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Báo cáo y học: " Administration of hydrogen sulfide via extracorporeal membrane lung ventilation in sheep with partial cardiopulmonary bypass perfusion: a proof of concept study on metabolic and vasomotor effects"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Administration of hydrogen sulfide via extracorporeal membrane lung ventilation in sheep with partial cardiopulmonary bypass perfusion: a proof of concept study on metabolic and vasomotor effects. | Derwall et al. Critical Care 2011 15 R51 http ccforum.eom content 15 1 R51 KS CRITICAL CARE RESEARCH Open Access Administration of hydrogen sulfide via extracorporeal membrane lung ventilation in sheep with partial cardiopulmonary bypass perfusion a proof of concept study on metabolic and vasomotor effects 1.2 t 1 t 1 1 1 1 Matthias Derwall Roland CE Francis Kotaro Kida Masahiko Bougaki Ettore Crimi Christophe Adrie Warren M Zapol1 Fumito Ichinose1 Abstract Introduction Although inhalation of 80 parts per million ppm of hydrogen sulfide H2S reduces metabolism in mice doses higher than 200 ppm of H2S were required to depress metabolism in rats. We therefore hypothesized that higher concentrations of H2S are required to reduce metabolism in larger mammals and humans. To avoid the potential pulmonary toxicity of H2S inhalation at high concentrations we investigated whether administering H2S via ventilation of an extracorporeal membrane lung ECML would provide means to manipulate the metabolic rate in sheep. Methods A partial venoarterial cardiopulmonary bypass was established in anesthetized ventilated fraction of inspired oxygen 0.5 sheep. The ECML was alternately ventilated with air or air containing 100 200 or 300 ppm H2S for intervals of 1 hour. Metabolic rate was estimated on the basis of total CO2 production VCO2 and O2 consumption VO2 . Continuous hemodynamic monitoring was performed via indwelling femoral and pulmonary artery catheters. Results VCO2 VO2 and cardiac output ranged within normal physiological limits when the ECML was ventilated with air and did not change after administration of up to 300 ppm H2S. Administration of 100 200 and 300 ppm H2S increased pulmonary vascular resistance by 46 52 and 141 dyn-s cm5 respectively all P 0.05 for air vs. 100 200 and 300 ppm H2S respectively and mean pulmonary artery pressure by 4 mmHg P 0.05 3 mmHg n.s. and 11 mmHg P 0.05 respectively without changing pulmonary capillary wedge pressure or cardiac output. .