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Biomedical subjects

S Sasaguri

Publications and source records attributed to S Sasaguri.

65 records · Page 4Linked to original sources

[Neuronal and adrenomedullary catecholamine response to cardiopulmonary bypass: with special reference to comparative studies based on functional classification].

Plasma epinephrine (E) and norepinephrine (NE) levels during cardiopulmonary bypass (CPB) were studied in thirty-eight cardiac patients with various grades of NYHA classification. Striking increases of both E and NE levels after release of aortic cross clamp (stage 4) were noted. A thirteen fold increase in E (from 0.05 +/- 0.05 ng/ml to 0.62 +/- 0.48 ng/ml) and sixfold increase in NE (from 0.21 +/- 0.18 ng/ml to 1.26 +/- 0.78 ng/ml) occurred from prebypass (stage 1) to stage 4. The values of E and NE were peaked at stage 4 and rapidly decreased after heart beating (stage 5). At chest closure (stage 7), E returned to close to prebypass control (stage 1) value, however NE remained still in moderately high level. Patients were divided into three groups: The mild group (NYHA class I and II, fourteen patients), the ill group (NYHA class III and IV, nineteen patients) and the IABP group (IABP support since prior to CPB due to unstable angina and ventricular septal perforation, five patients). Whereas E value at either stage 4 or stage 5 in the mild group was statistically significantly higher (p less than 0.05) than each E value at corresponding stages in the ill group. NE value at each stage 3 (prior to aortic cross clamp), stage 4 or stage 5 in ill group significantly higher than each NE value at same stages in the mild group respectively. These data suggest that depletion of E and compensatory increase of NE in the ill group may be occurred during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[A case of myonephropathic metabolic syndrome treated with limb washout using a roller pump and cell saver].

We operated on a 65 year old male for the saddle embolism presenting the signs of MNMS. Before the reperfusion of the ischemic limbs which were successfully embolectomized with the use of Fogarty catheter, we performed limb washout using roller pump and cell saver. The washout was done in the high flow and large volume by the roller pump. The red blood cells in the efflux were saved using cell saver and retransfused to the patient. The patient recovered without deterioration of MNMS. The limb washout was effective for the prevention of the deterioration of MNMS.

Acute Disease↗

Early change of myocardial water during acute cardiac allograft rejection.

To determine the changes in myocardial water during acute cardiac rejection and the effects of Ciclosporin (CYA) on the myocardial water, 90 heterotopic cardiac transplants were performed in rats which were divided into 3 groups, namely those receiving 1) Lewis X Lewis isografts, 2) Lewis X Brown Norway allografts and 3) CYA treated allografts (15 mg/kg/day). The water content was measured in both recipient and donor hearts at 2, 4, 6 and 8 days after transplant. Pathological specimens were examined by light and electron microscopy, and scored on a 0 to 4+ scale of increasing evidence of rejection. The water content of the isografts showed no significant change throughout the post operative period. In contrast, the allografts had significant increase of water content as early as 2 days after transplant, compared to the isografts and recipients hearts. A significant difference in cellular infiltration was noted between isograft and allograft 4 days after transplant. CYA suppressed significantly the increase of myocardial water and cellular infiltration in the allografts. These data suggest that myocardial edema may precede cellular infiltration during the rejection process and it may be suppressed with CYA treatment. The measurement of myocardial water may be useful in early detection of acute cardiac allograft rejection and for examining the therapeutic effects of CYA.

Animals↗

Early detection of cardiac allograft rejection with proton nuclear magnetic resonance.

