Calcium-channel blockade in canine hemorrhagic shock.

The effect of verapamil (VER) resuscitation from shock on cardiac function, regional blood flow, as well as skeletal muscle transmembrane potential (TMP) and electrolyte redistribution were studied. Two hours of hypotensive shock in the dog significantly impaired cardiac function and coronary perfusion; TMP fell from 89.9 +/- 0.9 to 75.1 +/- 1.2 mV. Skeletal muscle (SMS) extracellular water decreased 40 +/- 2%, whereas intracellular sodium and chloride increased and intracellular potassium fell. Serum hypocalcemia was accompanied by a significant rise in total myocardial tissue calcium (from 312 +/- 20 to 415 +/- 21 micrograms/g dry wt; P = 0.01); total SMS tissue calcium tended to increase during this time (from 259 +/- 24 to 305 +/- 46 micrograms/g dry wt). After 2 h of shock, all dogs received shed blood and lactated Ringer solution (60 ml/kg); 21 dogs received VER, 20 micrograms/kg with fluid resuscitation; 21 dogs received fluid resuscitation only. Volume replacement improved hemodynamic function to a similar extent in all dogs. However, TMP, intracellular water, sodium, and potassium returned closer to base-line values after VER compared with dogs given only fluid resuscitation. SMS calcium was lower in VER dogs (148 +/- 4 micrograms/g) compared with dogs treated with fluid alone (322 +/- 24 micrograms/g, P = 0.01). Myocardial calcium fell in all dogs after volume replacement regardless of calcium-channel blockade (VER: 148 +/- 8, Ringer: 165 +/- 17 micrograms/g; P greater than 0.05). Our data indicate a potential role for calcium-entry blockade in the treatment of hemorrhagic shock.