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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 631 records · Page 35Linked to original sources
PubMed1983

[Effect of regional phase delay on left ventricular performance studied by radionuclide angiography].

When cardiac hypokinesis in myocardial infarction is analyzed by means of phase analysis of radionuclide (RI) angiography, there are some cases in which the amount of regional wall movement of the left ventricle does not so decline, but the phase delay of regional wall movement is great. Hence, a simulation experiment was performed with a computer to evaluate the influences of regional phase delay on cardiac work. It was assumed that the radius of the model of the left ventricle varies from 3 cm in the late diastolic phase to 2 cm in the late systolic phase, and that in the initial 1/3 time of diastole, the radius alters by 90% of the change. One cardiac cycle (360 degrees) was divided into 60 fractions (1 fraction = 6 degrees), 0 degree being the end of diastole and 180 degrees the end of systole. An ischemic area was supposed to cover S% of the whole volume of the left ventricle, its amount of regional wall movement being P% of the normal area, and the phase delay being R degrees. By varying S, P and R, and taking weighted means of volume curves and normal ones, their assumed volume curves of the left ventricle were computed. Stroke volume (SV) and ejection fraction (EF) obtained from these curves were compared to those obtained from the normal curves, and were expressed in percentage (%SV, %EF). The influences of the changes of S, P and R on the volume curve and on the cardiac work were examined. Then the count curves of the left ventricle (LV) were obtained by gated RI angiography in 22 cases of myocardial infarction and 8 healthy controls, and LV regional wall movements were examined by means of the Fourier analysis. The circular volume was partitioned from the center into eight sections on the LV image of LAO 45 degrees, and the amount of wall movement and the phase delay of each section were evaluated from the count curves of each section. The following results were obtained. %SV and %EF declined with sole occurrence of regional phase delay. Occurrence of the regional phase delay flattened the slope of the volume curve of the initial diastolic phase and formed shoulders on this curve. This was observed also on the count curves actually determined from cases with myocardial infarction. When regional wall movement was markedly decreased, the influence of the regional phase delay on the pattern of the volume curve was slight even if the phase delay was extensive.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1983

[Characteristic findings of mitral valve and mechanism of mitral valve prolapse in Marfan syndrome].

To elucidate the mechanism of generation of mitral valve prolapse (MVP) in Marfan syndrome, we studied the relations of the length of the anterior mitral leaflet to the diameter of the mitral ring. In 13 cases of Marfan syndrome associated with MVP (Group I), 21 of isolated MVP (Group II), and 24 controls free from valvular disease (Group C), the maximal length of the anterior mitral leaflet (L) and the end-diastolic and end-systolic diameters of the mitral ring (Rd and Rs) were measured in the long-axis views on two-dimensional echocardiograms. In addition, the measurements were corrected with the body surface area; designated as L(c), Rd(c) and Rs(c), respectively. Furthermore, L/Rd and L/Rs, and the percentage of shortening of the mitral ring in systole, (Rd-Rs)/Rd X 100, were obtained. The body surface area in Group I was greater than that in Group II (p less than 0.05), but there was no significant difference between Groups II and C. The L was obviously different between Groups I and II or C (p less than 0.001, respectively). Similarly, there was a significant difference in L(c) between Groups I and II (p less than 0.02) or C (p less than 0.001), indicating the remarkably long anterior mitral leaflet in Group I. The Rd in Group I and II was greater than that in Group C (p less than 0.01 and p less than 0.02, respectively), while there was no significant difference in the Rd(c) among the 3 groups. There was also no statistical difference in either Rs or Rs(c) among the 3 groups. Both L/Rd and L/Rs in Group I were remarkably higher than those in Groups II and C (p less than 0.001, respectively), whereas these parameter did not differentiate Group II from Group C. (Rd-Rs)/Rd X 100 was higher in Group I than that in Groups II and C (p less than 0.05 and p less than 0.01, respectively), but it was not significantly different between Groups II and C. These results suggested that one of the probable mechanisms of generation of MVP in Marfan's syndrome is the redundant mitral valve resulting from a remarkably long leaflet and increased systolic shortening of the enlarged mitral ring.

Adolescent↗
PubMed1983

[Mitral valve prolapse in the heart with pressure overload of the right ventricle].

