Treatment of hemorrhagic shock with a new vasodilator

54 dogs and 14 rhesus monkeys were anesthetized with sodium pentobarbital (30 mg/kg, iv). 13 unanesthetized cross bred sheep were also used. Changes in arterial and central venous blood pressures, EKG, and heart rate were continuously recorded, and determinations of pH, pO₂ and pCO₂ were made hourly. Cortical EEG was also monitored in the sheep as an indicator of brain oxygenation. All animals were bled to a mean arterial pressure of from 45 to 50 mm Hg and maintained at that level for 8 hr. 3 hr after hemorrhage, animals were paired at random into either a control or a treated group. Control animals received no therapy, while the treated groups were given WR 2823, 50 mg/kg, iv. Prior to treatment, all animals showed progressive deterioration of the cardiovascular system, generalized acidosis, and pooling of blood. Controls continued to deteriorate and exhibited an early bradycardia, peripheral acidosis, and generalized pooling of the peripheral circulation. They expired from 8 to 24 hr. In contrast, treated animals showed slow yet sustained recovery of most parameters to prehemorrhage levels. At 8 hr, arterial blood pH was stable and venous pO₂ and arterial pCO₂ approached normal values. A significant improvement in survival populations was noted in all groups of treated animals.