[Effects of calcium antagonists, especially nifedipine, on variant angina, resting angina and unstable angina (author's transl)].
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Biomedical subjects
Publications and source records attributed to N Hata.
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We describe a new double-antibody enzyme radioimmunoassay for thyroxin-binding globulin (TBG) in serum. A TBG-beta-D-galactosidase complex was prepared with m-maleimidobenzoyl N-hydroxysuccinimide ester. The mean analytical recovery of TBG added to serum was 99%, sample volume and TBG value were linearly related, and values for TBG determined by this method and those determined by radioimmunoassay correlated well (r = 0.98). Coefficients of variation averaged 7.6% within assay, 6.6% between assay. The measurable range of TBG in the serum was 3.3 to 52 mg/L, but higher TBG concentrations could be measured by diluting the test serum with TBG-free serum. Mean (and SD) serum TBG concentrations as determined by this method were as follows: for 20 normal subjects, 21.2 (3.7) mg/L; for 10 pregnant women, 50.1 (9.5 mg/L; and for 10 patients with TBG deficiency, not detectable.
Hypoxic-hypercapnic interaction in mild hypoxia was studied in 12 healthy males. Steady state ventilatory responses to hypercapnic-hypoxia [delta V(s)] were obtained as the difference in ventilation between hypoxia (mean values +/- S.D. of PETO2 = 7.36 +/- 0.20 kPa or of PaO2 7.10 +/- 0.41 kPa) and hyperoxia (PETO2 greater than 26.7 kPa) with the same degree of hypercapnia (PETCO2 6.12 +/- 0.22 kPa). On the other hand, withdrawal responses [delta V(w)] were obtained as the magnitude of depression in ventilation caused by two breaths of O2 from the above mentioned hypoxic hypercapnia. Averaged delta V(s) and delta V(w) were 9.57 +/- 5.45 and 6.45 +/- 4.90 l/min, respectively, the difference being statistically significant (P less than 0.01). Furthermore, if we assume the presence of ventilatory depression to be due to tissue PCO2 fall resulting from an increase in cerebral blood flow caused by hypoxia, the magnitude of central hypoxic-hypercapnic interaction was estimated to be as great as the value of delta V(w).
During 90 min of spontaneous or controlled CO2 breathing in splenectomized dogs, the acid-base parameter changes of the thoracic duct lymph were compared with those of the arterial and postcaval venous blood. (1) The lymph reached an apparent steady state in the acid-base parameters at least 10 min after the blood. (2) The lymph bicarbonate concentration gradually increased almost in parallel with the lymph PCO2 elevation, while the raised plasma bicarbonate concentration remained nearly unchanged until the end of CO2 inhalation. (3) The in vivo buffer slope of the lymph increased strikingly within 10 min, reaching three times the in vitro slope at 90 min after inception of CO2 breathing. After 10 min, the lymph value became higher than the venous value, suggesting early cellular contribution to ECF buffering. (4) Considering the lymph values as representative of the interstitial fluid values, cellular contribution to ECF buffering was computed; they were 7.8, 15.6, and 10.7% in the spontaneously breathing group, and 8.9, 10.6, and 12.0% in the controlled ventilation group at 30, 60, and 90 min of CO2 breathing, respectively.
Chelating agent, such as CaEDTA, CaDTPA, D-penicillamine, DMSA, desferoxamine, NTA, cysteine ethyl ester, BAL, alpha-MPG, phthalein complexone, were tested as a possible contrast enhancing agent for tumor imaging with 67Ga-citrate. The intravenous administration of a chelating agent to Ehrlich's tumor bearing mice, one hour after the injection of 67Ga-citrate, accelerated the blood clearance with only a very slight change of activity in the target, increasing the tumor-to-blood ratio, and consequently achieving a better visualization. Among the tested chelating agents, D-penicillamine showed the highest target-to-nontarget ratio at a shorter time: a good tumor-to-blood ratio, performed after 24 hr with non-treated animals, was achieved in only 1-3 hr with post-treated animals. Thus, D-penicillamine hold a considerable promise as a contrast enhancing agent for future clinical use.
