 When man or animal is exposed to organophosphorous poisons such as nerve agents, a vital nervous system enzyme colonesterase is inhibited. This enzyme splits or causes hydrolysis of acetylcholine. The resulting respiratory failure along with other effects will cause death within a few minutes due essentially to overstimulation. One symptom of organophosphorous poisoning is neuromuscular block, failure of muscles needed for respiration, inducing anoxia and cardiovascular collapse. Another symptom is bronchoconstriction, contraction of the smooth muscles of the tracheobronchial tree causing increased resistance to airflow. These physiological manifestations may be readily demonstrated. Prior to exposure, inspiration and expiration require little effort. However, when the bellows simulating the lungs is restricted, a decided increase in pressure is required to move air. Likewise, tightening the clamp on the apparatus which simulates the tracheobronchial tree decreases the airflow into the bellows. Consequently, increased pressure would be needed to move the same volume of air into and out of the bellows or into and out of the lungs of man. At the U.S. Army-Edward Arsenal Chemical Research and Development Laboratories, experiments to improve resuscitative methods and devices for treating nerve agent casualties constitute an important program. This goat has been anesthetized with pentobarbital sodium and an endotracheal tube inserted to facilitate control resuscitation. A pneumotachograph is attached to record airflow. The animal's vital signs such as blood pressure, electrocardiogram, airflow and transpulmonary pressure are recorded for later evaluation. Three resuscitative methods were tested during this experiment. First, a low pressure-cycled commercially available resuscitator not designed for nerve agent therapy. Second, a man's lungs used as a bellows to force air into the animal's lungs. This method is based on the moth-demoth principle of resuscitation. Third, a military model resuscitator is tested. This bellows pressure assembly works somewhat like a mechanical man as it applies ventilation. The device increases pressure only when needed to overcome resistance of the casualties airway. For an animal under conventional anesthesia, any of the three resuscitative methods will provide adequate ventilation to supplement breathing. Five times the lethal dose of nerve agent is administered. Colonesterase inhibition results in the usual symptoms of a nerve agent casualty. In particular, decrease in lung compliance, increased airway resistance, generalized muscular twitching and both thick and copious salivation. The commercial resuscitator is a low pressure-cycled device not adequate to provide sufficient inflating pressure to overcome the constriction of the bronchiolar musculature. This suck and blow device cycles at a low pressure limit and activates rapidly, but does not move air, as indicated by the rapidly oscillating needle on the pressure gauge. The mouth-to-tracheal tube method does overcome the smooth muscle constriction and provides proper ventilation by raising the pressures applied to the lungs. The operator is aware of his efforts because he can observe the excursions of the chest, indicative of air movement into the lungs. As he inflates the animal's lungs, he can sense the pressure necessary to overcome the increased lung airway resistance. After allowing the nerve agent to again take full effect, the military resuscitator, which is volume-limited pressure-cycled, is attached. This too has sufficient reserve pressure to overcome the broncho constriction. The impedance or resistance offered by the animal determines the pressure required to give adequate ventilation. As resistance to airflow increases, higher pressures are needed to affect air movement. When the military model is made a more patent airway, the commercial resuscitator is temporarily able to function. But the smooth muscles will constrict again unless antidotes are administered. The antidotes are atropine and 2-pan chloride. Atropine, the classic drug, is administered to block the adverse effects of accumulated acetylcholine. No anticholinergic drug has been found to warrant replacement of atropine in the treatment of nerve agent poisoning. The 2-pan chloride is used to reduce the neuromuscular block. This reactivator helps in quicker regeneration of the cholinesterase, which has been inhibited by the nerve agent. The nares, which may be hyperactive during labored breathing, show a response to therapy by moving less. Experimentation has shown these drugs to be apparently successful in treating anticholinesterase intoxication. But adequate ventilation is also vital, and no matter what method of resuscitation is used, the airway must be open. In the light of this knowledge, there is genuine promise that superior and more effective resuscitative devices and procedures can be developed.