Maria Theresa Voelker1, Andreas Bergmann2, Thilo Busch3, Nora Jahn4, Sven Laudi5, Katharina Noreikat6, Philipp Simon7, Sven Bercker8. 1. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: theresa.voelker@medizin.uni-leipzig.de. 2. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: andibergmail@gmx.de. 3. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: thilo.busch@medizin.uni-leipzig.de. 4. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: nora.jahn@medizin.uni-leipzig.de. 5. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: sven.laudi@medizin.uni-leipzig.de. 6. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: katharina.noreikat@medizin.uni-leipzig.de. 7. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: philipp.simon@medizin.uni-leipzig.de. 8. University of Leipzig, Medical Faculty; Department of Anaesthesiology and Intensive Care Medicine, Liebigstrasse 20, 04103 Leipzig, Germany. Electronic address: sven.bercker@medizin.uni-leipzig.de.
Abstract
INTRODUCTION: Hemoglobin-based oxygen carriers (HBOC) have been developed as an alternative to blood transfusions. Their nitric-oxide-scavenging properties HBOC also induce vasoconstriction. In acute lung injury, an excess of nitric oxide results in a general vasodilation, reducing oxygenation by impairing the hypoxic pulmonary vasoconstriction. Inhaled nitric oxide (iNO) is used to correct the ventilation perfusion mismatch. We hypothesized that the additional use of HBOC might increase this effect. In a rodent model of ARDS we evaluated the combined effect of HBOC and iNO on vascular tone and gas exchange. METHODS: ARDS was induced in anaesthetized Wistar rats by saline lavage and aggressive ventilation. Two groups received either hydroxyethylstarch 10% (HES; n = 10) or the HBOC hemoglobin glutamer-200 (HBOC-200; n = 10) via a central venous infusion. Additionally, both groups received iNO. Monitoring of the right ventricular pressure (RVP) and mean arterial pressure (MAP) was performed with microtip transducers. Arterial oxygenation was measured via arterial blood gas analyses. RESULTS: Application of HBOC-200 led to a significant increase of MAP and RVP when compared to baseline and to the HES group. This effect was reversed by iNO. The application of HBOC and iNO had no effect on the arterial oxygenation over time. No difference in arterial oxygenation was found between the groups. CONCLUSION: Application of HBOC led to an increase of systemic and pulmonary vascular resistance in this animal model of ARDS. The increase in RVP was reversed by iNO. Pulmonary vasoconstriction by hemoglobin glutamer-200 in combination with iNO did not improve arterial oxygenation in ARDS.
INTRODUCTION: Hemoglobin-based oxygen carriers (HBOC) have been developed as an alternative to blood transfusions. Their nitric-oxide-scavenging properties HBOC also induce vasoconstriction. In acute lung injury, an excess of nitric oxide results in a general vasodilation, reducing oxygenation by impairing the hypoxic pulmonary vasoconstriction. Inhaled nitric oxide (iNO) is used to correct the ventilation perfusion mismatch. We hypothesized that the additional use of HBOC might increase this effect. In a rodent model of ARDS we evaluated the combined effect of HBOC and iNO on vascular tone and gas exchange. METHODS: ARDS was induced in anaesthetized Wistar rats by saline lavage and aggressive ventilation. Two groups received either hydroxyethylstarch 10% (HES; n = 10) or the HBOC hemoglobin glutamer-200 (HBOC-200; n = 10) via a central venous infusion. Additionally, both groups received iNO. Monitoring of the right ventricular pressure (RVP) and mean arterial pressure (MAP) was performed with microtip transducers. Arterial oxygenation was measured via arterial blood gas analyses. RESULTS: Application of HBOC-200 led to a significant increase of MAP and RVP when compared to baseline and to the HES group. This effect was reversed by iNO. The application of HBOC and iNO had no effect on the arterial oxygenation over time. No difference in arterial oxygenation was found between the groups. CONCLUSION: Application of HBOC led to an increase of systemic and pulmonary vascular resistance in this animal model of ARDS. The increase in RVP was reversed by iNO. Pulmonary vasoconstriction by hemoglobin glutamer-200 in combination with iNO did not improve arterial oxygenation in ARDS.