It is presumed that systemic hypotension resulting from high concentration of 1, 1, 1-trichloroethane (1, 1, 1-TCE) inhalation may be induced by functional depression of the central nervous system. However, it is still uncertain the possibilities that one of the site of action where 1, 1, 1-TCE acts in systemic hypotension existed in the portion without the central nervous system. The present experiment was performed to investigate the role of the peripheral vessels as a site of action in the systemic hypotension following 1, 1, 1-TCE inhalation.
The right hindlimb of a dog anesthetized with sodium pentobarbital (25-30 mg/kg, intravenously) was amputated at the central level of the thigh bone leaving muscles and nerves. The isolated hindlimb was perfused with blood at a constant flow rate using a pump. Venous blood circulated in the isolated hindlimb was returned to the femoral vein. To measure the perfusion pressure of the isolated hindlimb, a small catheter was inserted into the artery and was connected to a pressure transducer (Nihon Kohden, MPU-0.5). In this perfusion experiment, the changes in perfusion pressure following 1, 1, 1-TCE inhalation are shown to be the reaction of peripheral vessels only as the site of action of 1, 1, 1-TCE. In other words, the effects of 1, 1, 1-TCE on central nervous system could be completely removed. Various concentrations of 1, 1, 1-TCE vapor, made by an inside circuit vaporizer, were inhaled during a period of approximately 2 min. Perfusion pressure was continuously recorded before, during and after the termination of inhalation. Concentrations of 1, 1, 1-TCE in the inspired air were measured by gas chromatography.
In an acute inhalation experiment, a fall in perfusion pressure was observed following 1, 1, 1-TCE inhalation. The fall in perfusion pressure gradually returned to the pre-inhalation level. The threshold concentration of 1, 1, 1-TCE to produce the fall in perfusion pressure was about 0.4 to 0.5% in inspired air, and a dose-response relationship was observed between the fall in perfusion pressure and the concentrations of 1, 1, 1-TCE exceeding the threshold level. The fall in perfusion pressure resulting from 1, 1, 1-TCE inhalation in concentration of 2.0 to 3.8% was not affected by pre-treatment with atropine (1.0 mg/kg, iv), propranolol (2.0 mg/kg, iv) or phentolamine (1.0 mg/kg, iv).
From these results, the following conclusions were arrived.
1) One of the sites of action for 1, 1, 1-TCE may be the peripheral vessels, and the peripheral vasodilator effect as a site of action may be related to systemic hypotension following 1, 1, 1-TCE inhalation.
2) The threshold concentration of 1, 1, 1-TCE required to induce a peripheral vasodilator effect is 0.4 to 0.5% in inspired air, and a dose-response relationship exists between the concentration of 1, 1, 1-TCE and peripheral vasodilatation.
3) The peripheral vasodilator effect as a site of action for 1, 1, 1-TCE is not related to the sympathetic and parasympathetic nervous system.
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