Asian cardiovascular & thoracic annals
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Asian Cardiovasc Thorac Ann · Feb 2012
Recombinant activated factor VII for hemorrhage after pediatric cardiac surgery.
Postoperative bleeding is a common complication after pediatric cardiac surgery. Use of recombinant activated factor VII for intractable hemorrhage after cardiac, pediatric, and neurosurgery has been shown to decrease postoperative bleeding, but data in children are limited. This retrospective study analyzed 20 children <15 years-old who underwent cardiac surgery and received recombinant activated factor VII for refractory postoperative hemorrhage. ⋯ The median number of doses found to be effective in these children was 1.76. There were significant decreases in mediastinal chest tube drainage and the volume of packed red blood cells, platelet concentrates, and cryoprecipitate administered after recombinant activated factor VII. No complications were observed during the therapy.
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Asian Cardiovasc Thorac Ann · Feb 2012
Phosphodiesterase-5 inhibitor and rat lung ischemia-reperfusion injury.
To explore the protective effect of the phosphodiesterase-5 inhibitor, sildenafil, on lung ischemia-reperfusion injury, 30 rats were randomly divided into 3 groups of 10: a sham-operated group A, a lung ischemia-reperfusion injury group B, and a sildenafil preconditioned group C. A 0.1% sildenafil solution was administrated orally 2 h before establishing an in-vivo lung ischemia-reperfusion model in group C; 0.9% normal saline solution was used in the controls. The lung wet-to-dry ratio, malondialdehyde content, myeloperoxidase and nitric oxide synthase activity in groups B and C were significant higher than those in group A, while the partial pressure of oxygen in arterial blood and cyclic guanosine-3',5'-monophosphate content in groups B and C were significant lower than those in group A. ⋯ The expected histological and cytological changes were significantly alleviated in group C. Oral preconditioning with sildenafil prevented rat lung ischemia-reperfusion injury and improved pulmonary function. The mechanisms of this effect might be prevention of cyclic guanosine monophosphate degradation and inhibition of nitric oxide synthase activity.