The prevalence of mitral valve prolapse (MVP) was examined in 16 patients with right ventricular pressure overload with a peak systolic pressure ranged from 60 to 204 mmHg (Group 1; 9 cases of primary pulmonary hypertension and 7 cases of pulmonary valve stenosis), and the clinical and echocardiographic data were compared to those of 12 patients with idiopathic MVP (Group 2) and 10 healthy persons (Group 3). MVP was defined when either or both of the mitral valve leaflets protruded into the left atrium beyond the plane of the mitral ring, and "gap" was defined as positive when one of the leaflets of the mitral valve slipped 3 mm or more without prolapse toward the left atrium than the other leaflet. Eccentricity of the left ventricle was obtained from the cross-sectional view of the left ventricle at the mid-ventricular level: the ratio of the internal diameter (S) passing through the mid-point of the interventricular septum (IVS) and perpendicular to the IVS divided by the longest internal diameter (L) parallel to the IVS, at end-diastole (S/L(d] and at end-systole (S/L(s], respectively. The following results were obtained. MVP was found in seven cases of 16 patients (43.8%) of Group 1. Two cases had positive "gap" (12.5%). Eccentricity of the left ventricle in Group 1 (S/L(d) 0.81 +/- 0.12, S/L(s) 0.78 +/- 0.15) was more marked than that of Group 2 (S/L(d) 0.98 +/- 0.09, S/L(s) 1.02 +/- 0.06) or of Group 3 (S/L(d) 1.03 +/- 0.08, S/L(s) 1.00 +/- 0.04) (p less than 0.001 in each).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

[Left ventricular regional wall motion after correction of tetralogy of Fallot].

Cardiac function and left ventricular regional wall motion were examined using two-dimensional echocardiography in 40 post-operative patients of tetralogy of Fallot (TOF) of an average of 13 years after the correction. From the data of treadmill exercise test and cardiac catheterization, patients were classified into two groups; cases with complete ability for treadmill test (Group A, n = 22), and disabled for the test and the right ventricular systolic pressure above 50 mmHg (Group B, n = 18). Compared with the control group (n = 10), the patient groups had greater cardiothoracic ratios (CTR) and right/left ventricular dimensions (RVd/LVd) (p less than 0.001), and Group B had a greater CTR and RVd/LVd than Group A (respectively p less than 0.001). Compared with the control group, the patient groups had no significant differences in corrected ejection time, fractional shortening and mean velocity of circumferential fiber shortening, and no difference was noted between Group A and Group B. Left ventricular regional wall was divided into 12 segments around the left ventricular circumference on the two-dimensional short-axis view and the regional wall motion was evaluated on the basis of [(diastolic-systolic)/diastolic left hemiaxial length X 100%] values. In Group B, akinetic or dyskinetic wall motion was visualized at the interventricular septum and left ventricular posterior wall, but there was no abnormal motion in the control group and Group A. We concluded that even in postoperative patients with preserved cardiac function at rest, some of them had abnormal left ventricular regional wall motion due to the persistent right ventricular overload or corrective patch, resulting in low exercise capacity.

Adolescent↗
PubMed1982

[Immunohistochemical demonstration of somatostatin-28 like immunoreactivity in the fetal and adult human gut and pancreas].

In order to examine whether somatostatin-28 originally isolated from porcine and ovine tissues was present in the human gut and pancreas or not, immunohistochemical methods using specific antisera against somatostatin-28 and somatostatin-14 antisera were carried out in the fetal and adult human gut and pancreas. The specific antisera against somatostatin-28 were prepared from somatostatin-28 antisera by absorption of somatostatin-28 antisera with sepharose 4B-somatostatin-14. Somatostatin-like immunoreactivity appeared in the epithelial endocrine-like cells of the gut and in the pancreatic islet cells at 11 week's gestation, and thereafter it was constantly present in the fetal and adult gut and pancreas. Although detection of somatostatin-28 like immunoreactivity was not inhibited in the sections in which specific antisera against somatostatin-28 pretreated with either somatostatin-14 or other kinds of peptide hormones were employed to replace primary antisera in the immunohistochemical staining process, it was completely inhibited after use of the specific antisera against somatostatin-28 absorbed with somatostatin-28. This finding suggested that detection of somatostatin-28 like immunoreactivity was due to the immunohistochemical reaction between specific antisera against somatostatin-28 and somatostatin-28 itself. Furthermore, observation of serial sections stained by using specific antisera against somatostatin-28 and somatostain-14 antisera revealed that cells reacting with the former antisera were identical to those reacting with the latter one. Although the finding seemed to imply that full sequences of somatostain-28 may be present in the human gut and pancreas, it remained obscure whether or not somatostatin-28 and somatostatin-14 like immunoreactivities may be present independently in the cells since somatostatin-14 antisera have a crossreactivity to somatostain-28.

Digestive System↗
PubMed1982

Presence of somatostatin-28 like immunoreactivity in the human pancreas.

Specific antisera against somatostatin-28 were prepared by absorption of somatostatin-28 antisera with sepharose 4B-somatostatin-14. Indirect immunofluorescence techniques using somatostatin-14 antisera and specific antisera against somatostatin-28 were carried out to elucidate the time of occurrence of somatostatin-28 in the fetal pancreatic islets and to ascertain whether somatostatin-28 was present in the adult pancreatic islets or not, and further to examine whether cells reacting with specific antisera against somatostatin-28 are identical to those reacting with somatostatin-14 antisera or not. Somatostatin-28 like immunoreactivity occurred in the fetal pancreatic islets at 11th week's gestation and was found in all fetal pancreatic islets examined in the present study. It was also found in the adult pancreatic islets. Furthermore, cells reacting with specific antisera against somatostatin-28 in the fetal and adult pancreatic islets were identical to those reacting with somatostatin-14 antisera. Thus, the present study elucidated the presence of somatostatin-28 like immunoreactivity in the human pancreas. However, it could not be decided whether cells reacting with somatostatin-28 antisera contain either only somatostatin-28 or both somatostatin-28 and somatostatin-14; in other words, whether somatostatin-14 is produced from somatostatin-28 or not, since somatostatin-14 antisera had a cross-reactivity to both somatostatin-14 and somatostatin-28.

