Biomedical subjects
Publications and source records attributed to S Tsunoda.
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Prostaglandin (PG) I2 and 6-keto-PGE1 were infused into the aortic arch, femoral vein, renal artery and portal vein in anesthetized dogs over a dose range to produce a stable decrease in systemic blood pressure after 7 min of infusion. Mesenteric artery blood flow was measured continuously with a non-cannulating electromagnetic flow probe. Parallel log dose-response relationship were seen for decreases in blood pressure and increases in mesenteric blood flow with both prostaglandins when infused into the aortic arch. The dose responses for intra-aortic and intravenous infusion of PGI2 were not different but were shifted to the right with intrarenal and intraportal infusions. With 6-keto-PGE1 the dose responses after intravenous, intrarenal and intraportal infusions were all shifted to the right. By comparing doses which reduced blood pressure by 10 mm Hg, the extraction of the PGs by the lungs, kidney and liver was calculated PGI2 had no significant pulmonary extraction. 31% renal and 75% hepatic extraction. In contrast, 6-keto-PGE1 had extractions of 40, 66 and 51% for pulmonary, renal, and hepatic vascular beds, respectively. We conclude that 6-keto-PGE1 is reasonably well extracted by the lungs, kidney, and liver.
A Japanese family in which a father, daughter and son had hypokalemia and hyperreninemia was investigated. Both father and daughter had reduced vascular sensitivity to angiotensin II; in addition, the daughter had juxtaglomerular cell hyperplasia and dwarf glomeruli. These features are consistent with Bartter's syndrome occurring in 2 successive generations in 1 family. The 12-year-old girl had growth retardation in spite of normal growth hormone secretion. No chromosomal abnormalities were found. Indomethacin administration to this patient in doses sufficient to reduce urinary prostaglandin excretion resulted in a marked improvement of polydipsia and polyuria, and an increase in serum sodium, potassium and chloride concentrations. Even though plasma aldosterone concentrations were reduced to within the normal range, serum potassium concentrations remained low, and plasma renin activity (PRA) remained elevated. Thus it is not likely that hypokalemia is induced only by aldosteronism. These results suggest that prostaglandins are the major determinant of polydipsia, polyuria and high plasma aldosterone levels and contribute to the hypokalemia observed in this patient. However, the failure of complete correction of the hypokalemia and the persistence of the raised PRA with a significant reduction of the prostaglandins suggest the possibility that additional factors are involved in the pathogenesis of Bartter's syndrome.
A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.
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Changes of distribution of immunoreactive gastrin (IRG) and molecular forms of intra-tissue gastrin in the growth course of rats were examined. The results obtained were as follows; 1) IRG concentrations and G cell counts were extremely low in the fetal antral mucosa. However, a gradual increase of the above was observed during the neonatal suckling period, accompanied by a rapid increase at the commencement of feeding. 2) IRG concentrations in the duodenal mucosa of the fetal and neonatal period were markedly higher than that of adult rat. 3) Jejunal IRG concentration was negligible in the fetal period. The value obtained from the postnatal rats was equal to or higher than that of adult rat. 4) The major form of antral gastrin was G-17 throughout the fetal and adult age. No qualitative change of antral IRG in the growth course of rats was seen. 5) The major form of the duodeno-jejunal mucosa was G-17 in the fetal period and thereafter G-34 increased gradually in the growth course of rats. These results suggested that, (1) suckling and feeding appeared to be a trigger of the production and release of antral gastrin in the growth course of rats. (2) In the initial stage of the growth, G cells distributed in the duodeno-jejunal mucosa as well as in the antral mucosa may participated in the production and release mechanism of gastrin.
Uric acid is the end-product of purine metabolism, and purines are the nitrogenous bases derived from the breakdown of nucleic acids. The CSF uric acid level is thought to be the index of the turnover of the nucleic acid and the degree of the cellular destruction in the brain. CSF uric acid levels were investigated in normal controls (30 cases) and in patients with brain tumor (20 cases), microcephalus (8 cases) and craniostenosis (4 cases). The mean values and standard deviations of CSF uric acid levels in normal controls were as follows; Newborn--9 yrs 0.34 +/- 0.09 mg/dl; 10 yrs--19 yrs 0.50 +/- 0.18 mg/dl; 20 yrs--29 yrs 0.46 +/- 0.05 mg/dl; 30 yrs--39 yrs 0.35 +/- 0.10 mg/dl; 40 yrs--49 yrs 0.35 +/- 0.23 mg/dl. Thereafter 0.72 +/- 0.21 mg/dl. The increased CSF uric acid levels after the age of 50 is thought to be due to the cellular destruction in the brain. CSF uric acid levels increased in patients with highly malignant brain tumor such as grade 3 or 4 astrocytoma and sarcomatous meningioma, but were normal in patients with grade 2 astrocytoma and meningiomas of meingothelial or fibroblastic type. CSF uric acid levels decreased in patients with microcephalus, but were almost normal in patients with craniostenosis. There is a significant correlation between CSF uric acid levels and the degree of brain atrophy in infants.
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Lung volumes in irreversible diffuse obstructive pulmonary syndromes (DOPS(I)) have been studied by using an analog of the lung that simulates an 18-breath nitrogen washout. The functional residual capacity (FRC), the dead space volume (Vd), the distribution of ventilation, as well as the pattern of lung emptying have been measured in normal subjects and those with obstructive syndromes. The Vd increased progressively with severity of the obstructive syndrome, as did FRC. For all subjects, both normal and obstructed, the ratio of Vd/FRC remained relatively fixed with the regression line of Vd upon FRC showing a minimal value for Vd of 67 cm(3). Vd increased by an average value of 33 cm(3) per liter of lung volume above this value. The increase in FRC resulted from the increased volume of the poorly ventilated compartment for the most part. X-ray evidence of emphysema was poorly correlated with the changes in Vd or FRC. A significant increase in anatomical Vd in DOPS(I) makes up an appreciable portion of the total Vd (physiological).
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