Peritoneal perfusion with oxygenated perfluorocarbon augments systemic oxygenation.

BACKGROUND: Despite maximal ventilatory support, many patients die from hypoxia in the setting of potentially reversible pulmonary failure. There remains a pressing need for additional pulmonary supportive care measures, especially techniques that do not require systemic anticoagulation. The objective of our experiments was to determine whether systemic oxygenation could be increased in a large animal, with induced hypoxia, by perfusing the abdominal cavity with oxygenated perfluorocarbons. METHODS: Fifteen pigs with a mean (+/- SD) weight of 45 +/- 5 kg were intubated and rendered hypoxic by ventilating them with a blend of nitrogen and oxygen to achieve subatmospheric concentrations of inspired oxygen ranging from 18 to 10%, resulting in baseline mean Pao(2) range of 65.9 +/- 9.7 to 26.6 +/- 2.8 mm Hg, respectively. Peritoneal perfusion was performed in eight animals with oxygenated perfluorocarbon and in seven control animals with oxygenated saline solution. RESULTS: The average increase in Pao(2) with oxygenated perfluorocarbon perfusion, compared to oxygenated saline solution perfusion, ranged from 8.1 to 18.2 mm Hg. A common treatment effect was estimated across all fraction of inspired oxygen (Fio(2)) values, representing the average mean difference in oxygen uptake between oxygenated perfluorocarbon and saline solution, irrespective of the level of Fio(2). This average was 12.8 mm Hg (95% confidence interval, 7.4 to 18.2; p \u3c 0.001). The most clinically relevant results occurred at an Fio(2) of 14%, resulting in a baseline mean Pao(2) of 39.4 +/- 5.0 mm Hg with oxygenated saline solution perfusion, and a mean Pao(2) of 55.3 +/- 7.6 mm Hg with oxygenated perfluorocarbon perfusion. This corresponded to an increase in arterial oxygen saturation from 73 to 89%. CONCLUSION: These results of our principle experiments demonstrate that the peritoneal cavity can be used for gas exchange and, in our model, yielded clinically relevant increases in systemic arterial oxygen levels. This technique may have the potential for the supportive care of patients dying from hypoxia in the setting of reversible lung injury

2,4,6,8-Tetra­kis(4-fluoro­phen­yl)-3,7-diaza­bicyclo­[3.3.1]nonan-9-one

In the title compound, C31H24F4N2O, the bicyclo­[3.3.1]nonane ring exists in a chair-boat conformation. Two of the four fluorine-substituted rings adopt equatorial dispositions with the piperidin-4-one rings. Mol­ecules are linked into a two-dimensional network parallel to (01) by N—H⋯O, C—H⋯F and C—H⋯O hydrogen bonds. Inter­molecular N—H⋯π and C—H⋯π inter­actions are also observed

4-Azido-2-chloro-6-methyl­quinoline

In the title compound, C10H7ClN4, the quinoline ring system is planar [maximum deviation 0.0035 (10) Å]. The crystal structure is stabilized by van der Waals and π–π stacking inter­actions [centroid–centroid distance 3.6456 (17) Å]

1,1′-[4-(2,4-Dichloro­phen­yl)-2,6-di­methyl-1,4-di­hydro­pyridine-3,5-di­yl]diethanone

In the title compound, C17H17Cl2NO2, the central 1,4-dihydro­pyridine ring adopts a flattened-boat conformation. The ethanone substituents of the dihydro­pyridine ring at positions 3 and 5 have synperiplanar (cis) or anti­periplanar (trans) conformations with respect to the adjacent C=C bonds in the dihydro­pyridine ring. The 2,4-dichloro­phenyl ring is almost planar [r.m.s. deviation = 0.0045 (1) Å] and almost perpendicular [89.27 (3)°] to the mean plane of the dihydro­pyridine ring. In the crystal, an N—H⋯O hydrogen bond links mol­ecules into a zigzag chain along the ac diagonal. C—H⋯Cl contacts form centrosymmetric dimers and additional weak C—H⋯O contacts further consolidate the packing

3-Acetyl-6-chloro-4-phenyl­quinolin-2(1H)-one

The title compound, C17H12ClNO2, crystallizes with two mol­ecules in the asymmetric unit. The main conformational difference between these two mol­ecules is the dihedral angle between the phenyl ring and the quinoline ring system [70.5 (1)° and 65.5 (1) Å]. The crystal packing is stabilized by N—H⋯O hydrogen bonds

4,8,9,10-Tetra­kis(4-fluoro­phen­yl)-1,3-diaza­tricyclo­[3.3.1.1]decan-6-one

In the title compound, C32H24F4N2O, all four six-membered rings that constitute the diaza­adamantanone cage adopt chair conformations. Two of the four fluoro­phenyl substituents occupy axial positions and the other two occupy equatorial positions relative to their respective C5N rings of the adamantane framework. The crystal structure is stabilized by C—H⋯O inter­actions, generating a C(5) chain along the a axis

l-Asparagine–l-tartaric acid (1/1)

In the title compound, C4H8N2O3·C4H6O6, the amino acid mol­ecule exists as a zwitterion and the carb­oxy­lic acid in an un-ionized state. The tartaric acid mol­ecules are linked into layers parallel to the ab plane by O—H⋯O hydrogen bonds. The amino acid mol­ecules are also linked into layers parallel to the ab plane by N—H⋯O and C—H⋯O hydrogen bonds. The alternating tartaric acid and amino acid layers are linked into a three-dimensional framework by N—H⋯O and O—H⋯O hydrogen bonds

Ethyl 2-methyl-5-oxo-4-(3,4,5-trimeth­oxy­phen­yl)-1,4,5,6,7,8-hexa­hydro­quinoline-3-carboxyl­ate

In the mol­ecular structure of the title compound, C22H27NO6, the dihydro­pyridine ring adopts a flattened boat conformation while the cyclo­hexenone ring is in an envelope conformation. In the crystal, mol­ecules stack parallel to the crystallographic a axis linked by inter­molecular N—H⋯O and C—H⋯O hydrogen bonds