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Biomedical subjects

A Suehiro

Publications and source records attributed to A Suehiro.

At least 55 records · Page 3Linked to original sources
PubMed1990

Inhibitory effect of vitamin E (alpha-tocopherol) on spontaneous platelet aggregation in whole blood.

Vitamin E (D-alpha-tocopherol) inhibited spontaneous human platelet aggregation in whole blood in the 20-200 micrograms/ml range. When alpha-tocopherol (20 micrograms/ml) and aspirin (0.5 mM), or alpha-tocopherol and the mixture of phosphocreatine (1.5 mM) and creatine phosphokinase (50 U/ml) (CP/CPK) were added to this reaction system, a synergic inhibitory effect on aggregation was observed. On the other hand, when both alpha-tocopherol and the specific inhibitor of platelet activating factor (CV-3988; 0.38 mM) were added to this system, the inhibition was the same as that caused by the addition of CV-3988 alone, suggesting there was no synergism, i.e., that the effect of alpha-tocopherol is related to the inhibition of platelet activating factor (PAF)-induced platelet aggregation in whole blood. However, alpha-tocopherol (20 or 50 micrograms/ml) did not inhibit PAF (10 nM) induced platelet aggregation in platelet rich plasma (PRP). These results suggest that the inhibition of platelet aggregation in whole blood by alpha-tocopherol is due to the inhibition of PAF synthesis, and is unrelated to adenosine diphosphate (ADP) or thromboxane A2.

Adenosine Diphosphate↗
PubMed1990

Efficacy of the high molecular weight fraction of plasma for the maintenance of pregnancy associated with thrombotic thrombocytopenic purpura.

We have investigated the methods for the maintenance of a pregnancy in a patient with thrombotic thrombocytopenic purpura (TTP), said condition, since 1984, having been controlled by a plasma infusion every 3 to 4 weeks. In a preliminary trial it was confirmed that an infusion of the high molecular weight fraction (HMW-F) of plasma, separated by an Evaflux 2A fractionator, improved the patient's thrombocytopenia as the plasma infusion, and maintained its beneficial effect for about 2 weeks during early pregnancy. Though an occurrence of a toxemia-like syndrome responded to repeated plasma infusion, the dose of plasma required to improve the thrombocytopenia gradually increased and reached 5,040 ml by the 20th week of pregnancy. Thus, instead of periodic infusions of whole plasma, periodic infusions of the HMW-F of plasma were used. Under this regimen the platelet count remained above 10.0 x 10(4)/microliters during late pregnancy, and the total dose (2,600 ml) of HMW-F of plasma that was administered until delivery at full term was less than the dosage of whole plasma that was used during early pregnancy. In this manner we were able to obtain a healthy baby by controlling the patient's TTP during pregnancy. This method of preventing thrombocytopenia appears to be safer with respect to volume loading during pregnancy in the TTP patient.

Adult↗
PubMed1990

[Management with antithrombin III concentrate in a pregnant woman with hereditary antithrombin III deficiency].

Pregnant women with hereditary antithrombin III (AT-III) deficiency are frequently associated with thromboembolic disorders. We have treated a pregnant woman with hereditary AT-III deficiency, who had suffered from thromboembolic disorders at her past three gestations, with AT-III concentrate. Dosage of AT-III concentrate to maintain plasma AT-III activity over 80% was 3,500 units per week during second and third trimesters, but more frequent administration was necessary around delivery. In recent reports, pregnant women with hereditary AT-III deficiency had been treated with heparin or warfarin except for during abortion and delivery, in which time AT-III concentrate was widely utilized. But the use of heparin or warfarin during gestation is occasionally harmful, AT-III concentrate should be chosen for management in pregnancy in women with hereditary AT-III deficiency.

Adult↗
PubMed1989

A new index for collagen induced platelet aggregation.

In this paper, we propose a new index of platelet aggregation for optical aggregometry, the "R" value. This represents the rate of change in the half time for platelet aggregation (T1/2) induced by collagen with changes in the platelet concentration and expresses the degree of platelet sensitivity to collagen. The "R" value has been shown to reflect the aggregability of platelets due to activation of the contact factors. The "R" values were significantly different in the acute and chronic phases of occlusive arterial disease, while ordinary platelet aggregation parameters did not change. A decrease in the "R" value appears to indicate a platelet hyperfunction and hypercoagulable state, in other words a prethrombotic state.

Adenosine Diphosphate↗
PubMed1988

Antiserum to endotoxin in hemorrhagic shock.

