Search PubMed⌕ Search

Biomedical subjects

H Toyoshima

Publications and source records attributed to H Toyoshima.

At least 181 records · Page 10Linked to original sources
PubMed1980

Effects of domperidone on serum prolactin levels in human beings.

Effects of domperidone, a dopaminergic antagonist, on serum prolactin levels were studied in 6 normal men and 6 normal cyclic women at the different phases of their menstrual cycles (i.e., the follicular, the preovulatory and the luteal phases). Domperidone (10 mg, i.v.) caused significant increases in serum prolactin in all cases within 15 min after the injection. The prolactin response was significantly (p < 0.01) higher in women than in men, and there was no significant difference in the prolactin responses among the three phases of the menstrual cycles. These results indicate that domperidone may be an effective stimulator of serum prolactin secretion in human beings.

Adult↗
PubMed1980

Parallel dysfunctions of pancreatic A, B and PP cells in insulin dependent diabetes.

To test the possibility that insulitis might play an etiological role in the pathogenesis of insulin dependent diabetes, functions of 3 kinds of islet constituting cells (A, B and PP cells) were estimated by quantifying secretory responses of glucagon-, C-peptide-and pancreatic polypeptide-producing cells to hyperglycemia and hypoglycemia. In insulin dependent diabetes, all 3 hormonal responses were severely impaired to the same extent. On the other hand, 3 islet cell functions were uniformly but less severely impaired in insulin independent diabetics without a diabetic family history. These results suggest that A, B, and PP cells of islet of Langerhans are evenly destroyed in parallel fashion at least in insulin dependent diabetes and in some insulin independent diabetes, suggesting insulitis as a possible cause of these types of diabetes.

Blood Glucose↗
PubMed1980

Urinary keratan sulfate of Morquio's disease.

To elucidate precise chemical nature of urinary keratan sulfate (KS) of Morquio's disease, crude glycosaminoglycans (GAG) were separated from 24-hr urines of 3 patients with Morquio's disease and from pooled urine of a healthy boy, using cetylpyridinium chloride. KS fractions were then separated from the crude GAG after removal of other GAG and acidic glycopeptide by successive digestion with testicular hyaluronidase and chondroitinase ABC, and by nitrous acid treatment, followed by Dowex 1 column chromatography. The distribution of KS in several fractions (1.5 M Fr-5.0 M Fr) obtained by Dowex 1 column chromatography suggested polydispersity of urinary KS. The relative amounts (micrograms/24-hr urine/kg body weight) of the KS fractions excreted into Morquio's urine were 52-63 times as much as that excreted into normal urine. The KS fractions contained galactose, glucosamine and sulfate as the major constituents, together with fairly amounts of galactosamine and sialic acid, and small amounts of mannose, L-fucose and glucose. The KS fractions resembled sulfated glycopeptide with respect to the sugar composition. The contents of sulfate and sialic acid in each KS fraction from Morquio's urine were higher than those in the corresponding one from normal urine, whereas opposite was the case for the ratio of glucosamine to galactosamine. The sulfate contents in the KS fractions from Morquio's urine indicated that the patient excreted over-sulfated KS into urine. The chemical compositions of the KS fractions from Morquio's urine suggest that the sulfatase specific for 6-sulfate linked to sugars with the galactose configuration may act in a early step of the catabolism of oversulfated KS in the normal tissues.

Adolescent↗
PubMed1979

Body surface potential distributions in posterior ventricular pre-excitation.

Waveform of the QRS complex during ventricular pre-excitation is subject to the influence of both the site of pre-excitation and the time of pre-excitation relative to that of excitation via the normal AV path. This paper reports a case in which lead V1 of the electrocardiogram (ECG) could be altered from an R to an rS pattern by the administration of atropine sulfate. The provable mechanism was that of reduced conduction time in the normal AV path with altered time phase of normal excitation and pre-excitation. This mechanism was simulated in experiments on dogs and yielded similar findings. Body surface mapping in both the patient and the dogs provided evidence that pre-excitation could be recognized by that means with varied time phase of normal excitation and pre-excitation. It was demonstrated that the QRS complex of right sided precordial leads could be altered from an R to an rS pattern by altering the time phase of normal excitation and pre-excitation of the posterior ventricular wall. This alteration was related to the degree to which negative potentials on the anterior chest wall due to right ventricular breakthrough of normal activation developed in relation to the time of pre-excitation.

Action Potentials↗
PubMed1978

Electrotonic interaction during canine ventricular repolarization.

Canine ventricular refractory periods were measured during test site drive, during drive of single ectopic sites, during fusion drive from two ectopic sites, and during fusion drive from an ectopic site and the test site. Refractory period duration was dependent on the driving modes employed. Refractory periods were 2.63 +/- 0.73%, 3.42 +/- 0.87%, 3.54 +/- 100%, and 4.68 +/- 1.36% (mean +/- SD) shorter during drive of single ectopic sites 2, 4, 6, and 40-60 mm, respectively, from the test site than during test site drive. During fusion drive from two ectopic sites, refractory periods were an average of 2.44 +/- 1.04 msec (mean +/- SD) less than during drive from a single ectopic site (P less than 0.005). When fusion of activation, induced by ectopic and test site drive, was located within 4 mm or less of the test site, refractory periods during fusion drive were also significantly shorter than during test site drive (P less than 0.05). Refractory periods were as much as 10 msec shorter when fusion occurred within 1 mm of the test site than their durations during test site drive. The differences in refractory periods measured during various driving modes were most likely due to electrotonic interactions during ventricular repolarization and are explicable on the basis of the intracellular distribution of potentials to be expected with each driving mode.

