Extracorporeal CO2 removal as bridge to lung transplantation in life‐threatening hypercapnia

In patients awaiting lung transplantation (LTX), adequate gas exchange may not be sufficiently achieved by mechanical ventilation alone if acute respiratory decompensation arises. We report on 20 patients with life‐threatening hypercapnia who received extracorporeal CO₂ removal (ECCO2‐R) by means of the interventional lung assist (ILA®, Novalung) as bridge to LTX. The most common underlying diagnoses were bronchiolitis obliterans syndrome, cystic fibrosis, and idiopathic pulmonary fibrosis, respectively. The type of ILA was pumpless arteriovenous or pump‐driven venovenous (ILA activve®, Novalung) in 10 patients each. ILA bridging was initiated in 15 invasively ventilated and five noninvasively ventilated patients, of whom one had to be intubated prior to LTX. Hypercapnia and acidosis were effectively corrected in all patients within the first 12 h of ILA therapy: PaCO₂ declined from 109 (70–146) to 57 (45–64) mmHg, P < 0.0001; pH increased from 7.20 (7.06–7.28) to 7.39 (7.35–7.49), P < 0.0001. Four patients were switched to extracorporeal membrane oxygenation due to progressive hypoxia or circulatory failure. Nineteen patients (95%) were successfully transplanted. Hospital and 1‐year survival was 75 and 72%, respectively. Bridging to LTX with ECCO2‐R delivered by arteriovenous pumpless or venovenous pump‐driven ILA is feasible and associated with high transplantation and survival rates.     

Inhibition of prolactin secretion by lergotrile mesylate: mechanism of action.

Lergotrile mesylate (2-chloro-6-methylergoline-8beta-acetonitrile, methane-sulphate salt) was shown to be a potent inhibitor of prolactin secretion in vivo and in vitro. The dopamine receptor blocker, pimozide, was able to reverse the inhibitory effect of lergotrile mesylate (LM) on prolactin release from rat pituitaries in vitro. Alpha-adrenergic or beta-adrenergic receptor blockers were unable to antogonize the action of LM on prolactin release. These findings indicate that ergolines such as LM inhibit prolactin release from pituitaries by activating an adenohypophyseal dopamine receptor. LM is currently undergoing clinical trial as a prolactin inhibitor and a dopamine agonist.