[The process of wound healing after a flap operation. Regeneration of the gingival epithelium and connective tissue examined by autoradiography].
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Biomedical subjects
Publications and source records attributed to K Kamoi.
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To clarify clinical evaluation of highly sensitive thyroid stimulating hormone (TSH) immunoradiometric assay (IRMA) using RIABEAD II kit, we measured serum TSH and its changes after TRH test in normal subjects and patients with hyper- or hypothyroidism due to Grave's disease, TSH-producing pituitary adenoma and chronic thyroiditis or Refetoff's syndrome. In 12 normals, basal TSH (0.23-1.85 microIU/ml) increased in 2.29-18.85 microIU/ml 30 min after TRH test. In patients whose serum TSH and thyroid hormone showed less than 0.10 microIU/ml and more than normal level, respectively, no response of TSH to TRH was observed, while in patients whose serum TSH and thyroid hormone showed more than 3.5 microIU/ml and less than normal level, respectively, hyperresponse of TSH to TRH was observed. In patients with hyper- or hypothyroidism, changes in serum TSH after treatment were normalized a few months later after normalizing of thyroid hormone. In patients with TSH-producing pituitary tumor or Refetoff's syndrome, serum TSH increased. These results show that serum TSH using IRMA-(RIABEAD II) kit indicates a precise function of pituitary TSH.
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A 62-year-old man with small cell carcinoma (oat cell type) of the lung who had hyponatremia and renal sodium loss with inappropriate antidiuresis is reported. Plasma levels of arginine vasopressin (AVP) were not elevated inappropriately. Plasma levels of atrial natriuretic peptide (ANP), however, were high, and increased after water loading and hypertonic saline infusion. The renin-aldosterone axis was normal, as were adrenal, thyroid, and renal functions. Water restriction to 500 to 700 ml/d resulted in a rise in serum sodium. Analysis of the tumor tissue failed to demonstrate the presence of AVP or ANP. The findings (1) suggest that hyponatremia and renal sodium loss with inappropriate antidiuresis observed in the patient is due to an antidiuretic substance distinct from AVP, and (2) point to the possibility that hypersecretion of ANP may play a role in the pathophysiology.
The effect of GnRH-associated peptide on PRL secretion by human pituitary lactotropes in culture was studied. Pituitary adenomas obtained at selective transsphenoidal adenomectomy from a patient with prolactinoma, and two patients with mixed GH- and PRL-secreting pituitary adenomas were cultured in monolayer. When cells were incubated with dopamine (10 nmol/l), a significant inhibition in PRL secretion was observed in all the experiments, which was blocked by co-incubation with haloperidol. In mixed GH- and PRL-secreting adenoma cells, dopamine likewise decreased GH secretion. Incubation of cells with synthetic GnRH-associated peptide at concentrations up to 100 nmol/l, on the other hand, failed to affect both PRL and GH secretion. These results suggest that synthetic GnRH-associated peptide has no inhibitory effect on PRL secretion in human pituitary lactotropes.
In an attempt to clarify the clinical significance of atrial natriuretic peptide (ANP) in man, plasma levels of immunoreactive ANP were studied in patients with heart diseases and in those with chronic renal failure. When ANP concentrations in pulmonary arterial plasma were compared with hemodynamic variables in patients with heart diseases who underwent cardiac catheterization, a significant positive correlation was found between plasma ANP levels and mean pulmonary capillary wedge pressure, while plasma ANP levels were not significantly correlated to mean right atrial pressure (MRAP). After the injection of contrast medium, both MRAP and plasma ANP levels increased and a significant positive correlation was observed between two variables. Plasma levels of ANP were elevated in patients with congestive heart failure according to the severity. In addition, patients associated with atrial fibrillation showed significantly higher plasma ANP levels than those on sinus rhythm. In patients with paroxysmal atrial arrhythmias, plasma ANP levels increased markedly during paroxysms. Patients with chronic renal failure had elevated plasma ANP levels, which fell after hemodialysis. These results suggest that both left and right atrial tissue can secrete ANP as a result of stretching of the cardiocytes in man and that plasma ANP levels are elevated in patients with congestive heart failure and in those with chronic renal failure by increased atrial pressure due to volume expansion. Abnormal atrial contraction per se, in addition, may stimulate ANP secretion.
