear to have potent reflex effects in spinal cord injury.

The Effect of Raveron on the Detrusor Muscle

Raveron (a European pharmaceutical consisting of swine prostate extract and m-creosal) was studied in vivo in female mongrel dogs and in vitro bladder studies were conducted on male New Zealand rabbits.Intravenous administration of raveron reduced both the passive and active pressure in dog detrusor in vivo. It did not act in a dose dependent fashion.Chronic treatment with raveron for three to four months caused changes in rabbits with vesical neck obstruction. An increase in contractility along with a reduced rate of increase in passive force (measurement of bladder stiffness) was observed in relation to obstructed rabbits without treatment. Parallel morphological changes were also observed in this group, consisting of increased muscular hypertrophy, decreased bladder wall thickness and reduced collagen content (readings taken from Masson-Trichrome sections). No influence was observed with bladder specimens from rabbits with six to eight week vesical obstruction or normals that received treatment.In vitro dose response studies showed that a 3.3% dose of raveron significantly reduced passive force in two groups (treated normals and treated rabbits with six to eight week vesical obstruction). Pharmacology studies with potassium chloride and acetylcholine suggest that raveron acts as a calcium antagonist by blocking the influx of extracellular calcium.

Effect of Vesical Outlet Obstruction on Detrusor Contractility and Passive Properties in Rabbits

Outlet obstruction was induced in 16 New Zealand rabbits by implanting a polyethylene tube (20 F) for a period of three months. The tube was slit longitudinally and placed around the bladder neck, between the ureters and vasa deferentia. It was left open to induce moderate obstruction and closed by a suture to induce severe obstruction. The animals were studied by cutting consecutive rings from each bladder, which were subjected to the following studies: morphology, contractility and mechanical properties.Morphology. Histology sections of the rings, studied by Hematoxylin and Eosin and Masson-Trichrome stains, demonstrated smooth muscle hypertrophy in moderate obstruction, while hyperplasia was the predominant response in severe obstruction. The average nuclear count per square millimeter of smooth muscle was 251 in controls, 87 in moderate obstruction and 705 in severe obstruction. Bladder wall thickness was significantly increased after both moderate and severe obstruction, as compared to controls.Contractility and mechanical properties. Each ring was tested in a muscle chamber under conditions of maximal electrical stimulation (100 V, 2ms, 40Hz). For each ring, full force-length relationships (active and passive) were obtained by stretching the rings in successive increments until length of maximal active force development was reached. Force was normalized per unit cross-sectional area (stress), and length according to a “reference” underformed state (per cent of unloaded length). The maximum active stress of the rings was taken as a measure of bladder contractility, and the rate of increase in passive force as a measure of detrusor stiffness. In all groups, the body of the detrusor exerted better contractility, as compared to a rigid, less contractile base. In the obstructed groups, detrusor contractility was significantly decreased at the body level, with increased stiffness, as compared to controls. The length at which maximum contractility was exerted, however, increased in moderate obstruction, and decreased in severe obstruction.