Stretch of mammalian nerve in vitro: Effect on compound action potentials

Abstract

Stretch of nerve has been reported to decrease the amplitude of the compound action potential (CAP) with a complete block appearing in approximately 30 minutes. But for the most part, those experiments were carried out in vivo , and it is generally accepted that the failure of responses was due to a closure of vessels supplying the nerve with a resulting ischemia and anoxia. These studies were undertaken to determine if stretch of nerve has effects that are independent of interference with its vascular supply. In the studies, lengths of rat sciatic and dog peroneal nerves were removed and placed in a chamber supplied with oxygen in which their CAPs were continuously elicited and recorded. This in vitro preparation obviated interference with the nerve's metabolism on stretching. We have previously shown that the form change termed 'beading,' appearing within 10 seconds and reversing as quickly on relaxation, can be elicited with tensions of only several grams. We wished to determine if stretch adequate to produce beading could alter CAPs with the same rapidity. Tensions below 2 g had little effect. On applying tensions of 10-100 g, levels well above those needed to bead the fibers, both increases and decreases of CAP amplitude were seen. The changes occurred within 10 seconds of stretch application, the time at which beading arises with stretch. Although the decreases of CAP amplitudes could be accounted for by beading, the degree of CAP change did not correspond to the amount of tension applied. We hypothesize that the constrictions in the beaded fibers increase axial resistivity and diminish local currents so as to block conduction. The lack of an increasing degree of decreased CAP amplitude with increases in tension is ascribed to the inhibition of elongation offered by the collagen fibrils present in nerve. Collagenase applied to nerves allowed a further increase in length, producing a 'hyperbeading,' showing much longer lengths of beading constrictions on stretch. This would further increase axial resistance and is taken to account for the greater decreases of CAP amplitudes seen following collagenase treatment. To account for those cases where increases of CAP amplitude were seen on stretch, we hypothesize that stretch can also cause an increase in the excitability of the nodes. The outcome of stretch in any given nerve would be the resultant of two opposing actions; beading of the internodes causes a decrease of local currents leading to block of CAPs, while an increased excitability of the nodes acts to augment the responses.

Peripheral nerves in the rat exhibit localized heterogeneity of tensile properties during limb movement

“…Mechanical tension is an important issue for reconstructive surgery and nerve repair and consequently a number of studies have investigated changes in tension in human cadaveric nerves during limb movement (Kleinrensink et al 1995; Wright et al 2001; Hicks & Toby, 2002; Byl et al 2002). Previous investigators have sought to place values on the degree to which nerves can be stretched before they become compromised through changes in conduction, blood flow, or integrity of intraneural structures (Lundborg & Rydevik, 1973; Rydevik et al 1990; Wall et al 1992; Kwan et al 1992; Millesi et al 1995; Ochs et al 2000). These studies have failed to agree on an absolute strain‐limit value, chiefly due to (i) difficulties in determining original length and disagreement on what constitutes nerve resting tension and (ii) differences in post mortem treatments (fixation, ligation, incubation, etc.).…”

“…Numerous studies have been undertaken to define the limits to which nerves can be stretched before their function is compromised. It is known that straining nerves beyond the physiological tension range can alter their conduction properties (Wall et al 1992; Ochs et al 2000) and intraneural blood flow (Lundborg & Rydevik, 1973) and can result in permanent loss of function believed to be related to a breakdown in integrity of the perineurium (Rydevik et al 1990; Kwan et al 1992).…”

The effect of stretching on nerve excitability

“…Rapid conduction loss has been observed at only 6.2% nerve strain (13). (40) argued that the decrease in action potential amplitude could be a side effect of stretching by reducing the supply of the axons leading to ischemia and anoxia after a long stretch. This might be true for some experiments, but is unlikely for experiments during which the onset of the decrease in excitability is fast and reversible.…”

Revisiting the Hodgkin-Huxley and Fitzhugh-Nagumo models of action potential propagation

“…will be reduced, resulting in the reduction of the action potential conduction velocity In this connection, it is pointed out that Wall et al [36] noticed a reversible reduction in the compound action potential (CAP) amplitude for a 6 % elongation of rabbit tibial nerves in stretching experiments in vivo, which is under the ischemia limit and without structural changes of the nerves. Similarly, Ochs et al [37] performed in vitro stretching experiments on canine peroneal nerves and rat sciatic nerves. After the possibility of nerve ischemia and hypoxia was excluded, a reversible (for a small deformation) reduction in the CAP amplitude and beading appearance of axons were observed.…”