Fetuses with cystic hygroma or loose skin of the neck were studied chromosomally and phenotypically to clarify the relation between neck abnormality and cardiovascular malformations. Of 12 fetuses, 9 had chromosome abnormalities: 4 with 45,X, 3 with trisomy 21, one each with trisomy 13, dup 6q. One had normal chromosomes. Two cases, in which chromosome analysis was unsuccessful, were morphologically suspected to be trisomy 13. Nine of the 12 fetuses had either bilateral cystic hygroma of the neck (7 cases) or nuchal bleb (2 cases: trisomy 13 and dup 6q). Two of the 3 remaining cases (trisomy 21) had loose skin of the neck, and one had edematous swelling of the skin of the neck. Except for the last case of trisomy 21, 11 fetuses (91.7%) had severe and/or rare cardiovascular malformations. They were divided into 3 major groups: a) spectrum of hypoplastic left heart syndrome (45,X and dup 6q), b) double outlet right ventricle, agenesis of semilunar valve (trisomy 13), and c) abnormality of atrioventricular orifice or valves (trisomy 21). One fetus with normal chromosomes had persistent left superior vena cava instead of absent right one and calcification of myocardium. Histological observation of edematous skin demonstrated the abnormal distribution of lymph vessels, including their absence. Some cases showed hypoplastic thymus. To integrate the findings of the present study and the descriptions in the literature, a pathogenesis is hypothesized in relation to migration of neural crest cells and extracellular matrix.

\s=b\The ischemic change of the vocal fold on phonation was studied with an oxygen electrode using the canine vocal fold. Oxygen pressures of a limited area of the vocal fold were measured in the lamina propria and vocal muscle at the middle of the membranous portion. The results are summarized as follows: oxygen pressure in each area decreased on phonation as compared with respiratory movement, an ischemic change of the vocal fold occurred on phonation, and the response in the lamina propria was less than that of the vocal muscle.

\s=b\To clarify the mechanisms of ischemic change in the vocal fold on phonation, model experiments were performed under various conditions by recording tissue oxygen pressure (Pto2) values under electrical stimulation of either the recurrent laryngeal nerves or external branches of the superior laryngeal nerves. In addition, autonomic nerve regulation of laryngeal vessels was estimated under administration of succinylcholine chloride. Oxygen pressures of the vocal fold were measured in the lamina propria and vocal muscle at the middle of the membranous portion. The Pto2 in the lamina propria showed a slight increase during lower-frequency stimulation and a slight decrease during higher-frequency stimulation of the recurrent laryngeal nerve. The Pto2 in the vocal muscle showed a decrease during stimulation of the recurrent laryngeal nerve. On the other hand, the Pto2 showed almost no change in the lamina propria or vocal muscle during stimulation of the external branch of the superior laryngeal nerve. It is supposed that an ischemic change in the vocal muscle on phonation results mainly from contraction of the vocal muscle. On the contrary, the ischemic change in the vocal mucosa on phonation does not appear to be directly caused by the contraction of the vocal muscle but by other factors, such as wavelike movement. (Arch Otolaryngol Head Neck Surg 1988;114:308-312) On phonation, it is assumed that circulation in the vocal fold is exposed to special conditions because the vocal fold is subjected to an ultra-high-frequency vibration. We have already reported that an ischem¬ ie change in the vocal fold obviously occurred on phonation as compared with at rest and that the response in the lamina propria was less than that of the vocal muscle.' From these results, we speculated that the is¬ chemie change on phonation was caused by several factors, including direct and/or indirect influence of contraction of the intrinsic laryngeal muscle and wavelike movement of the vocal fold. In addition, these factors may include regulation by the auto¬ nomie nervous system. Therefore, we undertook this study to evaluate the responses in laryngeal circulation of intrinsic laryngeal muscle contraction and laryngeal mucosa during electri¬ cal stimulation of the laryngeal nerves. These findings might also (Dr Matsuo). reveal valuable information concern¬ ing the autonomie vasomotor influ¬ ence in regulating laryngeal vessels. MATERIALS AND METHODSTissue oxygen pressure (Pt02) measure¬ ments were used to study the responses in vocal fold circulation during electrical stimulation of laryngeal nerves. The details of this technique were published earlier.1 Ten mongrel dogs, weighing from 8 to 10 kg, were anesthetized intravenously with an initial dose of 25 mg of pentobarbital sodium per kilogram of body weight. Sup¬ plemental doses were administered as needed. Before experiments, tracheostomy was performed and an air passage was maintained. Endolaryngeal microsurgical technique was used to insert a platinum electrode into the mucosa ...

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