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Verapamil treatment of canine hemorrhagic shock
R G Carroll1, S G Iams, P L Farmer
1Department of Physiology, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4354.
Insights
Verapamil, a calcium channel blocker, significantly prolonged survival and delayed decompensation in dogs experiencing hemorrhagic shock. This suggests calcium channel blockade is a promising treatment for this condition.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Pharmacology
Background:
- Calcium influx into ischemic cells initiates irreversible damage.
- Hemorrhagic shock leads to cellular damage and decreased blood pressure.
- Verapamil may inhibit calcium influx, potentially mitigating injury.
Purpose of the Study:
- To investigate verapamil's effect on survival during hemorrhagic shock.
- To determine if verapamil delays or reduces calcium influx-induced injury.
- To assess verapamil as an intervention for hemorrhagic shock.
Main Methods:
- Utilized chronically instrumented dogs subjected to rapid hemorrhage.
- Administered verapamil before or after hemorrhage in different groups.
- Monitored mean arterial blood pressure, decompensation time, and survival time.
Main Results:
- Verapamil pretreatment significantly increased time to decompensation and survival time.
- Verapamil initiated post-hemorrhage improved survival rate to 75%.
- Verapamil did not affect initial arterial pressure recovery post-hemorrhage.
Conclusions:
- Calcium channel blockade with verapamil shows potential as an initial treatment for hemorrhagic shock.
- Verapamil's ability to prolong survival suggests a role in managing ischemic cellular damage.
- Further research into verapamil's efficacy in hemorrhagic shock is warranted.
Abstract:
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.