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Effects of radiographic contrast media on pulmonary vascular resistance of normoxic and chronically hypoxic pulmonary hypertensive rats

C J Emery, PhD1, L Fang, MD2, E A Laude, PhD1 and S K Morcos, FRCS, FFRRCSI, FRCR2

1Respiratory Medicine, Sheffield University Medical School, Sheffield S10 2JF and 2Department of Diagnostic Imaging, Northern General Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield S5 7AU, UK



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Figure 1. Schematic diagram of the isolated blood-perfused rat lung preparation. PA, pulmonary artery; LA, left atrium.

 


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Figure 2. Change (mean±SEM) in pulmonary artery pressure ({Delta}Ppa mmHg) from baseline in response to cumulative volumes of radiographic contrast media (RCM) in the normal rat isolated perfused lung preparation (normoxic ventilation). ****Iopromide vs other RCM (p<0.05); ***ioxaglate vs iotrolan and diatrizoate and iopromide (p<0.05); **ioxaglate vs iotrolan (p<0.05); *iopromide vs iotrolan (p<0.05).

 


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Figure 3. Rise in pulmonary artery pressure (Ppa) (mean±SEM) in response to a cumulative volume of 0.95 ml of radiographic contrast media (RCM), mannitol solutions (osmolar control) or normal saline (volume control) in normal rat isolated perfused lung preparation (normoxic ventilation) from baseline (n=6–9). IOP, iopromide; IOT, iotrolan; IOX, ioxaglate; D, diatrizoate; IOPM, IOTM and IOXM, RCM-matched mannitol (osmolar control) solutions (for diatrizoate the osmolar control solution DM was saturated mannitol); S, normal saline; *Saline vs D, IOX, IOT and SM (p<0.05); **RCM vs matched mannitol (p<0.01). All tested solutions, with the exception of iotrolan mannitol control and normal saline, induced a significant (p<0.05) rise in Ppa compared with the baseline.

 


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Figure 4. Effects of (a) diatrizoate, (b) ioxaglate, (c) iotrolan and (d) iopromide on pulmonary artery pressure (Ppa mmHg) when raised by ventilation with hypoxia (2% O2+5% CO2). Results are expressed as percentagechange (mean±SEM) of the rise in Ppa with hypoxia from baseline (HPV). A schematic diagram of the changes in Ppa in response to 0.3 ml of RCM is shown. (N.B. The time-scale of the schematic diagram is the same for each figure.)

 


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Figure 5. Initial maximum acute changes (mean±SEM) in pulmonary artery pressure from baseline in chronic hypoxic pulmonary hypertensive rats in response to radiographic contrast media. (a)Schematic diagram of the changes in Ppa in response to 0.5 ml of iopromide shows an initial fall followed by a rise in Ppa within 2 min of exposure (*p<0.05 in comparison with baseline). (b) Schematic diagram of the changes in Ppa in response to iotrolan shows an initial fall followed by a rise in Ppa with 0.1 ml and 0.3 ml of iotrolan, but no initial fall and an immediate rise in Ppa with a 0.5 ml dose (*p<0.05 in comparison with baseline). (c) Schematic diagram of the changes in Ppa in response to ioxaglate shows a significant sustained fall in Ppa that lasted for approximately 20 min (**p<0.01 in comparison with baseline). (N.B. The time-scale of the schematic diagram is the same for each figure.)

 


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Figure 6. The maximum rise in pulmonary arterial pressure (Ppa) (mean±SEM) from baseline in response to cumulative 0.95 ml of radiographic contrast media and normal saline in chronic hypoxic-induced pulmonary hypertensive rats. IOP, iopromide; IOT, iotrolan; IOX, ioxaglate; S, normal saline. All solutions caused a significant rise in Ppa from baseline (p<0.05). *, Saline vs IOT and IOX (p<0.05).

 





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