Search PubMed⌕ Search

Biomedical subjects

I Sato

Publications and source records attributed to I Sato.

At least 325 records · Page 18Linked to original sources
PubMed1987

Maladaptation after successful revascularization in anginal patients without transmural infarction.

In order to elucidate how peripheral or cardiac function maladaptations play a role in deconditioning after coronary bypass surgery, we have evaluated effects of successful coronary artery bypass grafting (CABG) and percutaneous transluminal angioplasty (PTCA) on exercise capacity in anginal patients without myocardial infarction. Symptom-limited treadmill exercise tests were performed in 46 patients before and after CABG and in 28 patients before and after PTCA. None of the patients carried out a cardiac rehabilitation program after their discharge. PTCA patients showed significant improvement of exercise capacity, from 6.4 +/- 1.6 to 10.5 +/- 2.5 METs in 4 weeks after PTCA, and even elderly PTCA patients showed improvement from 6.0 +/- 1.1 to 10.3 +/- 2.5 METs. However, the exercise capacity of CABG patients improved only from 5.9 +/- 1.4 to 8.5 +/- 3.1 METs in the first 6 months after CABG, and from 5.9 +/- 1.7 to 10.0 +/- 3.6 METs thereafter. The 15 elderly CABG patients showed only slight increase of physical activity, from 6.0 +/- 1.7 to 6.9 +/- 1.9 METs in the first 6 months after CABG and from 6.3 +/- 1.9 to 8.7 +/- 2.9 METs thereafter. Furthermore, 6 of 15 elderly CABG patients showed no improved exercise capacity after CABG. There was no correlation between the duration of anginal symptoms before CABG and exercise capacity before or after CABG. These findings suggest that CABG itself and/or physical restriction during admission produces peripheral function maladaptation and may be the main contributors to deconditioning after CABG, especially in elderly patients. This deconditioning can be treated by a rehabilitation program after the discharge.

Aged↗
PubMed1987

Immunoreactive corticotropin-releasing hormone present in human plasma may be derived from both hypothalamic and extrahypothalamic sources.

Immunoreactive CRH concentrations were determined in human plasma using an immunoaffinity chromatographic extraction procedure and sensitive RIA. Immunoreactive CRH was detectable in the plasma of all normal subjects (mean +/- SD, 6.2 +/- 2.4 pg/mL; n = 15). Basal (0800-1000 h) plasma immunoreactive CRH levels were significantly lower in patients with Cushing's syndrome due to adrenal (2.8 +/- 1.1 pg/mL; n = 4) or pituitary adenomas (2.9 +/- 0.8 pg/mL; n = 5), in patients with hypothalamic hypopituitarism (3.2 +/- 0.9 pg/mL; n = 5), and in glucocorticoid-treated patients (3.9 +/- 1.9 pg/mL, n = 8). Basal plasma CRH levels were also low in patients with acromegaly (2.8 +/- 0.8 pg/mL; n = 14) and insulin-treated diabetic patients whose pituitary-adrenal function was normal (3.6 +/- 1.0 pg/mL; n = 12). In normal subjects plasma CRH levels increased after insulin-induced hypoglycemia; this response was abolished by the prior administration of dexamethasone. In contrast, basal plasma CRH levels were not affected by prior administration of metyrapone or dexamethasone. No evidence for diurnal variation in plasma immunoreactive CRH was found in normal subjects. In addition, in normal subjects oral glucose administration elicited a significant increase in plasma CRH (basal, 7.3 +/- 0.9 pg/mL; peak 30 min after glucose, 16.7 +/- 5.8 pg/mL; n = 5; P less than 0.05) without concomitant changes in ACTH. Gel filtration of extracts of pooled plasma from normal subjects revealed a major component of immunoreactive CRH in the position of synthetic rat CRH. Immunoreactive CRH-sized material had the same retention time as authentic rat CRH in a reverse phase high pressure liquid chromatography system. The content of immunoreactive CRH in human placenta, pancreas, and adrenal gland was much larger than that in hypothalamus. These findings suggest that immunoreactive CRH is present in peripheral plasma; the increase in plasma immunoreactive CRH after insulin-induced hypoglycemia may reflect stimulation of hypothalamic CRH release; the increase in plasma immunoreactive CRH after glucose administration may reflect extrahypothalamic CRH release; and the lack of diurnal variation in plasma immunoreactive CRH together with the lack of suppression of CRH by dexamethasone suggest that basal plasma CRH is of extrahypothalamic origin.

Adolescent↗
PubMed1987

[Non-invasive assessment of the peak pressure gradient between the aorta and pulmonary artery in patent ductus arteriosus].

