Experimental studies by Dunn (1) demonstrated that multiple embolism of the pulmonary arterioles and capillaries is followed by a temporary inhibition of respiration succeeded by rapid shallow breathing. Dunn attributed this phenomenon to the stimulation of sensory nerve endings in the lungs. This explanation was favored by the fact that the injection of starch produced no alteration in the respiratory rate when both vagi had been previously sectioned.Attracted to this problem by its bearing upon the occurrence of rapid and shallow respiration in lobar pneumonia, Binger and Moore and their associates (2-6) have carried out a carefully planned series of experiments. Their studies chiefly concern the effects of the embolism of pulmonary arterioles and capillaries produced by the intravenous injection of starch grains under varying conditions. These observations were supplemented by other experimentally induced modifications of the pulmonary circulation. In their conclusion (6) to this instructive series of papers they state: "Since rapid and shallow breathing is not the result of (1) anoxemia, (2) increased pCO, and hydrogen ion concentration of the serum, (3) restriction of pulmonary vascular bed by nearly half, (4) increase in resistance to the flow of blood to and from the lungs, (5) the presence of starch grains in the lungs acting as a local irritant, it must be the result of the secondary pathological changes which occur in the pulmonary parenchyma following embolism. The nature of these changes, congestion and edema has been discussed elsewhere. Whether they operate directly on nerve endings or through their influence on lung volume and tissue elasticity is not certain." In their discussion the authors are inclined toward the hypothesis of direct irritation of the vagal nerve endings, 531 on

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There appears a striking lack of similarity between observations that record the effects of slow compression of the pulmonary artery in animals and the phenomena that may follow a partial occlusion of the same artery in man by a massive embolus.Cohnheim's (1) description of the effects of slowly produced pulmonary stenosis is so classical that it is worthy of quotation particularly as other experimental studies have simply confirmed his findings. The experiments of Cohnheim recorded simultaneously the pressure in the right auricle and femoral artery. A ligature was passed about the pulmonary artery and slowly tightened. Even when the constriction was carried to a marked degree there was not " the slightest change in thefemoral curae or in the manometer in the jugular. A change occurs only when the stenosis is carried beyond a certain point. The arterial pressure then undergoes a steep and sudden descent, while at the same time the level of the venous manometer rapidly rises; and, if the ligature be not loosened, life is in extreme danger." This finding is used by the author to illustrate his concept of the ability of the heart to accommodate itself to increased work until a point is reached " when the resistance becomes so considerable that the cardiac contractions are no longer capable of completely overcoming it," and " the circulation is instantly at an end. An intermediate state where the blood stream, though not quite normal, continues; where at each systole the heart still throws a certain quantity of blood into the arteries, though not the former normal, average amount, and thus maintains the arterial and venous pressures at levels lower and higher respectively than is normally the case; such an intermediate state, that is to say, as we become acquainted with in connection with increased pericardial tension, does not exist here. The physiological heart-muscle can meet the demands on its work, or it cannot meet them; in the former case, we have a regular physiological circulation, in the latter, death."The abrupt failure of the circulation under these circumstances has been described repeatedly. Haggart and Walker (2) produced occlusion of the pulmonary artery by slowly approximating the jaws of a clamp. As in Cohnheim's experiments, no effect upon systemic blood pressure or 543

FROM THE MASSACHUSETTS GENERAL HOSPITALA VISIBLE and palpable tumor in the neck stimulated surgical interest in disorders of the thyroid gland so long ago that no date can be assigned to its origin. In his classical "Operative Story of Goitre" Halsted wrote: "For thousands of years, probably, goitre has been a familiar malady. This conspicuous tumor of the neck was a perpetual challenge to the physician, and to the surgeon a stigma as well." Years after the perfection of the surgical technic of thyroidectomy came the isolation of thyroxin by Kendall in I9I5.Quite in contrast stands the order of the unfolding of knowledge concerning disorders of the parathyroid glands. Although a background of information concerning parathyroid deficiency served to link these glands with calcium metabolism, little or nothing was known about a state of hyperfunction until the isolation of a physiologically effective extract of the gland by Hanson in I923, and by Collip working independently in 1925. Classical studies in morbid anatomy centering largely in the laboratory of Erdheim contributed little of clinical significance until the bold surgical experiment of Mandl reversed the interpretations that had been based oln theory. A brief period of confusion then followed, during which surgical endeavors were controlled by neither pathological findings nor chemical data.In their eagerness to explore a new territory, surgeons became incautious and floundered in a field beset with pitfalls and blind alleys. During this period, however, the chemical and metabolic laboratories continued their efforts and ultimately built a foundation that the surgeon can rely upon in undertaking the operative treatment of hyperparathyroidism.The pathology of the living controlled by accurate pre-operative and postoperative data has again been found more illuminating than the findings of the deadhouse. As surgical specimens have been placed under the microscope of the pathologist, new data are emerging that are already providing a better rounded concept of the disease.Only in the light of very recent pathological studies may a classification of diseases of the parathyroids be formulated so that a hitherto nebulous subject begins to assume an orderly and familiar form. The following grouping is suggested as a working basis, subject of course to extension and modification in the future:(I) Generalized enlargement of the parathyroid glands due to functional hyperplasia but not associated with hyperparathyroidism. (Rickets, osteomalacia, pregnancy, nephritis.) 606