Objective To evaluate the cardioprotective effect of dexmedetomidine in patients undergoing off-pump coronary artery bypass grafting. Methods Forty-six ASA Ⅱ or Ⅲ patients aged 37-64 yr weighing 54-81 kg undergoing off-pump coronary artery bypass grafting were randomized into 2 groups ( n = 23 each): control group (group C) and dexmedetomidine group (group D) . Dexmedetomidine was infused at 0.5 μg·kg-1·h-1 starting after induction of anesthesia until the end of operation in group D. Radial artery was cannulated and Swan-Ganz catheter placed via right internal jugular vein. HR, MAP, mean pulmonary arterial pressure, pulmonary capilary wedge pressure, central venous pressure, and cardiac output were recorded and stroke volume index, left and right ventricular stroke work index, systemic vascular resistance and pulmonary vascular resistance were calculated at the beginning of operation (T1 ), immediately (T2 ) and at 30 min after reestablishment of coronary blood flow (T3 ) and the end of operation (T4 ) . Venous blood samples were taken before induction of anesthesia (T0 , baseline) , at T4 and 4 h (T5 ) and 24 h (T6 ) after operation for determination of plasma concentration of cardiac troponin I by ELISA. Results Stroke volume index and left ventricular stroke work index were significantly higher at T4 while systemic vascular resistance was lower at T34 in group D than in group C. Plasma cardiac troponin Ⅰ concentration was significantly lower at T6 in group D than in group C. Conclusion Dexmedetomidine infusion at 0.5 μg ·kg-1·h-1 during operation can protect myocardium in patients undergoing off-pump coronary artery bypass grafting.

ObjectiveTo investigate the effects of dexmedetomidine on cerebral oxygen and glucose metabolism in patients undergoing mitral valve replacement under cardiopulmonary bypass (CPB).Methods Fiftyeight ASA Ⅱ or Ⅲ patients of both sexes aged 32-64 yr weighing 52-90 kg undergoing mitral valve replacement were randomly divided into 2 groups (n =29 each): control group (group C) and dexmedetomidine group (group D).Dexmedetomidine was infused iv at 0.5 μg· kg- 1 · h- 1 starting after tracheal intubation until the end of operation in group D,while in group C equal volume of normal saline was infused instead of dexmedetomidine.Blood samples were collected from radial artery and jugular venous bulb for blood gas analysis and determination of glucose and lactate concentrations before CPB (T1,nasopharyngeal temperature =36 ℃ ),during CPB (T2,nasopharyngeal temperature =30 ℃ ),immediately and 30 min after restoration of spontaneous heart beat ( T3,T4 ).Arterial O2 content ( CaO2 ),arteriovenous O2 content difference ( Da-jvO2 ),cerebral extraction of O2 ( CEO2 ),arteriovenous glucose and lactate content differences (Da-jvGlu and Da-jvLac) were calculated.ResultsThe Da-jvO2 and CEO2 were significantly decreased at T2 in group D as compared with group C.There was no significant difference in CaO2,Da-jvGlu and Da-jvLac between the 2 groups.ConclusionDexmedetomidine can reduce cerebral O2 metabolism and help maintain the balance between cerebral O2 supply and demand but has no effect on cerebral glucose metabolism in patients undergoing mitral valve replacement under CPB.

Objective To investigate the efficacy of prostaglandin E1 administered via the pulmonary artery for treatment of pulmonary hypertension in patients.Methods Thirty ASA Ⅱ or Ⅲ patients undergoing offpump coronary artery bypass grafting complicated with pulmonary hypertension,with pulmonary arterial systolic pressure (PASP) ＞ 40 mm Hg,were randomly divided into 2 groups (n =15 each):administration via the central vein group (group C) and administration via the pulmonary artery group (group P).Anesthesia was induced with midazolam,etomidate,cisatracurium and sufentanil.The patients were tracheal intubated and mechanically ventilated.Swan-Ganz catheter was placed via the right internal jugular vein for monitoring of hemodynamic parameters after induction of anesthesia.The central vein and pulmonary artery were cannulated for infusion of prostaglandin E1.Prostaglandin E1 was infused at a rate of 20-50 ng· kg-1 · min-1 starting from the end of skin incision until PASP was decreased to 20-30 mm Hg.Heart rate (HR),mean arterial pressure (MAP),central venous pressure (CVP),PASP,pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were recorded at 5 rain before administration (To) and 5 min after administration (T1).The pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) were calculated.The amount of prostaglandin E1 consumed was recorded.Results Compared with group C,the amount of prostaglandin E1 consumed was significantly reduced,PASP and PVR were decreased at T1,while MAP and SVR were increased at T1 in group P(P ＜ 0.05).Conclusion Administration via the pulmonary artery can increase the potency of prostaglandin E1 for treatment of pulmonary hypertension and exerts no influence on the systemic hemodynamics.