The validity of continuous wave Doppler ultrasound estimation of the peak pressure gradient between the aorta (Ao) and pulmonary artery (PA) in patients with patent ductus arteriosus (PDA) was evaluated. Ten patients, all without other anomalies, underwent cardiac catheterization and cine-angiography, and the peak pressure gradient between the Ao and PA (dP(C)) was measured during catheterization. In all cases the mean PA pressure was less than 35 mmHg. According to the angiographic findings, the patients were categorized as Group A, consisting of seven patients whose features of the ductus were wedge- or tube-like in configuration; Group B, consisting of two patients whose features were termed "orifice-like" stenosis including one with abrupt narrowing on the PA side of the ductus and the other with a short segmental ductus. Group C consisted of one patient who had a long curved segmental ductus. The maximum velocity of ductus flow was measured by continuous wave Doppler ultrasonography, and the estimated peak pressure gradient between the Ao and PA by Doppler (dP(D] was calculated using the simplified Bernoulli equation (dP = 4V2). In group A, dP(D) was overestimated compared to dP(C) in all patients by 19 to 51 mmHg (mean 34 mmHg). However, in group B, the difference between dP(D) and dP(C) was small, 5 mmHg and 7 mmHg, respectively. In group C, dP(D) was underestimated as opposed to dP(C). Thus, in the limited cases, the simplified Bernoulli equation could be used in estimating the peak pressure gradient between the Ao and PA. However, this equation leads to overestimation in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗
PubMed1987

[Mitral regurgitation in the acute phase of Kawasaki disease: scrutiny using real-time two-dimensional Doppler flow imaging].

To study valvular lesions in the acute phase of Kawasaki disease, 17 patients who were admitted to our institution before the 12th day of their illness were examined using real-time two-dimensional Doppler flow imaging (2DD: Toshiba SSH 65A) from January to September 1986. Pulsed Doppler, continuous wave Doppler, and M-mode echocardiography were also performed. Patients were examined daily from their admission to 12th day of illness, and after that, more than twice a week until the 28th day of illness. Fourteen of the 17 patients underwent Ga-67 scintigraphy. Cardiac catheterization, including selective coronary arteriography, was performed in 15 patients in the convalescent phase. Mitral regurgitation (MR) was detected in eight of the 17 cases (47%). MR appeared on 2DD 7.5 +/- 1.6th day of illness (mean +/- SD), lasting until 11.9 +/- 5.7th day of illness. MR was transient and mild in degree in all cases, and the regurgitant jet was directed towards the left atrial posterior wall. Neither prolapse nor deformity of the mitral valve was detected. The left ventricular volume indices (determined by the Pombo method) measured by M-mode echocardiography in the acute and convalescent phases were compared. In the group with MR in the acute phase, the end-diastolic volume index was 66.9 +/- 19.9 ml/m2 and the end-systolic volume index was 21.0 +/- 11.7 ml/m2. These were significantly greater than those in the convalescent phase (51.3 +/- 13.1 ml/m2, 14.1 +/- 4.0 ml/m2, respectively). However, no significant differences were observed in the group without MR. Positive uptake of Ga-67 was observed in six patients with MR, but in none of the seven without MR. The incidence of positive uptake was significantly higher in the patients with MR. Cardiac catheterization performed in the convalescent phase revealed that no patient had the findings of MR, other valvular lesions, coronary arterial lesions, or abnormal ventricular performance.

Acute Disease↗
PubMed1986

Pathohistological and immunohistochemical studies on Castleman's disease of the lymph node.

Histological and immunohistochemical examinations were carried out on lymph nodes in 9 cases with Castleman's disease. In all cases, there were whorled follicle centers and proliferation of blood vessels. These findings were also considered to be important criteria for diagnosis of the plasma cell type of this disease. The whorled follicle centers often consisted of smaller concentrical structures and contained factor VIII-positive cells. In some cases, there were many small whorled structures surrounding postcapillary venules within the interfollicular areas of lymph nodes. These structures had factor VIII-positive granules indicating their endothelial origin. In 2 cases of the plasma cell type, monoclonal plasma cell proliferation (IgA, lambda and IgG, lambda, respectively) and cellular atypia were identified. These findings showed that extramedullary plasmacytoma could occur not only in the multicentric form, but also in the solitary form of Castleman's disease. In the lymph node of a case of the hyaline-vascular type, there were scattered tumour nodules consisting mainly of factor VIII-positive, atypical spindle cells suggesting associated Kaposi's sarcoma. It is conceivable that an abnormal immune state plays a role in pathogenesis of Castleman's disease.

Adult↗