Antiserum to Escherichia coli J5, a mutant endotoxin (LPS) which contains only core determinants, has proven effective in reducing mortality from endotoxic shock due to a wide variety of gram-negative bacteria. Twenty New Zealand white rabbits with coliforms in the gut were subjected to hemorrhagic shock of 36 mm Hg for 3 hr. Treated rabbits were resuscitated with 15 cc of rabbit J5 antiserum (hemagglutinating antibody titer against J5 lipopolysaccharide of 1:1024), remaining shed blood, and lactated Ringer's to achieve a mean arterial blood pressure (MABP) within 20% of baseline. The control group was similarly resuscitated but received 15 cc normal rabbit serum (titer 1:2). Catheters were removed and rabbits were returned to their cages until death or 5 days of survival. Hemodynamic parameters (heart rate, MABP, cardiac output, and total peripheral resistance) did not differ significantly between groups. However, six treated rabbits survived 5 days (60%) and no control rabbit lived past the third postexperimental day (P less than 0.019). Our data suggest that systemic endotoxemia may contribute to morbidity and mortality in severe hemorrhagic shock.

Alanine Transaminase↗
PubMed1986

Regional myocardial blood flow in experimental myocardial infarction after pretreatment with aspirin.

The effects of aspirin on myocardial blood flow in an area of ischemia were studied in 12 baboons. In each, a diagonal branch of the left anterior descending coronary artery was ligated. Six of the baboons received aspirin (2 X 600 mg orally, 12 hours and 1 hour before ligation); the other six did not receive aspirin and served as a control group. The extent of myocardial ischemia was delineated with an electrode wire grid on the surface of the anterior left ventricular wall. The maximal area circumscribed by electrodes with 2 mV or more ST segment elevation was compared with the area of reduced myocardial blood flow. Myocardial blood flow was measured with the radioactive microspheres method using strontium-85-labeled carbonized spheres. Two areas of reduced myocardial blood flow were noted, one with severely reduced flow in the center of the myocardial infarct (0 to 49% of noninfarcted myocardium) and another with mild to moderately reduced myocardial blood flow at the border of the myocardial infarct (50 to 90% of noninfarcted myocardium). Myocardial blood flow in the border area (margins of ST elevation area) for the total wall was 85 +/- 8% of normal in the aspirin-treated animals and 40 +/- 4% in the control group (p less than 0.01); for the epicardium it was 67 +/- 10% of normal in noninfarcted myocardium after aspirin and 37 +/- 5% for the control group (p less than 0.05); and for the endocardium it was 78 +/- 8% of normal in noninfarcted myocardium after aspirin and 39 +/- 6% in the control group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Differences in platelet aggregation kinetics in normal and hyperlipidemic rabbits.

The difference in the aggregation mechanism between normal and hyperlipidemic rabbits was studied by kinetic analysis of changes in the number of residual single platelets in adenosine diphosphate (ADP)-induced platelet aggregation. When ADP was added to platelet rich plasma (PRP) obtained from normal rabbit, the number of single platelets decreased exponentially, but with PRP from hyperlipidemic rabbit, it decreased hyperbolically. However, the aggregation of platelets isolated from plasma of hyperlipidemic rabbit and resuspended in normal plasma showed an exponential decay, while that of normal rabbit platelets resuspended in hyperlipidemic rabbit plasma showed a hyperbolic decay. The results suggested that these aggregation mechanisms are altered mainly due to changes in the plasma components, such as the cholesterol levels.

Adenosine Diphosphate↗
PubMed1983

The effect of oxygen on the development of atherosclerosis in WHHL rabbits.

The effect of hyperoxic or hypoxic inhalation on blood lipid levels and on the development of atherosclerosis was studied in young male WHHL rabbits. They were exposed to ordinary room air containing different concentrations of oxygen: 6 animals were exposed to 40% oxygen (hyperoxia group) or 5-10% oxygen (hypoxia group) for 5 h a day, 5 days a week for 8 weeks. Four control rabbits inhaled ordinary room air. The following results were obtained. (1) The severity of aortic lesions significantly decreased in the hyperoxia group and increased in the hypoxia group, when these two groups were compared. However, both hypoxic and hyperoxic groups did not statistically differ from the control. (2) Plasma cholesterol levels were not changed either by hyperoxic or hypoxic inhalation. (3) Plasma triglyceride levels were elevated only in the hypoxia group, with significant differences from the values in both control and hyperoxia groups. (4) There was no significant correlation between mean plasma lipid level and severity of aortic lesions. From these results, we conclude that hyperoxic or hypoxic inhalation respectively regresses or aggravates the development of atherosclerotic lesions, not by an indirect action on blood lipid concentrations but by a direct action on the vascular wall.

