17 research outputs found

    MOESM8 of Effect of nitric oxide on postoperative acute kidney injury in patients who underwent cardiopulmonary bypass: a systematic review and meta-analysis with trial sequential analysis

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    Additional file 8. Forest plot for the risk of postoperative hemorrhage, i.e., requiring blood transfusion after the operation or reoperation. RR, risk ratio. CI, confidential interval; NO, nitric oxide

    Image3_Non-carbonic buffer power of whole blood is increased in experimental metabolic acidosis: An in-vitro study.tiff

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    Non-carbonic buffer power (βNC) of blood is a pivotal concept in acid-base physiology as it is employed in several acid-base evaluation techniques, including the Davenport nomogram and the Van Slyke equation used for Base excess estimation in blood. So far, βNC has been assumed to be independent of metabolic acid-base status of blood, despite theoretical rationale for the contrary. In the current study, we used CO2 tonometry to assess βNC in blood samples from 10 healthy volunteers, simultaneously analyzing the electrolyte shifts across the red blood cell membrane as these shifts translate the action of intracellular non-carbonic buffers to plasma. The βNC of the blood was re-evaluated after experimental induction of metabolic acidosis obtained by adding a moderate or high amount of either hydrochloric or lactic acid to the samples. Moreover, the impact of βNC and pCO2 on the Base excess of blood was examined. In the control samples, βNC was 28.0 ± 2.5 mmol/L. In contrast to the traditional assumptions, our data showed that βNC rose by 0.36 mmol/L for each 1 mEq/l reduction in plasma strong ion difference (p 2 titration. Although no significant difference was found between the electrolyte shifts in the two types of acidosis, we observed a slightly higher rate of chloride change in hyperchloremic acidosis, while the variation of sodium was more pronounced in lactic acidosis. Lastly, we found that the rise of βNC in metabolic acidosis did not induce a clinically relevant bias in the calculation of Base excess of blood and confirmed that the Base excess of blood was little affected by a wide range of pCO2.</p

    Image4_Non-carbonic buffer power of whole blood is increased in experimental metabolic acidosis: An in-vitro study.TIF

    No full text
    Non-carbonic buffer power (βNC) of blood is a pivotal concept in acid-base physiology as it is employed in several acid-base evaluation techniques, including the Davenport nomogram and the Van Slyke equation used for Base excess estimation in blood. So far, βNC has been assumed to be independent of metabolic acid-base status of blood, despite theoretical rationale for the contrary. In the current study, we used CO2 tonometry to assess βNC in blood samples from 10 healthy volunteers, simultaneously analyzing the electrolyte shifts across the red blood cell membrane as these shifts translate the action of intracellular non-carbonic buffers to plasma. The βNC of the blood was re-evaluated after experimental induction of metabolic acidosis obtained by adding a moderate or high amount of either hydrochloric or lactic acid to the samples. Moreover, the impact of βNC and pCO2 on the Base excess of blood was examined. In the control samples, βNC was 28.0 ± 2.5 mmol/L. In contrast to the traditional assumptions, our data showed that βNC rose by 0.36 mmol/L for each 1 mEq/l reduction in plasma strong ion difference (p 2 titration. Although no significant difference was found between the electrolyte shifts in the two types of acidosis, we observed a slightly higher rate of chloride change in hyperchloremic acidosis, while the variation of sodium was more pronounced in lactic acidosis. Lastly, we found that the rise of βNC in metabolic acidosis did not induce a clinically relevant bias in the calculation of Base excess of blood and confirmed that the Base excess of blood was little affected by a wide range of pCO2.</p

    DataSheet1_Non-carbonic buffer power of whole blood is increased in experimental metabolic acidosis: An in-vitro study.XLSX

    No full text
    Non-carbonic buffer power (βNC) of blood is a pivotal concept in acid-base physiology as it is employed in several acid-base evaluation techniques, including the Davenport nomogram and the Van Slyke equation used for Base excess estimation in blood. So far, βNC has been assumed to be independent of metabolic acid-base status of blood, despite theoretical rationale for the contrary. In the current study, we used CO2 tonometry to assess βNC in blood samples from 10 healthy volunteers, simultaneously analyzing the electrolyte shifts across the red blood cell membrane as these shifts translate the action of intracellular non-carbonic buffers to plasma. The βNC of the blood was re-evaluated after experimental induction of metabolic acidosis obtained by adding a moderate or high amount of either hydrochloric or lactic acid to the samples. Moreover, the impact of βNC and pCO2 on the Base excess of blood was examined. In the control samples, βNC was 28.0 ± 2.5 mmol/L. In contrast to the traditional assumptions, our data showed that βNC rose by 0.36 mmol/L for each 1 mEq/l reduction in plasma strong ion difference (p 2 titration. Although no significant difference was found between the electrolyte shifts in the two types of acidosis, we observed a slightly higher rate of chloride change in hyperchloremic acidosis, while the variation of sodium was more pronounced in lactic acidosis. Lastly, we found that the rise of βNC in metabolic acidosis did not induce a clinically relevant bias in the calculation of Base excess of blood and confirmed that the Base excess of blood was little affected by a wide range of pCO2.</p

    MOESM5 of Effect of nitric oxide on postoperative acute kidney injury in patients who underwent cardiopulmonary bypass: a systematic review and meta-analysis with trial sequential analysis

    No full text
    Additional file 5. Forest plot for sensitivity analysis including studies that had lower risk of bias and reported AKI using KDIGO criteria. RR, risk ratio. CI, confidential interval; AKI, acute kidney injury; NO, nitric oxide
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