A child with isolated Horner's syndrome after blunt neck trauma.

Horner's syndrome is the triad of miosis, ptosis, and anhidrosis that results from disruption of the sympathetic pathways between the brain and the eye. Although the individual signs of Horner's syndrome do not constitute an emergency, their presence makes any Horner's syndrome a potential vascular emergency due to the proximity of the internal carotid artery to the sympathetic ganglia. We present a case of Horner's syndrome in a 5-year-old child after blunt trauma to the neck, and discuss the management and implications of a potential carotid artery injury.

[Nitric oxide activates Ca2+ activated potassium current in rat tail artery smooth muscle cells via cGMP-dependent mechanism]. / NO aktiviruet vykhodiashchii Ca2+-aktiviruemyi K+-tok gladkomyshechnykh kletok khvostovoi arterii krysy cherez cGMP-zavisimyi mekhanizm.

Mechanisms of nitric oxide (NO) action on K(Ca) channels were investigated using patch-clamp technique and freshly isolated smooth muscle cells from rat tail artery. In whole-cell experiments, the outward current was increased 6,64-/+0,72-fold (n=10) by 100 microM sodium nitroprusside (SNP), which was significantly different compared with 1,07-/+0,03-fold (n=8) increase of the outward current by addition of experimental bath solution. In the presence of 300 nM iberiotoxin, the specific blocker of K(Ca) channels, the outward current was not altered by 100 microM SNP. In addition, in the presence of 1 microM Rp-8-Br-PET-CGWS, the specific protein kinase G-inhibitor, the outward current was not affected by 100 microM SNP. These results suggest that NO released from NO-donors stimulates K(Ca) current in rat tail artery smooth muscle cells by activating protein kinase G and not by direct effect on the channel 1.