We investigated whether the adenosine triphosphate (ATP)-sensitive K+ (K(ATP)) channel activation by bimakalim, at concentrations devoid of both negative inotropic and action-potential duration (APD) shortening effects, might exhibit myocardial protection after hypoxia and reoxygenation in human atrial myocardium by using 112 preparations. The recovery of contractility of human atrial trabeculae, subjected either to short-duration (5 min) or to long-duration (60 min) and severe (high pacing rate) hypoxia followed by reoxygenation, was assessed by challenging with dobutamine. Treated preparations were exposed to 10 or 100 nM bimakalim, 1 microM glibenclamide, or both before hypoxia. Variations of isometric developed tension (%DT) or APD90 were studied. At concentrations <100 nM, bimakalim showed no negative inotropic effects and did not modify significantly APD90 either in normoxia or in hypoxic conditions. In the short-duration hypoxia protocol, preparations treated with bimakalim showed a dobutamine-induced %DT increase significantly higher (p < 0.001) than in controls and similar to that observed in the absence of hypoxia. This bimakalim effect was blocked by glibenclamide. In the long-duration hypoxia protocol, %DT after dobutamine was 50% of that observed in normoxic preparations. Preparations treated with bimakalim showed after dobutamine %DT more than twofold above controls (p < 0.001), whereas in the glibenclamide group, recovery of DT with dobutamine remained 50% of what observed in normoxia (p < 0.001). In conclusion, exposure to hypoxia (either short- or long-lasting) and reoxygenation affects contractility of human atrial myocardium with pronounced reduction of the positive inotropic action of dobutamine. Pretreatment with bimakalim restores the response expected in the absence of hypoxia, and glibenclamide blocks the effect of bimakalim or further impairs the response to dobutamine when used alone before long-duration hypoxia. Evidence is provided for protective effects of the K(ATP) opener bimakalim on the human myocardial contractile function in conditions of hypoxia/reoxygenation, at concentrations at which negative inotropism and APD90 shortening are not contributory.
We assessed some Japanese bedding on the assumption of the effects of air trapping using an infant mannequin. The change of CO2 concentration in the airway of a mannequin head placed on bedding was continuously monitored using a CO2 analyzer during simulated breathing. To compare the level of CO2 dispersal among different items of bedding, CO2 half time (t1/2) values were used. The t1/2 values were calculated by measuring the time required for the expired percent CO2 to reach 1/2 the initial percent end-tidal PCO2. We also measured softness and resistance to airflow (R) of the same items. As for the bedding, 4 types of futon and several types of bottom sheets/towels were combined. The t1/2 value in supine position was 9.8 seconds. When the model was placed prone on futon, the t1/2 values increased to 14.1 seconds (hard mattress type)--17.2 seconds (soft cotton-like futon). With respect to present Japanese baby futon (hard mattress type), there may be a relatively low potential for rebreathing to occur, compared with soft futon. In every case, the t1/2 value was prolonged by the use of a towel spread on the futon. CO2 dispersal may depend not only on the softness of the futon, but also on the combination of bottom sheet/towel and mattress. There was no relationship between R values and t1/2 values. The potential of rebreathing increased in face down position among all bedding, and supine position was the best CO2 dispersal position.
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