Congenital dilation of the cervical epidural venous plexus: neuroradiology and endovenous management.

We report a case of a 15-year-old girl suffering from cervicobrachialgia who was admitted to our service due to an enlarged neural foramen suspicious for a neurinoma. The cervical phlebography, however, revealed a space-occupying dilated epidural vein with increased blood supply from the suboccipital venous plexus. Lesions like this are absolutely rare, presumably of congenital origin and have not been described before. The lesion was treated by feeder occlusion applying platinum coils and enbucrilate via the internal jugular vein.

Effects of corticotropin-releasing factor on isolated rat heart activity.

We investigated effects of bolus administration of corticotropin-releasing factor (CRF) on parameters of cardiac activity in isolated working rat hearts. Effects at a dose of 5 micrograms of CRF were compared in hearts perfused with Krebs-Henseleit solution, norepinephrine (NE, 10(-9) M), propranolol (3 x 10(-6) M), NG-nitro-L-arginine (L-NNA, 3 x 10(-5) M), or indomethacin (3 x 10(-5) M). CRF increased coronary flow for > 30 min (P < 0.01) with maximum increases of 31.7%, suggesting a prolonged vasodilatory action of the peptide. CRF, in addition, induced transient (lasting < 10 min) increases in maximum aortic pressure and oxygen consumption (P < 0.01), suggesting an inotropic action of the peptide. Perfusions of NE and propranolol did not change the cardiac response to CRF. L-NNA, inhibiting release of endothelium-derived relaxant factor (EDRF), and indomethacin diminished the vasodilatory response to CRF, as indicated by significantly shortened increases in coronary flow after CRF (P < 0.05). Indomethacin also enhanced peak increases in maximum aortic pressure after CRF (P < 0.01). The data confirm direct effects of CRF on cardiac activity. They also suggest that the mediation of coronary vasodilation by CRF involves the endothelial release of prostacyclin and EDRF.