An animal model of chemotherapy-induced vagal neuropathy.

In this study we establish an animal model of chemotherapy-induced autonomic neuropathy. Rats were injected with vincristine (30 and 100 microg/kg/day) for 2 weeks while cardiovascular parameters were collected telemetrically. Vincristine caused a dose-dependent decrease in vagal activity expressed by decreased parasympathetic parameters of heart rate variability, without expression of damage to the cardiac sympathetic innervation.

Vagal damage enhances polyneuropathy pain: additive effect of two algogenic mechanisms.

While the major pain generation in polyneuropathy is in the somatic peripheral nerves, pathologies at visceral nerves might be involved as well. Decreased vagal afferent activity is known to disinhibit pain perception, and therefore might contribute to pain in polyneuropathy. In this study we explored this potential contribution by employing a rat model of vincristine (VCR)-induced pain after sub-diaphragmatic vagotomy (SDV).

Electrical activity from rat corpora is affected by pharmacological but not mechanical intracorporal manipulation.

Smooth muscle electromyographic (EMG) recording from the corpora cavernosa is a potentially useful clinical tool for the diagnosis of impotence. Controversy still exists regarding the nature of this signal, which could be resolved using animal models. The signal recorded from denuded rat corporal surface was Fourier transformed, and power at 0.

Smooth muscle electromyography from rat urethra.

Electrical signals recorded from the penis have been suggested as reflecting electromyographic activity in the underlying smooth muscles. In order to verify this assertion, we manipulated the signal recorded from rat urethra surface. Stimulation of the pelvic nerve brought about a reduction of activity (965 +/- 826 to 166 +/- 143 microV, root mean square of the power at range 0.