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Ten healthy subjects were tested for their peripheral respiratory chemosensitivities by the withdrawal technique two times on separate days. Hypoxic hypercapnia of PET, O2 75, 65 AND 55 mmHg with PET, CO2, 5 mmHg higher than the control level was replaced by 100% O2 two times with spontaneous respiration. Then, breath-by-breath depression calculated in minute ventilation (delta V) was observed during the period 5-20 sec after the first O2 inhalation. The results were analyzed by the linear relationship between PET, O2 and 1n delta V, and PaO2 and 1n delta V. Delta V at P02 50 mmHg, delta V50, was 9.09 +/- 6.81 liters/min (mean +/- SD) in PET, O2-1n delta V analysis and 9.22 +/- 7.46 liters/min in PaO2-1n delta V analysis, respectively. The averaged day to day variation of delta V50 expressed by SE in % was 5.3% in PET, O2-1n delta V analysis and 11.5% in PaO2-1n delta V analysis, respectively.
Incubation of bovine lenses over a period of 24 h in Krebs-Ringer solution effects a decrease in the content of GSH. This decrease can be blocked by addition of 2 mM/1, each of glycine, glutamic acid, and cysteine. The content in GSSG is in no way influenced by incubation with or without addition of the three amino acids.
The effects, on respiration, of the acute administration of sodium bicarbonate were studied in 10 normal subjects. Carbon dioxide responses curves and tidal volume v. PCO2 relationships were obtained under hyperoxic conditions using a closed-circuit breathing system. During alkalosis, a decrease in the slope, and a displacement of the response curves to the right, were observed. These findings indicate that metabolic alkalosis, induced acutely by the administration of sodium bicarbonate, alters the respiratory response to carbon dioxide and that sodium bicarbonate may have a depressant effect on respiration.
On fundi of pigmented rats, with Argon laser constantly 300 mW of power. 2 seconds exposure time and 50 microns spot diameter, coagulations have been performed. The eyes have been observed up till 3 months after the intervention, then angiographies were performed, and the following enucleated eyes have been examined with the fluorescence microscope. Neovascularizations and dye diffusions were observable mainly in the marginal zones of the arised cicatrices. The neovascularizations were starting from the choroid and penetrating into the outer retinal layers.
The effect of chlorpromazine (CPZ), imipramine (IMP), nitrazepam (NZP) and amobarbital sodium (AMOB) on the REM period of sleep (REMP) was investigated on four subjects by means of all-night sleep polygraphy with the schedule PPPDDDPP where P is placebo and D active drug. CPZ 25 mg resulted in a slight increase in %REMP, and no significant change in REM density (1 second fraction method) and total REM activity during the drug and withdrawal nights. IMP 25 mg produced moderate decrease in %REMP in the three drug nights, whereas REM density decreased only in the first drug night. NZP 5 mg resulted in a slight parallel suppression of %REMP, REM density and total REM activity during the drug nights. AMOB 200 mg produced a slight decrease in %REMP and marked decrease in REM density during the drug nights. Rebound increase of %REMP and a tendency of carry over decrease of REM density were observed in the withdrawal nights. Decrease in the REM density was more marked in AMOB than in NZP drug night. The importance of the simultaneous analysis of %REMP and REM density for the study of effects of psychotrophic drugs on sleep was emphasized.
The effects of laser coagulation on rat fundi were studied angiographically and with the fluorescence microscope. The coagulations were performed using constantly 300 mW and 0.2 second exposure time and 50 microns spot diameter. We observed the animals for 3 months, after which we could still observe dye diffusion by fluorescence angiography. With the fluorescence microscope we could localize these diffusions as originating from neovascularisation starting from the choroid. These new vessels penetrated subsequently into the exterior retinal layers. At the beginning of our observation time, the retinal vessels showed some sinuosities, dilatations and solitary stenosis, but no disturbance of circulation was demonstrable.
1. Both cardiovascular and antidiuretic hormone (ADH) responses to some neural inputs were examined in paralysed anaesthetized cats.2. Carotid occlusion elicited cardiovascular responses and increased ADH secretion. When the electrical stimulation of discrete loci of the cerebellar fastigial nucleus (fastigial pressor area) was superimposed on carotid occlusion, cardiovascular responses were further facilitated, while ADH secretion was inhibited.3. The fastigial stimulation alone elicited facilitory cardiovascular responses composed of hypertension and tachycardia, and the fastigial pressor response (FPR), but did not evoke any consistent ADH response.4. These facts indicate that cerebellar modulation of ADH secretion occurs not directly via the hypothalamo-hypophysial system but through the lower brain stem to which both carotid sinus nerves and outflows from the fastigial pressor area project.5. We conclude that the fastigial pressor area is specific for not only cardiovascular and other autonomic responses but pituitary hormonal response.
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