Animals↗
PubMed1983

The effects of thoracic aortic cross-clamping and declamping on visceral organ blood flow.

Blood flow was measured using radioactive microspheres in 11 macaque monkeys 1) before hemorrhage shock, 2) after onset of shock, 3) after aortic cross-clamping and resuscitation, and 4) after release of the cross-clamp and stabilization. Hemodynamic parameters (cardiac output, arterial, right atrial and left atrial pressure) and blood gases were also monitored. Total abdominal organ flow fell with hemorrhage and fell further with aortic clamping. Reinfusion of shed volume did not restore abdominal organ flow (4.7% baselines) but increased LAP and cardiac output to the upper body. Release of the cross-clamp produced profound acidosis that was treated effectively with NcHCO3. After stabilization of blood, flow to kidney remained low (49% baseline) although intestinal flow was increased threefold (320% of baseline). It is clear that thoracic aortic cross-clamping in shock further compromises already reduced visceral blood flow and may contribute to the problem of ischemic multiple organ failure after resuscitation from hemorrhagic shock.

Abdomen↗
PubMed1983

Mechanism of hematuria in glomerular disease. An electron microscopic study in a case of diffuse membranous glomerulonephritis.

From an electron-microscopic study in a case of diffuse membranous glomerulonephritis, we would like to propose a possible mechanism of hematuria in glomerular disease. There are several factors we should consider: (1) the deforming force of the red blood cell (RBC); (2) the deformability of the RBC; (3) the size of the gaps in the glomerular basement membrane (GBM), and (4) the thickness of the GBM. The deforming force is due to increased capillary pressure in the glomerulus that alters the contour of the RBCs. If these gaps are larger than 0.25 micron, the stretching and retracting force of the internal chamber of the GBM, combined with the capillary pulse, cause the deformed RBCs to pass through the gaps and proceed to the urinary space.

Adult↗
PubMed1982

The role of platelet hyperfunction in thrombus formation in hyperlipidemia.

The mechanism of thrombus formation in hyperlipidemia was studied. Attempts at artificial creation of an arterial thrombus in control rabbits stenosing the femoral artery by ligature were not successful unless ellagic acid was administered by injection. However, in rabbits with hyperlipidemia, mere creation of stenosis in the femoral artery resulted in a high percentage of thrombus formation. In rabbits with hyperlipidemia, both thromboxane (Tx) A2 biosynthesis in platelets and prostacyclin (PGI2) biosynthesis in the aorta were increased and these changes were noted at the level of cyclooxygenase in the arachidonic acid metabolic pathway. Therefore, these results suggest that thrombi are likely to be formed in hyperlipidemia and that such thrombus formation is due largely to platelet hyperfunction.

Animals↗
PubMed1981

Effect of left ventricular--to--aortic bypass on infarct size and infarct microcirculation in baboons.

A major diagonal branch of the left anterior descending coronary artery (LAD) was acutely occluded in 17 baboons. Complete left ventricular (LV) decompression was achieved with a left heart bypass (LHB) system in six baboons while 11 baboons served as untreated controls. In the treated group, LHB was initiated after 30 minutes of coronary occlusion. For a period of 6 hours after occlusion, aortic pressure, LV pressure, left atrial pressure, and cardiac output were monitored. During the same monitoring period, electrograms were recorded from a high resolution matrix of fixed epicardial electrodes. Regional myocardial blood flow was determined prior to and at intervals following the initiation of LHB with radioactive microspheres. Infarct size was assessed histologically from serial cross sections of the left ventricle. The degree of salvage achieved by LHB was assessed by comparing the epicardial area of infarction 6 hours after occlusion (AI) to the area of epicardial St-segment elevation (STE) 30 minutes after occlusion (maxAST). In the LHB-treated group, 40.0% +/- 8.1% (SEM) of maxAST showed subsequent infarction; in the control group, 79.8% +/- 2.7% of maxAST showed eventual infarction (p less than 0.01). STE overlying the region of ischemia in the LHB-treated group did not undergo the spontaneous decline observed in the control group, which is normally associated with the progression of necrosis. Regional myocardial blood flow did not change significantly in the ischemic region during the period of occlusion following LHB. LHB. The results suggest that LHB is capable of substantial salvage of acutely ischemic myocardium by reducing myocardial work and thus reducing myocardial oxygen requirements.

Animals↗