Although we did not expose the pigs to OP in this preliminary study, we followed local clinical recommendations for the

treatment of OP casualties, which includes hyperventilation, to reduce OP-induced hypercapnia. In both cases respiratory rate was kept on 30 breaths per minute, and ventilation lasted for 25 minutes, with no oxygen supplementation. Both devices were effective in ventilating the animals. Physiological parameters were monitored continuously and no significant changes were observed. Vital signs included heart rate derived from ECG, O2 saturation by pulse-oximetry placed on the animals’ tails, non-invasive blood pressure and EtCO2. Ventilation was monitored by watching chest wall movement and blood saturation. Restrained pigs were fitted with an intravenous line Apoptosis Compound Library order and anesthetized using Propofol (3.5 mg/kg, iv) to enable the insertion of an arterial cannula into the pigs’ ear. About 40 minutes later, when the pig regained full neck muscle tone,

exposure to paraoxon was performed. An intramuscular dose of 600 μg/kg paraoxon (the equivalent of 1.4LD50) was followed eight minutes later by a single administration of atropine (0.05 mg/kg, i.m.) alone, to simulate a realistic scenario, in which severe respiratory distress is likely to develop [21]. Following the paraoxon exposure three possible treatments were evaluated: Ventilation SCH772984 support using the biphasic cuirass device (Cuirass group, n = 7), ventilation support using a bag-valve mask (Mask group, n = 7) and a control

group that received no ventilation support (Control, n = 9). No oxygen enrichment was provided (FiO2 = 0.21). Ventilation was initiated 15 minutes following exposure and regardless of clinical manifestations was terminated 25 minutes later. Rate of ventilation was kept at 30 breaths per minute in O-methylated flavonoid both groups, with the same MRTX settings as in the preliminary study. Animals were closely observed for chest wall movement and post exposure signs. The following parameters were monitored continuously for one hour after paraoxon exposure: ECG, Heart rate (derived from ECG), O2 saturation by pulse-oximetry placed on the animals’ tails, and blood pressure by using an arterial line placed in the animals’ ear. Arterial blood gases (arterial pO2, arterial pCO2, arterial pH and BE) were collected from the arterial line before poisoning (0’) and 10, 20, 30, 40, and 50 minutes following exposure. The following clinical signs were recorded every 10 minutes during the first hour post exposure and 24 h later: fasciculation, salivation, teeth clenching, tremor, dermal patches, convulsion, and respiratory distress. The score ranged from 0 (no effect) to 3 (severe effect). Time of death within the 24 h was also recorded. All animals were allowed to recover with no further help, for a period of 24 hours. After 24 hours all animals were euthanized using i.v. overdose of sodium pentobarbital (200 mg/ml).