A bioassay model has been developed to test the time course and degree of in capacitation produced by exposures to thermal decomposition products from polymeric materials. A battery of physiological tests was used during separate exposures to atmospheres of carbon monoxide, hydrogen cyanide, hypoxia, hypercapnia and heated air. Each atmosphere was designed to simulate one aspect of the conditions commonly encountered in fires. Measurements were made of the animals' respiration, cardiac function and respiratory blood gases. Neurological function was monitored by measurements of the elec troencephalogram, auditory cortical evoked potentials and peripheral nerve con duction velocity. Hypoxia (10% oxygen) caused muscle weakness, a decrease in nerve conduction velocity, abnormal cardiac function accompanied by a fall in blood pressure and central nervous system depression. At 1000 ppm carbon monoxide, venous carboxyhaemoglobin levels reached 30%. There was a reduc tion of nerve conduction velocity and in some cases severe central nervous system depression. At 60 ppm hydrogen cyanide had a slight depressive effect on the central nervous system, while at 80-150 ppm severe central nervous system depression and incapacitation occurred. The main result of 5% carbon dioxide exposure was a three-fold increase in respiratory minute volume. It is concluded that the model is capable of detecting early physiological signs of in capacitation induced by fire conditions. It is suggested that exposures to a com bination of hydrogen cyanide and carbon monoxide with accompanying changes in cerebral blood flow during attempts to escape from fires may be a cause of col lapse and subsequent death.
Network interactions within the canine intrinsic cardiac nervous system: implications for reflex control of regional cardiac function