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Usefulness of three kinds of TSH kits by immunoradiometric assay (IRMA) was evaluated. They were able to measure low levels (less than 0.1 microIU/ml) in serum thyroid stimulating hormone (TSH) with incubation of short time (4 hours). In particular, RIABEAD II kit had a highly specific affinity for TSH and the normal range (+/- 2 S.D.) using it showed from 0.20 to 3.50 microIU/ml in 150 normal subjects. In patients with hyperthyroidism and in patients with hypothyroidism, the values of TSH were lower and higher than those of normal subjects, respectively. Another kits showed similar results. These results indicate that these TSH-IRMA kits are useful to evaluate serum TSH levels exactly.
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Clinical usefulness of a radioimmunoassay of plasma arginine vasopressin concentration (AVP) during hypertonic saline infusion for the assessment of posterior pituitary function was studied in comparison with the conventional water deprivation test. Infusion of 5% saline at a rate of 0.05 ml/kg/min for 120 min in 15 normal subjects induced an elevation of plasma osmolality (Posm) from 290.3 +/- 0.7 to 307.5 +/- 2.1 mOsm/kg with a resultant increase in AVP from 2.4 +/- 0.4 to 9.9 +/- 2.2 pg/ml. During the infusion, a highly significant correlation between AVP and Posm was observed with a regression line expressed as AVP = 0.40 (Posm - 283.0). In 22 polyuric patients, on the other hand, the infusion induced a marked elevation of Posm from 302.6 +/- 2.5 to 321.3 +/- 2.9 mOsm/kg, but caused a slight (less than 5.8 pg/ml) or no increase in AVP from the basal levels (0.5 +/- 0.1 pg/ml). A conventional water deprivation test was carried out in ten patients with neurogenic diabetes insipidus, including one who had coincidental nephrogenic diabetes insipidus. As would be expected, urine osmolality (Uosm) did not rise beyond Posm in seven of them. However, two of three other patients, who had a complete lack of AVP response to the hypertonic saline, were able to concentrate their urine with a maximal Uosm/Posm of 1.3 and 1.1 respectively. The concurrent decrease in creatinine clearance to 49 and 57% of the initial values, respectively, indicated that a marked reduction in glomerular filtration rate due to severe dehydration was responsible for the unexpected concentration of urine in the patients with totally impaired AVP secretion. Based on these results, we conclude that the direct measurement of AVP during hypertonic saline infusion is an essential procedure for the accurate evaluation of posterior pituitary function.
In an attempt to clarify the mechanisms regulating the release of atrial natriuretic peptide (ANP) in man, ANP levels in pulmonary arterial plasma determined by RIA were correlated to hemodynamic variables in 17 patients with heart disease who underwent cardiac catheterization and angiocardiography. In addition, plasma ANP levels in various blood vessels were determined in 7 patients with heart disease and in 7 normal subjects to determine the source and the site of removal of circulating ANP. A significantly positive correlation was found between plasma ANP levels and mean pulmonary arterial wedge pressure, while the correlation between plasma ANP levels and mean right atrial pressure was not significant. After the injection of contrast medium, both mean right arterial pressure and plasma ANP levels increased, and a significant positive correlation was found between the two variables. When ANP levels in plasma collected from various blood vessels were compared, the highest levels were found in the coronary sinus. Plasma ANP levels in the renal vein were the lowest and were 50% of the levels in the aorta. Plasma ANP levels in the superior vena cava and internal jugular vein were higher than that in the antecubital vein. Analysis of immunoreactive ANP in pooled plasma by high performance liquid chromatography revealed that the retention time of the main ANP peak coincided with that of synthetic human alpha ANP. These results indicate that circulating ANP mainly originates from the heart, the kidney rapidly takes up a significant amount of ANP from the circulation, and an increase in both left and right atrial pressure triggers ANP release in man.
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