Adult↗
PubMed1982

His-bundle electrogram in the convalescent stage of inferior myocardial infarction complicated with complete A-V block.

Twelve patients with inferior wall myocardial infarction complicated with complete atrioventricular block during the acute stage were studied. The His-bundle electrogram was studied in the convalescent stage at an average of 6 months after the acute attack. The age of the patients was 62 +/- 16 years. The width of the QRS complex was within the normal range and the PR interval was less than 200 msec. AH time was 74 +/- 18 msec (mean +/- SD). No split H activity was observed. HV time however, was significantly prolonged in the 12 patients; 54 +/- 12 msec vs. 42 +/- 9 msec in the control group (p less than 0.02). Five patients had HV time equal to or more than 60 msec. Intra-His block was suggested to exist in a high frequency in the patients who had previous complete AV block during the acute stage of myocardial infarction of the inferior wall.

Blood Pressure↗
PubMed1982

Somatostatin-28 like immunoreactivity in normal and tumour tissue from duodenum and pancreas.

Radioimmunoassay using labelled somatostatin-14 revealed that components of somatostatin-28 antisera cross-reactive to somatostatin-14 were removed by absorption of somatostatin-28 antisera with sepharose 4B-somatostatin-14. Indirect immunofluorescence techniques using specific antisera against somatostatin-28 were carried out in normal pancreas, duodenum, a somatostatinoma in the duodenum, and pancreatic tumour cells containing somatostatin-14 positive cells, in order to establish if somatostatin-28 is present in normal and pathological tissues. Somatostatin-28 like immunoreactivity was present in pancreatic islets cells and in the epithelial cells of the duodenum as well as in the duodenal somatostatinoma and in pancreatic tumour cells. Furthermore, cells reacting with specific antisera against somatostatin-28 were identical to those with somatostatin-14 antisera in normal and pathological tissues. The findings suggested that somatostatin-28 like immunoreactivity may be constantly present in the tissues where somatostatin like immunoreactivity was detected using somatostatin-14 antisera. However, further studies were necessary to clarify whether somatostatin-28 and somatostatin-14 were independently present in these tissues, in other words, whether somatostatin-14 may be produced from somatostatin-28 or not, since somatostatin-14 antisera had cross-reactivities to somatostatin-28.

Adenoma, Islet Cell↗
PubMed1982

Somatostatin-28-like immunoreactivity in the stomach.

Localization of somatostatin-28 and somatostatin-14 immunoreactive cells in the human, canine and cat's stomach was studied by an indirect immunoperoxidase method using somatostatin-14 antisera and specific antisera against somatostatin-28. The somatostatin-28 immunoreactive cells belonged to the endocrine-like cells of the fundic glands and pyloric antrum of the human, canine and cat's stomach. These cells were identical to somatostatin-14 ones. Since immunocytochemical cross-reaction between specific antisera against somatostatin-28 and somatostatin-14 was not found, it was suggested that the coexistence of N-terminal amino acid sequence of somatostatin-28 and somatostatin-14 in one and the same cell seemed to be most likely. Thus, it seems probable that somatostatin-28 originally isolated from porcine and ovine tissues may be constantly present in other mammals.

Animals↗
PubMed1982

Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders.

Blood coagulation and fibrinolysis were studied in 65 patients with chronic myeloproliferative disorders (MPD). They consisted of 28 patients with chronic granulocytic leukemia (CGL) in chronic phase, 7 with CGL in blast crisis, 9 with polycythemia vera (PV), 13 with primary thrombocythemia (PTh) and 8 with primary myelofibrosis (MF). Hemorrhagic and thrombotic complications were observed in 19 and 8 patients, respectively. Activated partial thromboplastin time and prothrombin time were prolonged in many patients. Low factor II levels were observed in some CGL patients. Factor V was decreased in CGL patients in chronic phase and in PV patients. Fibrinogen was either normal or increased in most patients, but an elevation of fibrin/fibrinogen degradation products (FDP) was found in some patients. The VIIIR: Ag/VIII:C ratio was increased in CGL patients in blast crisis, in PV patients and in PTh patients. Antithrombin III and plasminogen were below normal in some patients. Most patients showed a decrease in alpha 2-plasmin inhibitor. These findings suggest that blood coagulation and fibrinolysis are involved in the pathogenesis of the thrombotic and hemorrhagic complications in these patients. Chronic low-grade intravascular coagulation might be present in some patients with MPD.

Adult↗