We have previously shown that
gamma-hydroxybutyrate (GHB) protects the small intestine against
ischemia/reperfusion injury. This study examined the effects of GHB on cardiovascular function and intestinal microcirculation following
hemorrhage.
Hypotension was induced in control group of hamsters by controlled
hemorrhage to a mean arterial pressure (MAP) of 40 mm Hg. Following 60 minutes of
hypovolemia the shed blood was returned. This procedure resulted in complete intestinal mucosal microvascular stasis 2 hours following the return of shed blood. A second group of animals was treated with GHB (600 mg/kg
body weight) and, despite the loss of 37% of total blood volume, GHB treatment completely prevented the microcirculatory stasis, following the reinfusion of shed blood. In male Wistar rats treated with GHB (200 mg/kg) after the induction of
hemorrhage, blood pressure rapidly increased to pre-
hemorrhage levels following treatment, even though the shed blood was not returned. Cardiac output (CO) also increased to pre-
hemorrhage levels.
Sodium chloride solution, in the same molar concentration as GHB (23% NaCl), produced much smaller, but statistically significant, increases in MAP and CO. In animals given an equal volume of
normal saline, a gradual increase in MAP was observed, reaching statistical significance at 75 minutes following treatment. Three hours following
hemorrhage, serum levels of
creatine kinase were 3-fold higher, whereas
aspartate aminotransaminase and
alanine aminotransferase levels were 2-fold higher in both
normal saline and hypertonic saline-treated animals than in GHB-treated animals. These experiments suggest that GHB can prevent ischemic complications following a
hypovolemic episode and may improve survival following severe
hemorrhage.