Hie-syndrome is common in females and complains of severe chillness of the hand and foot in cold season. Although endocrinological or autonomic disfunctions were proposed, there were few reports regarding the etiology of Hie-Syndrome. From the findings of chillness and dark coloring of the extremities, we supposed increased venous contraction by cold. Then we studied the effects of cold exposure on body temperature, venous gas and the effects of phosphodiesterase-5 inhibitor Tadarafil (TDF).
[Subjects and Methods]
Subjects were 10 females with Hie-syndrome and 7 females without Hie under 50yrs. Studies were done at November to March, on outdoor temperature below 12 centi-degree. A Teflon tube was placed in cubital vein to take blood for venous pO2 and pCO2 measurement. Finger pulse-oximeter was set, and sulingual temperature was examined by electronic thermistor and limb temperature by ultra-red ray thermometer after 30min sitting in warm room and cold room (12 degree). Then 10mg TDF was administered, and same studies were done on next day.
Finger tip O2-saturation and sublingual temperature at warm room (23℃) was normal in both groups. Hie group showed, compared to No-Hie group, marked decrease in sublingual and limb temperature and venous pO2 pressure at cold room (12℃). The improvements after 10mg TDF on limb temperature and venous pO2 and pCO2 during cold exposure were observed more prominently in Hie-group.
Normal finger oximeter (arterial O2-saturation) in both groups, marked decrease in body temperature and venous pO2 after cold exposure in Hie-syndrome indicated that Hie-syndrome has not arterial but venous abnormality. Prominent improvement of body temperature and venous gas by TDF seem to highly suggest excess cold contraction of peripheral vein in Hie-syndrome, possibly due to disturbed venous NO-synthesis.