Animals↗
PubMed1977

Diagnosis of right ventricular infarction: experimental study through the use of body surface isopotential maps.

This investigation was designed to diagnose right ventricular infarction, which is difficult to diagnose by the standard twelve-lead ECG, through the use of body surface isopotential maps which have significant diagnostic information. Right ventricular infarction was experimentally caused by ligation of the canine right coronary artery. Each dog had a series of maps recorded before and a week after experimentally-induced myocardial infarction. The common features of maps in right ventricular infarction are: 1. In the early stage of the ventricular depolarization the negative area occupies a comparatively large part of the right anterior chest surface, and in the middle stage, the larger part of the right anterior surface is also occupied by the negative area. 2. A minimum appears on the right anterior chest surface in the early stage. The delayed excitation resulting from intraventricular conduction disturbance caused by infarction, as verified by the epicardial isochronic map, is also well represented by the body surface isopotential map. In conclusion, through the use of body surface isopotential maps, it is much easier to diagnose right ventricular infarction and intraventricular conduction disturbance caused by infarction even in cases in which the standard twelve-lead ECG does not show the abnormalities clearly.

Animals↗
PubMed1977

Experimental study of myocardial infarction through the use of body surface isopotential maps: ligation of the anterior descending branch of the left coronary artery.

This investigation was undertaken to diagnose the location and extent of myocardial infarction with the use of maps which give significant information about the ventricular activation process. Myocardial infarction was experimentally caused by ligation of the anterior descending branch of the left coronary artery. All classes were classified into three groups (A,B, and C) according to the location and extent of infarction. The map of each group had its own characteristics, as follows. In Group A no pisitive potentials appeared on the left anterior chest surface all through ventricular depolarization. In Group B, like Group A, the negative area occupied the whole left anterior chest surface in the early stage. But in the later stages there appeared a positive area on the left anterior surface. As to Group C, there was no abnormality in its early stage, but in its middle stage, the negative area was found on the left anterior chest surface. Thus the sequential maps can be helpful in diagnosing the location and extent of myocardial infarction, and will be applied to clinical use much more.

Animals↗
PubMed1976

Comparison of the changes in plasma human growth hormone (HGH) and immuno-reactive glucagon (IRG) after intravenous and subcutaneous injection of glucagon.

Ten healthy male volunteers were studied to compare the effectiveness of intravenous and subcutaneous injections of 1 mg of glucagon on HG secretion. Plasma HGH level rose to a peak of 6 ng/ml or greater 120 minutes after the subcutaneous injection of glucagon (sc glucagon) in all subjects, whereas the intravenous injection of glucagon (iv glucagon) caused comparable increments in plasma HGH in only six out of ten subjects. Furthermore, in comparison to those in sc glucagon the periods required to show maximum responses were less consistent in iv glucagon. Plasma IRG levels reached a peak of 102.4+/-22.6 ng/ml at two minutes following iv glucagon, and a peak of 3.33+/-1.08 ng/ml at 15 minutes following sc glucagon. These fell to initial levels at 60 minutes and at 180 minutes, respectively. There was no definite correlation either between the magnitudes of changes in plasma IRG and HGH levels or between the velocities of decrement in blood sugar and HGH responsiveness. Judging from its simplicity and reproducibility it may be concluded that sc glucagon is more suitable for a clinical provocative test of HGH release than is iv glucagon. In regards to the mechanism of glucagon-induced HGH release, neither glucagon per se nor the fall of blood sugar after hyperglycemia was assumed to play any major role. The sustained elevation of plasma IRG for a certain period might be responsible for the glucagon-induced HGH release.

Adult↗
PubMed1976

Correlations between the spread of ventricular activation and map patterns of measured and difference maps.

Three kinds of torso surface isopotential maps (measured, simulated, and difference maps) were delineated at every 1.5 (or 3) msec. during the QRS duration from the 85 unipolar lead ECG's led from the surface of a cylindrical torso model filled with perfusate and containing a canine heart undergoing Langendorff's perfusion. These three maps were compared as to the propagation process of ventricular activation obtained from the same heart and close correlations were found between the spread of ventricular activation and the map patterns of measured and difference maps. The difference map mainly reflected the proximity potential at each instant of ventricular activation in QRS duration and, when used in combination with the measured map, it was useful to estimate the spread of ventricular activation, especially around the stage of epicardial breakthrough of the activation front. It was confirmed that the interpretation of the difference map expressed in the present paper would not be misleading even if applied to a difference map obtained in a human torso model experiment.

Action Potentials↗