To study the effect of monocrotaline on the pulmonary alveolar-capillary membrane permeability, cardiac catheterization, extravascular lung water content and absorption of ¹⁴C-compoundsfrom the rat lungs in combination with morphological observations were studied in the early stage of monocrotaline intoxication. Purified monocrotaline or its pyrrole was administered to rats with various doses. Single dose of 50mg/kg of monocrotaline was enough to induce pulmonary hypertension 4 weeks later, but neither immediate nor direct pressor effect was observed by monocrotaline or active pyrrole. Only 3 to 5mg/kg of pyrrole was enough to produce alveolar flooding with increased extravascular lung water content and accelerated absorption of ¹⁴C-mannitol and ¹⁴C-inulin from lungs 24 hours after administration. In contrast with fast and potent effect of pyrrole, effect of monocrotaline was mild and delayed in development. These findings suggested that monocrotaline increased the porosity of not only endothelial but also alveolar membraneby active metabolite.

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To evaluate the sympathetic nervous activity in chronic hypoxic states, the plasma concentrations of norepinephrine (NE), cyclic adenosine 3', S'-monophosphate (cyclic AMP), cyclic guanosine 3', 5'-monophosphate (cyclic GMP) and dopamine-β-hydroxylase (DBH) enzymeactivity were measured in 32 patients with pulmonary tuberculosis and 30 normal volunteers. Moreover, the peripheral arterial-venous difference of concentration of these substance, arterial blood gas levels and spirometric data were studied in these patients. The results of this study demonstrated that the plasma NEand cyclic AMPconcentrations were directly related to the degree of hypoxemia and some of the spirometric parameters in these patients. It is concluded that sympathetic nervous activity was augmented in chronic hypoxic states, especially with chronic respiratory failure.

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It has been generally assumed that contrast media used for excretory urography are safe even in the presence of renal insufficiency. Recently, however, several reports of acute oliguric renal failure have been documented in diabetic patients after excretory urography. Wealso have experienced three cases of acute renal failure following contrast media study in diabetic patients. For the purpose of investigating the effect of contrast media on renal function, we examined serum creatinine, BUN, K⁺ levels and urine volume before and after intravenous pyelography (IVP), drip-infusion pyelography (DIP) or angiography in twenty diabetic patients. As controls, twenty patients with non-diabetic renal diseases were selected. From this study, it is concluded that contrast media study had better be avoided in diabetic patients providing with renal disturbance (creatinine level more than 3.0 mg/dl) and severe retinopathy.

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Plasma renin activity (PRA) and plasma aldosterone (PA) were measured under conditions of bed rest and after administration of furosemide and/or angiotensin II to adultonset diabetics and age-matched controls. Seventeen of the diabetics had no proteinuria (non-proteinuria group) while in the other ten subjects, there was a persistent proteinuria, but no hypertension and renal dysfunction (proteinuria group). In the non-proteinuria group, changes in PRAand PA levels during both bed rest time and after the stimulation with furosemide did not significantly differ from findings in the control group. In the proteinuria group, PRA and PA levels were significantly lower than in the other two groups. PA and diastolic pressure respsnses to angiotensin II were slightly increased in diabetics (N.S.). PA responses to furosemide had significant positive correlation with those to angiotensin II. These findings suggest that the renin-aldosterone system responds normally in adultonset diabetics without proteinuria, but shows lower response in diabetics with persistent proteinuria, even without complications of hypertension and a decreased renal function.

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The incidence and pathologic features of cardiac lesions in 184 autopsied aged patients with disseminated intravascular coagulation (DIG) were reported. Coronary thrombosis was noted in 31 (16.8%), fresh myocardial necrosis in 60 (32.6%) and massive myocardial hemorrhage in 49 (26.6%) of these patients. Fresh myocardial infarction was present in 16 (8.7%) patients, 13 of whommanifested coronary thrombosis. The site of thrombi deposition was closely related to preexisting stenotic lesions of the coronary arteries. Only 3 of 16 patients with disseminated intravascular coagulation and acute myocardial infarction had typical cardiac symptoms.In most patients, the electrocardiographic changes were equivocal or not diagnostic for the diagnosis of acute myocardial infarction. Wesuggest the possibility that coronary thrombi in disseminated intravascular coagulation may gradually increase in extent and severity, leading to confluent areas of myocardial necrosis. The possibility of death due to heart failure, arrhythmia or cardiac rupture, points to the importance of recognizing the frequent cardiac involvement in aged patients with disseminated intravascular coagulation.

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A 24-year-old female had juvenile rheumatoid arthritis since the age of 3, with systemic manifestations such as fever, polyarthralgia, micrognathia, splenomegaly, hepatomegaly, lymphadenopathy, subcutaneous nodules, hidden rheumatoid factor of IgG type. Particularly noteworthy is selective IgA deficiency in this patient, with increases in concentration up to 50 mg/dl in the serum concurrently with the repeated febrile attacks in the clinical course.

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Batter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis, normotensive hyperreninism, hyperalodosteronism, hyporesponsiveness to pressor agent and juxtaglomerular cell hyperplasia. Recently, metabolic mimicry of Batter's syndrome by vomiting, diarrhea, laxatives and diuretics abuse has been reported. We had a 30 year-old female patient whodeveloped so-called pseudo-Bartter's syndrome as the result of surreptitious self-administration of furosemide for about six years. In this case, calcification of bilateral renal medulla was demonstrated. Such adverse reaction has not been reported to date. Moreover, a total 14 cases of pseudo-Bartter's syndrome reported in Japanese literature is reviewed.

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The availability of thyrotropin releasing hormone (TRH) has made it possible to determine whether tropic hormone deficiency is caused by pituitary or hypothalamic dysfunction. A case of hypothalamic hypothyroidism was described in a 17 year old woman. This patient was admitted for the evaluation of hypothyroidism and secondary amenorrhea. Her T₃ and T₄ were decreased, with an undetectable level of base line thyrotropin. The TRH test revealed normal but delayed response of TSH. Her base line prolactin and its response to TRH were normal. Adenocorticotropic hormone (ACTH), cortisol, growth hormone (GH), and urinary 17-hydroxysteroids were also normal. ACTH response to metyrapone was normal. Evaluation of the pituitary-gonadal axis revealed a normal increase in both lutenizing hormone (LH) and follicle stimulating hormone (FSH) following the intravenous administration of lutenizing hormone releasing hormone (LHRH). These results suggest that she had hypothalamic hypothyroidism as an isolated disturbance in the hypothalamic-pituitary axis. A deficiency of TRH is probably caused by a disorder of hypothalamic function of unknown etiology since the extensive studies did not reveal any secondary causes. It is recommendedthat patients with amenorrhea and hypothyroidism be evaluated for possible hypothalamic hypothyroidism.

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Increased TdT activity was demonstrated in 2 cases of AML. One of them had Ph positive chromosome due to a standard translocation of t(9: 22). Treatment with cytosine arabinoside, daunorubicin, 6-mercaptopurine and prednisolone was ineffective or only partially effective. Switching to the vincristine and prednisolone therapy resulted in a complete remission in both cases.

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