This study describes the synthesis of modular diquinolineanthracene and polydiquinolineanthracene derivatives. The reported facile and scalable aza-Diels-Alder-based approach requires mild conditions, proceeds in two steps, uses commercially available starting materials, and accommodates varying functionalities. Given the known utility of the acene and quinoline motifs, the synthesized molecules and polymers hold promise for organic electronics applications.

value because of their hypotensive effects on the systemic Pulmonary hypertension is a well known, though uncirculation. [4][5][6] In contrast, inhaled nitric oxide is a potent pulcommon complication of end-stage liver disease (ESLD).monary vasodilator without apparent systemic effects as it Patients with severe pulmonary hypertension and ESLD is removed from circulation rapidly by hemoglobin. 6 Nitric undergoing orthotopic liver transplantation (OLT) may oxide is a lipophilic gas, which can be introduced into the develop right ventricular failure and death. This study inspiratory limb of a breathing circuit and delivered to the investigates the reversibility of pulmonary hypertension alveoli. 7 Here it is absorbed by the capillaries supplying the by the inhalation of nitric oxide in patients under evaluventilated alveoli where it activates guanylate cyclase that ation for OLT. Ten patients with ESLD who were discovleads to an increase in cyclic 3 5 -monophosphate that causes ered to have moderate to severe pulmonary hypertensmooth muscle relaxation and vasodilation. 8 Nitric oxide has sion were administered nitric oxide via face mask in been used successfully in infants with persistent pulmonary concentrations ranging from 0 to 80 ppm. Inhaled nitric hypertension and also to treat pulmonary hypertension and oxide is a potent pulmonary vasodilator without apparshunting in adult respiratory distress syndrome. 7,9 The preent systemic effects. Nitric oxide had no demonstrable transplantation evaluation of patients with ESLD and puleffect on mean pulmonary artery pressure (PAP) (37 vs.monary hypertension with nitric oxide might determine those 37 mm Hg), transpulmonary gradient (TPG) (26 vs. 26 patients that have reversible pulmonary hypertension, which mm Hg), or pulmonary vascular resistance (PVR) (295 might be an indicator of resolution following OLT. It might vs. 288 dynesrsecrcm 05 ). Two patients were discovered also provide evidence of a potential mechanism for treating to have an elevated pulmonary artery occlusion presan exacerbation of pulmonary pressures during transplantasure (PAOP) on baseline readings. The cause of pulmotion. 10 nary hypertension in these two patients was secondary to volume overload as a result of hepato-renal syndrome rather than primary pulmonary arteriolar pathology PATIENTS AND METHODS and was responsive to diuresis or dialysis but not toTen patients under evaluation for OLT were found to have pulmonitric oxide therapy. In conclusion nitric oxide does not nary hypertension determined by clinical symptoms, chest radioreverse pulmonary hypertension associated with ESLD.graphs, precordial echocardiograms, and right-heart catheterization.(HEPATOLOGY 1997;25:524-527.)After institutional review board approval and informed consent each patient underwent a repeat right-heart catheterization so that pulAdvanced liver disease is associated with a hyperdynamic monary artery pressures could be monitored during the administracirculatory state. It is characterized by a decreased systemic tion...

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Three separate episodes of acute pulmonary edema are described that developed in two otherwise healthy individuals during heavy exertion at high altitudes. Detailed physical examination and laboratory studies failed to demonstrate pulmonary infection or cardiac disease. Data obtained by cardiac catheterization during one of these episodes revealed elevation of the pulmonary artery pressure and a normal left atrial pressure. This syndrome appears to be the consequence of pulmonary vascular obstruction distal to the capillary bed, presumably in the pulmonary veins. It is brought about by exposure of susceptible individuals to high altitudes, and is completely reversed by oxygen administration.

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