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Biomedical subjects

M Sugihara

Publications and source records attributed to M Sugihara.

At least 91 records · Page 5Linked to original sources

Kinetics of indium-111-labeled leukemic cells in patients with acute nonlymphocytic leukemia.

The distribution within the body of autologous leukemic cells labeled with indium-111 oxine was studied in seven patients with acute nonlymphocytic leukemia. The leukemic blood cells initially entered the spleen and liver, and the major site of localization was the former rather than the latter. The majority of the leukemic cells had not left the spleen and liver within 48 hr. Liver radioactivity fell transitorily up to the third hr after the initial rise. The clearance curve of radioactivity from the blood showed a plateau or the appearance of a "hump" from 1 to 5 hr after injection of labeled leukemic cells. These results might reflect recirculation of a portion of the leukemic cells between these organs and the bloodstream. In a patient with acute monoblastic leukemia. OKM1 monoclonal-antibody-treated monoblasts showed the lowest recovery into the blood and a greater increase of liver than splenic radioactivity at 30 min after injection. These results suggest the removal of damaged cells by the cytotoxic effects of antibody mediated by reticuloendothelial clearance mainly of the liver and others. In one patient with acute promyelocytic leukemia, leukemic cells accumulated in both kidneys, indicating the possible infiltration of these cells. Since indium-111 oxine stays firmly attached to the cells in spite of the possibility of radiation damaged in a long-term survey, it seems an ideal label for studying leukemic cell kinetics.

Acute Disease↗

Hemorheological approach to oxygen transport between blood and tissue.

A mathematical model is developed to elucidate micro-hemorheological factors of the oxygen transport between blood and tissue. A two-fluids model is introduced for capillary blood flow, including the non-equilibrium and relative motion between red blood cell (RBC) and plasma. A capillary-tissue unit is devised to describe the oxygen supply to tissue from a couple of capillaries with symmetric antiparallel input and output. Non-equilibrium flows are examined numerically on the basis of the model for various geometrical and dynamical parameters such capillary hematocrit, RBC velocity and flux. It is found that both RBC flux and capillary hematocrit have important influences on the oxygen transfer to tissue. Especially under low capillary hematocrit flow, the lowest oxygen pressure within tissue may appear at the maximal diffusional distance from the capillary between arterial and venous side.

Animals↗

Numerical approach to the motion of a red blood cell in Couette flow.

The motion of a red blood cell in a plane Couette flow is studied theoretically, introducing a two-dimensional microcapsule model for the cell. It is assumed that the microcapsule is deformed into an elliptical shape with a constant area and that its membrane moves like a tank-tread around the interior. The flow fields both inside and outside the microcapsule are analyzed using the finite element method in the Stokes equations and the obtained viscous forces on the membrane are used to determine its deformation and tank-treading motion. It is shown that a decrease in viscosity ratio of internal to external fluids causes the microcapsule to be more elongated, with its inclination angle increasing, whereas the microcapsule becomes more elongated at a smaller inclination angle with a longer tank-treading period as the elastic compliance of the membrane or the shear rate of the Couette flow increases. The force acting on the wall is also examined in relation to the abnormal viscosity of blood.

Blood Flow Velocity↗

Kinetics of 111In-labelled leukaemic cells in blast crisis of chronic myelocytic leukaemia.

The distribution within the body of autologous leukaemic cells labelled with 111In oxine was studied in 4 patients with blast crisis of chronic myelocytic leukaemia (CML) by means of serial samples and gamma camera imaging. Leukaemic cells of the blood initially entered the spleen and liver, and the major site of localization was the former rather than the latter. A portion of leukaemic cells, which rapidly entered the liver, left temporarily 3 h after reinjection. Leukaemic cells entered the spleen maximally at 3 or 24 h and then continued to leave gradually or rapidly up to 48 h. The majority of leukaemic cells in acute myelocytic leukaemia did not leave the spleen for up to 48 h. It is suggested that the destruction of sinusoidal structures of the spleen due to marked infiltration of leukaemic cells in CML impairs the effects of filtration in endothelial cells of sinusoids and facilitates the entry of leukaemic cells into sinusoids from splenic cords.

Adult↗

Kinetics of indium-111-labelled T lymphocytes in a patient with adult T-cell leukaemia.

