The entry of calcium (Ca++) into ischemic cells is the first of a series of steps leading to irreversible cellular damage. This study examined the ability of verapamil, which may delay or diminish the injury-induced influx of Ca++, to prolong survival in three groups of chronically instrumented dogs subjected to a single, rapid hemorrhage. In untreated animals (group 1, N = 6), hemorrhage decreased mean arterial blood pressure from 101 +/- 3 mm Hg to 23 +/- 2 mm Hg. Following hemorrhage, arterial pressure recovered to 61 +/- 5 mm Hg before the secondary fall (decompensation) occurred. As decompensation progressed, arterial pressure fell to 25 mm Hg, and the animals were euthanized. In group 2 (N = 6), verapamil treatment (2 mg bolus, 1 mg/hr infusion) was initiated 30 minutes before the hemorrhage. This treatment significantly increased both the time to decompensation (184 +/- 15 minutes vs 72 +/- 9 minutes) and survival time (262 +/- 20 minutes vs 128 +/- 8 minutes). Arterial pressure recovery during the first 60 minutes following hemorrhage, however, was not affected by the verapamil pretreatment. Verapamil treatment immediately after the hemorrhage (group 3, N = 4) increased the survival rate to 75% (three of four animals). These results indicate that calcium channel blockade may be a useful initial intervention in the treatment of hemorrhagic shock.