Jacek Przybylski, Artur Stolarczyk, Łukasz Sawionek, Klaudiusz Papierski, Małgorzata Łukowicz

Jacek Przybylski, Artur Stolarczyk, Łukasz Sawionek, Klaudiusz Papierski, Małgorzata Łukowicz – The mechanisms of functional hyperemia in spinal nerves. Fizjoterapia Polska 2003; 3(2); 164-174

Abstract
Background. The purpose of this research was to examine the impact of the stimulation of heat and pain receptors on the surface of the sole of the foot on the quantity of blood flow in the sciatic nerve in rat and rabbit. An attempt was also made to examine the phenomenon of reactive hyperperfusion in the sciatic nerve of both species in subjects with experimentally evoked diabetes and in rats with genetically conditioned hypertension (SHR). Material and methods. The experiments were performed on 180 male rats of natural strain, 20 male Okamoto-Aoki rats with genetically conditioned hypertension (SHR), and 28 rabbits. The rats were anesthetized with chlorohydrate, 32 mg/kg, administered peritoneally, while the rabbits were anesthetized by intramuscular administration of ketamine (20 mg/kg) and xylazine (5 mg/kg). During the experiment the animals’ temperature was controlled. An ALF21 flow meter was used to measure flow in the sciatic nerve. Results. An increased o thermode temperature to 70°C caused no statistically significant changes in either the volume of blood flow in the sciatic nerve or the vascular resistance in this nerve. When the temperature exceeded 70°C there was a significant decline in the vascular resistance in the sciatic nerve, accompanied by a significant increase of blood flow in this vascular region. A further thermode temperature increase did not cause any intensification of changes in these parameters. The dependency between the volume of the thermal stimulus and the response of the sciatic vessels did not differ in either rats or rabbits. The application of a painful stimulus on the surface of the sole of the foot caused a significant increase in flow in the ipsilateral sciatic nerve. This vascular reaction disappeared after the KATP channels were blocked, as well as nitrous oxide synthase. The phenomenon of functional hyperperfusion in the sciatic nerve in response to a painful stimulus did not occur in the animals with experimentally induced diabetes or in the rats with genetically conditioned hypertension. Conclusions. 1. Increased bioelectrical activity in spinal nerves causes reactive hyperemia. 2. Reactive hyperemia in spinal nerves is associated with excitation of thin C fibers. 3. The disappearance of reactive hyperemia in response to a pain stimulus is a sensitive sign of neuropathy. 4. One of the factors responsible for reactive hyperemia is the opening of ATP-dependent potassium channels.

Key words:
functional hyperemia, Spinal Nerves, pain receptors

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