No reliable, noninvasive technique is currently available for the early detection of cardiac transplant rejection. In this study, pulse nuclear magnetic resonance (NMR) spectroscopy was used (20 MHz) to detect cardiac allograft rejection in rats. Proton spin-lattice relaxation time (T1), proton spin-spin relaxation time (T2), and water content were measured in both recipient and donor hearts at 2, 4, 6, and 8 days after transplantation. Pathologic specimens were scored on a 0 to 4+ scale of increasing evidence of rejection by light microscopy. Three kinds of heterotopic transplants were performed for a total of 90: (1) Lewis rats received Lewis rat isografts, (2) Lewis rats received Brown Norway rat allografts, and (3) Lewis rats received cyclosporin A-treated allografts (15 mg/kg/day). T1 in group 2 was significantly higher than that in group 1 as early as day 2 (670 + 25 vs 616 + 11 msec, p less than .001), when histologic scores were not different. T2 in group 2 was also higher than that in group 1 (48.0 +/- 5.0 vs 41.1 +/- 2.6, p less than .005). T1 and T2 in group 2 increased from day 4 and correlated well with the water content of the hearts (r = .70 and r = .75, respectively). Cyclosporin A completely suppressed the increase of T1 and T2 in group 2. Treatment with cyclosporin also suppressed the histologic rejection scores. Our data suggest that proton relaxation time measurement may be a sensitive technique for detecting the onset of rejection and examining the therapeutic effects of cyclosporin. NMR imaging, which highlights T1 and T2 separately, should provide a sensitive noninvasive means of assessing myocardial graft rejection.

Animals↗

Immunohistochemical characterization of p57KIP2 expression in human esophageal squamous cell carcinoma.

Functional defects in the CIP/KIP family of cyclin-dependent kinase inhibitors (CDKIs) have been shown to be associated with human malignancies. We immunohistochemically examined p57KIP2 (p57) expression in 92 patients with human esophageal squamous cell carcinoma (SCC) to determine the relationship between this expression and those of cyclin D1 and E. The p57 labeling index (LI) (defined as the percentage of p57-positive cells) in esophageal SCC was 43.3 +/- 3.2% (mean +/- standard error of the mean). In non-neoplastic esophageal epithelium, p57 staining was more frequently observed in the basal and parabasal cells than in surface layer cells. Immunostaining for cyclin D1 and E was observed in 28.2% (28/92) and 32.6% (30/92) of tumors, respectively. The median p57 LI in cyclin D1-positive cases was 66.2, and significantly higher than that in negative cases (31.9%) (p = 0.0009). There was no significant relationship between p57 LI and cyclin E expression (p = 0.147). As determined using Kaplan-Meier's method, loss of p57 immunoreactivity was not a prognostic factor for esophageal SCC (p = 0.548). Our in vivo findings suggested that p57 protein expression was positively correlated with cyclin D1 expression and that loss of p57 protein expression alone does not affect progression of esophageal SCC.

Adult↗

Role of smooth-muscle cells and macrophages in cardiac allograft arteriosclerosis in rabbits.

Accelerated coronary arteriosclerosis is one of the major complications in allogeneic cardiac transplantation, despite the significant improvement in immunosuppressive therapy. In this study we sought to clarify the cellular components in cardiac allograft arteriosclerotic lesions with monoclonal antibodies specific to either the muscle cell (HHF-35) or the macrophage (RAM-11). Four kinds of heterotopic transplantations were performed in the rabbit: (1) low cholesterol-fed (n = 5), (2) 1% cholesterol-fed (n = 5), (3) low cholesterol-fed and immunosuppressed (n = 6), and (4) 1% cholesterol-fed and immunosuppressed (n = 6). The donor hearts were removed after cardiac arrest in groups 1 and 2, and at 5 weeks after transplantation in groups 3 and 4. In groups 1 and 2 acute rejection was associated with slightly thickened intimal lesions composed of abundant infiltrating mononuclear cells and sparsely intermingled smooth-muscle cells. In group 3 the arterial intima were moderately thickened with the predominant proliferation of smooth-muscle cells. In group 4 coronary lumina were almost completely occupied with the intimal foam cells, which were derived mostly from macrophages and some from smooth-muscle cells. These data suggest that the proliferation of smooth-muscle cells might be a major factor contributing to arteriosclerosis in chronic cardiac rejection and that long-term exposure to hypercholesterolemia could induce the accumulation of smooth-muscle cells or macrophage-derived foam cells.

Animals↗