Our aim was to examine the effects of small volumes (0.7-1 mL/kg intravenous) of 7.5% NaCl with different colloids on cardiac stability, hemodynamics, and mortality after severe hemorrhagic shock.
Methods: Male fed Sprague-Dawley rats (300-450 g, n = 48) were anesthetized and randomly assigned to one of six groups: (1) untreated (bleed only), (2) 7.5% NaCl, (3) 7.5% NaCl/6% FDA-approved Drug Library mouse dextran-70, (4) 7.5% NaCl/6% hetastarch (HES), (5) 6% HES alone, and (6) 7.5% NaCl/10% HES. Hemorrhagic shock
was induced by phlebotomy until the mean arterial pressure (MAP) was 35 mm Hg to 40 mm Hg and continued for 20 minutes until similar to 40% blood loss. Animals were left in shock for 60 minutes at 34 degrees C. 0.3 mL (<4% of shed blood) was injected as a 10 seconds bolus into the femoral vein. Lead II electrocardiogram, blood pressures, MAP, and heart rate were monitored.
Results: Untreated rats were highly arrhythmogenic with 38% mortality. 7.5% NaCl increased MAP from 39 mm Hg to 44 mm Hg with no severe
arrhythmias or mortality. Dextran-70 increased MAP from 38 mm Hg to 49 mm Hg, transiently increased QRS amplitude (1.5 times) and was arrhythmogenic affecting 50% of animals with no deaths. Addition of 6% HES to hypertonic saline resulted in aberrant arrhythmias and 38% mortality. Six percent HES alone was proarrhythmic and led to 38% mortality. 7.5% NaCl with 10% HES resulted in 100% mortality (p < 0.05) AZD8931 from arrhythmias within 5 minutes of MK-0518 datasheet resuscitation.
Conclusions: Small
volumes of 7.5% NaCl led to fewer arrhythmias and a 2.6 times survival benefit over untreated rats, and a partial resuscitation of MAP into the “”permissive range.”" Dextran-70 or HES in 7.5% NaCl were proarrhythmic and HES led to increased mortality (p < 0.05). Because optimal heart function is critical for successful resuscitation, care should be exercised when using dextran-70 or 6 and 10% HES in small volume hypertonic saline solutions for early hypotensive resuscitation.”
“OBJECTIVES: Approximately 40-60% of obsessive-compulsive disorder patients are nonresponsive to serotonin reuptake inhibitors. Genetic markers associated with treatment response remain largely unknown. We aimed (1) to investigate a possible association of serotonergic polymorphisms in obsessive-compulsive disorder patients and therapeutic response to selective serotonin reuptake inhibitors and (2) to examine the relationship between these polymorphisms and endocrine response to intravenous citalopram challenge in responders and non-responders to serotonin reuptake inhibitors and in healthy volunteers.