Clinical studies using indium-111 oxine labelling of leukaemic T lymphocytes from a patient with adult T-cell leukaemia are presented. Leukaemic T lymphocytes did not take less than 48 h to traverse the spleen. This result was different from that of normal subjects, in which T lymphocytes continue to fall up to 44 h after the initial rise. Liver activity was seen to accumulate progressively up to 68 h. This could be explained by the infiltration of the liver by T lymphocytes or phagocytosis of damaged T lymphocytes due to Kupffer cells. Leukaemic T lymphocytes entered the enlarged, inguinal lymph nodes at 3 h and left after 68 h, but few T lymphocytes crossed the axillary lymph nodes, which were enlarged as much as the inguinal lymph nodes. This observation suggests that the degree of migration of leukaemic T lymphocytes to each lymph node differs.

Humans↗

Plain radiographic diagnosis of thrombosis of left atrial appendage in mitral valve disease.

Conventional posteroanterior chest radiographs of 42 patients with mitral valve disease who had had surgery were analyzed, and particular attention was directed to the presence or absence of the convexity of the left lower midcardiac border (left atrial segment). The flatness or concavity of this segment, despite other evidence of left atrial enlargement, was observed in six (60%) of 10 patients who had left atrial thrombosis, and in three (9%) of 32 patients who did not have thrombosis (false positive diagnosis). Four of the 10 patients who had left atrial thrombosis did not show this finding on the radiographs (false negative diagnosis). One of these four had a thrombus only against the posterior wall of the body of the left atrium. Therefore, the accuracy in the diagnosis of thrombosis of the left atrial appendage was 66.7% (six of nine) for patients who had thrombosis of the appendage. Standard chest radiographs are important in the evaluation of the patient with thrombosis of the left atrial appendage.

Adult↗

Hemorheological factors of oxygen transfer in capillary tissue unit.

The supply of oxygen to tissue from capillaries may be influenced by hemorheological factors. A hemorheological model is developed for elucidating which factors play a major role in the oxygen transport to tissue. For a capillary tissue unit, a modified cylindrical model of Krogh is used. For blood, two fluids model of red blood cells (RBCs) and plasma is used where hemoglobin release effect is included. Non-equilibrium flows as well as equilibrium flows are examined for various parameters (total flow Q or RBC velocity Vr, discharge hematocrit Hd and capillary hematocrit Hc). In equilibrium flow, Hd and Q determine the oxygen transport. In non-equilibrium flow, Hc also becomes important. Especially, hemoglobin release effect becomes significant in low Hc flow, which affects the area of lethal region in tissue.

Capillaries↗

Blood rheology near a stagnation point.

Blood rheology at a stagnation point is studied in views of microhemorheology. Special emphasis is put on the effect of both non-Newtonian and unhomogeneous properties of blood on the fine structure of blood flow impinging on the wall. It is shown that "non-flow" region exists just at the stagnation point due to the non-Newtonian viscosity when its yield stress is large enough, compared with the viscous stress far from the wall. When the yield stress becomes negligibly small, RBC and plasma behave individually near the stagnation point; RBC is deviated from the plasma streamline and impinges on the wall. Finally, a microhemorheological factor of legional metabolic disorder is discussed on basis of the fine structure near a stagnation point.

Blood Circulation↗

[Evaluation of the left ventricular function by myocardial scintigram and radionuclide angiocardiography with technetium-99m pyrophosphate in patients with acute myocardial infarct (author's transl)].

Myocardial scintigrams with 99mTc-pyrophosphate (PYP) were performed in 30 patients with acute myocardial infarct (AMI) and positive scintigrams were obtained in the 24 patients. In 12 patients the size of the AMI estimated from the scintigram with 99mTc-PYP was compared with the pulmonary capillary wedge pressure (PCWP). In the 7 patients with PCWP below 10 mmHg the mean area of the AMIs was 22 +/- 5.5 cm2 and that of in the 5 patients with PCWP beyond 10 mmHg was 41 +/- 12.4 cm2. This difference was statistically significant (p less than 0.05). In comparison with chest X-ray findings, the average size of the AMIs among 6 patients with alveolar and/or interstitial edema was 43 +/- 11.9 cm2 and that of among 8 patients without pulmonary edema was 25 +/- 9 cm2. The left ventricular ejection fraction (LVEF) was obtained by first pass method. In 12 patients LVEF and PCWP was compared. The 7 patients with PCWP below 10 mmHg did show significantly larger LVEF (49 +/- 8.2%) than that of 5 patients with PCWP beyond 10 mmHg (33 +/- 6.1%) (p less than 0.01). The mean LVEF in the 7 patients with pulmonary edema was 35 +/- 10.2% and that of in the 8 patients without pulmonary was 48 +/- 5.3%. Myocardial scintigram and radionuclide angiocardiography with 99mTc-PYP were useful for evaluation of the left ventricular function as well as detection of the AMI.

Acute Disease↗