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Biomedical subjects

R Tegnèr

Publications and source records attributed to R Tegnèr.

2 recordsLinked to original sources

Experimental uremic neuropathy. Part 1. Decreased nerve conduction velocity in rats.

Acute and chronic renal failure were induced in adult male albino rats by conventional surgical methods. The glomerular filtration rate of rats with chronic uremia was reduced to approximately 15% of normal. Despite this drastic degree of renal failure, the motor nerve conduction velocity (MCV) increased from 47.5 +/- 6.4 m/s, preoperatively, to 55.6 +/- 4.0 m/s after 4 weeks. In rats with acute uremia, MCV decreased from 51.4 +/- 3.0 m/s to 45.2 +/- 2.7 m/s after 48 h. The conduction velocity, measured in vitro of excised sciatic nerves was 55.2 +/- 4.4 m/s in acute uremia and 64.7 +/- 4.7 m/s in a control group. There was no difference in the refractory period between these groups. It is concluded that this decrease in the nerve conduction velocity was not caused by changes in the composition of the extracellular fluid but rather by changes in the nodal membrane function.

Acute Kidney Injury↗

Experimental uremic neuropathy. Part 2. Sodium permeability decrease and inactivation in potential clamped nerve fibers.

Potential recordings and potential clamp of isolated myelinated fibers from the sciatic nerve of acutely uremic rats showed a marked decrease in excitability related to a decrease in the specific Na permeability (P Na) of the nodal membrane. Mean value of the available P Na in the resting node of the uremic rats was 24% of the P Na in a control group. This change explained the decreased nerve conduction velocity in the acutely uremic rat. The Na current reversal potential was decreased in some fibers, reflecting an axoplasmic Na accumulation. The decrease in P Na was to a large extent caused by an increased inactivation, due to a negative shift (about 10 mV) of the steady state inactivation curve along the potential axis. The activation of P Na was similarly shifted (about 10 mV) to a more negative potential region. Such changes may be caused by elevated intracellular [Ca], suggesting a disturbance in Ca metabolism or an intracellular accumulation of cationic metabolites (which possibly have a similar effect) in rats with acute uremia.

Acute Kidney Injury↗