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Hyperglycemia and pancreatic insulitis were detected in all NOD/Scid recipients (n = 6) of NON.NOD DNCD3 splenic cells (5×105 cells/mouse) infused 1 month prior to co-infusion of diabetogenic splenocytes (5×105 cells/mouse) (Figure 2G).
Co-infusion of sumatriptan with GTN completely inhibits this effect.
Transient hyperkalaemia is a frequent side effect of AA co-infusion during PRRT.
Importantly, NS solutions are compatible with co-infusion of blood products.
Co-infusion of GTN with sumatriptan was performed in 6 rats.
Fig. 4 Significant decrease in bicarbonate (HCO3−) after ERT and 2.5% Arg/Lys amino acid co-infusion Fig. 5 Significant drop in base excess after ERT and 2.5% Arg/Lys amino acid co-infusion.
Fig. 1 Significant increase in potassium after ERT and 2.5% Arg/Lys amino acid co-infusion (Cobas Analyzer) Fig. 2 Significant rise in potassium after ERT and 2.5% Arg/Lys amino acid co-infusion (blood gas analysis).
Co-infusion of sumatriptan with GTN prevents the GTN-evoked increase of the magnitude of the EMG.
As we lack a control group which did not get an AA co-infusion, this question remains open.
Amino acid co-infusion during ERT leads to severe metabolic acidosis which induces hyperkalemia by potassium hydrogen exchange.
Only GFR and creatinine levels at 24 h varied significantly between the two co-infusion protocols (p?0.05).
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