Functional rehabilitation of the larynx after unilateral vocal cord paralysis was attempted in the dog by selective reinnervation of the laryngeal muscles. The intralaryngeal branches of the right recurrent nerve were dissected. The adductor branch was anastomosed with the ansa cervicalis; the abductor branch was anastomosed with the trunk of the phrenic nerve either within the larynx or through the recurrent nerve, the adductor branch of which was sectioned. Results could be analyzed in seven dogs: mobility of the vocal cord was checked, and electromyography, stimulation of the nerves, and histologic studies were performed. Functional reinnervation of both the adductor and abductor muscles was obtained in only one case, with good abduction. Adduction was recorded in five cases. False-positive results emphasize the necessity of collecting several types of data before concluding that functional reinnervation has been accomplished. The reliability of the procedure can and must be improved.
A patient with type I pseudohypoparathyroidism was found to have mild hypothyroidism. The patient had an elevated basal TSH level and an exaggerated TSH response to TRH. There was no goiter despite increased TSH levels, and the 131I thyroidal uptake was low before and after exogenous TSH administration. These studies suggested that the patient might have partial resistance to TSH. The binding of radioiodinated TSH to thyroid membranes obtained by biopsy was next studied. The displacement of iodinated TSH by unlabeled TSH was found to be identical to that in normal control membranes. The adenylate cyclase stimulation by a supramaximal dose of TSH, however, was blunted (120.1 +/- 11.5 vs. 387.2 +/- 40.3 pmol cAMP/min/mg protein), while basal and NaF-stimulated activities were quite similar to the activities in normal membranes. These findings suggested a lack of signal transmission between the TSH receptor and the catalytic unit. Incubation of control membranes with TSH and GTP resulted in a synergistic effect on the adenylate cyclase activity. This was not found with the patient's membranes and suggested that the coupling failure was due to a defective guanine nucleotide regulatory protein. We conclude that in this case of type I pseudohypoparathyroidism, the associated mild primary hypothyroidism was due to a partial TSH refractoriness caused by a coupling defect between the TSH receptor and adenylate cyclase. This observation suggests that a common pathogenetic mechanism might underly type I pseudohypoparathyroidism and its associated hypothyroidism.
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