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Biomedical subjects

T Motomiya

Publications and source records attributed to T Motomiya.

At least 55 records · Page 3Linked to original sources
PubMed1988

Platelet adenine nucleotides in patients with primary glomerular disease.

Total platelet adenosine diphosphate (ADP) and adenosine triphosphate (ATP) contents and amounts of ADP and ATP released from platelets by 3 micrograms/ml of collagen were studied in 20 patients with primary glomerular disease (PGD) to examine the metabolism of these platelet substances in the disease. ADP and ATP were measured by Holmsen's firefly luciferase method. The patients had significantly lower total platelet ATP compared with controls and total platelet ATP was significantly lower in nephrotic patients than in patients whose serum albumin levels were normal. Releasable platelet ADP and ATP were both significantly decreased in patients. Releasable ADP: total ADP ratio and releasable ATP: total ATP ratio were both significantly lower in patients' platelets than in normal platelets. There was no significant difference in platelet counts between patients and controls. Platelet aggregation induced by ADP and adrenaline were significantly higher in patients compared with controls. We conclude that total ATP content and the amount of ADP and ATP released by collagen are decreased in PGD patients' platelets.

Adenosine Diphosphate↗
PubMed1984

[Transient obstruction of the left ventricular outflow tract induced by excessive alcohol intake: a case report].

A case of transient obstruction of the left ventricular outflow tract after excessive intake of alcohol was reported. This 41-year-old man was admitted to the Hiroo Hospital because of a syncopal attack experienced while walking. He had been drinking excessively for one week until the day before admission. On admission, physical examination revealed a bifid carotid pulse and a grade 3/6 systolic ejection murmur accentuated by Valsalva maneuvers and prompt standing. The second heart sound was paradoxically split. Echocardiography showed typical systolic anterior motion of the mitral valve (SAM). The interventricular septal and left ventricular posterior wall thicknesses were 13 mm and 11 mm, respectively. No enlargement or displacement of the papillary muscles was noted. The redundant mitral chordae tendineae protruded into the left ventricular outflow tract in systole, and both the anterior and posterior mitral valve leaflets were retracted upwards approximating the interventricular septum by these chordae, resulting in obstruction of the left ventricular outflow tract. All signs of left ventricular outflow obstruction, including SAM, disappeared within several days after admission, and prolapse of the anterior mitral leaflet became evident. Since ejection fraction was markedly increased and the corrected QT interval was prolonged on admission, this patient was considered to be in hyperadrenergic state induced by excessive alcohol intake. In this case, left ventricular outflow tract obstruction was attributed to hyperadrenergic state and a redundant mitral apparatus.

Adult↗
PubMed1983

Influence of lipids metabolism on platelet activation in vivo.

Platelet aggregability and plasma factor VIII-related antigen (F. VIIIR:AG) level in 16 ischemic heart disease (IHD) patients were increased by isometric exercise and these changes were prevented by administration of a lipid lowering agent, simfibrate, a derivative of clofibrate. Serum total cholesterol (TC) level decreased and the high density lipoprotein-cholesterol (HDL-C)/TC ratio increased with the treatment. Another 7 hyperlipidemics were administered with simfibrate. Platelet malondialdehyde (MDA) production decreased with improvement in lipid profile. In an in vitro study, platelet aggregability and the plasma level of von Willebrand factor (vWF) and F.VIIIR:AG of normal citrated blood were increased by passing it through a glass bead column. Combining above results of the three separate studies, it would be suggested that hyperlipidemia might enhance platelet activation in vivo, which occurred through contact of platelets to atherosclerotic rough vessel surface. The anti-platelet effect of simfibrate might be mediated through its effect on arachidonic pathway in platelets.

Adult↗
PubMed1983

Activation of platelets in cancer, especially with reference to genesis of disseminated intravascular coagulation.

Seventy-five cancer patients were evaluated on a scale of coagulation abnormalities related to DIC, one point given for each of the following criteria fulfilled and the score (0 to 4) being used. 1. Platelet count less than 150 x 10(3)/mu 1. 2. PT prolonged more than 1 sec over control or APTT prolonged more than 10 sec over control. 3. Fibrinogen less than 250 mg/dl (mean fibrinogen value of the cancer patients minus 1SD). 4. FDP greater than or equal to 20 micrograms/ml. The patients were distributed with 27% for score 0, 38% for 1, 20% for 2, 7% for 3 and 8% for 4. Platelet mode volume in score 4 was smaller than that of the other groups. Platelet aggregation by epinephrine was decreased in score 3 and 4 (P less than 0.01), while it was increased in score 0 (P less than 0.05). ADP-induced aggregation was increased in score 0 and 1 (P less than 0.01 - 0.05). The mean value of beta-thromboglobulin in cancer patients (44 +/- 24 ng/ml) was significantly higher than that of control (22 +/- 13 ng/ml) (P less than 0.01). These results suggest the existence of hyperfunction of platelets in cancer patients and possibility of a triggering mechanism of such activated platelets in the genesis of DIC in cancer.

Adult↗
PubMed1982

Activation of platelets in patients with chronic proliferative glomerulonephritis and the nephrotic syndrome.

Platelet count, volume and aggregation and plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) were measured in 54 patients with chronic glomerulonephritis (CGN). Platelet count and platelet aggregation induced by ADP, adrenaline and collagen were significantly higher in the patients than in normal subjects, and platelet aggregation was markedly increased in the cases with progressive glomerular lesions. Plasma levels of beta-TG and PF-4 were significantly higher in the patients than in the normal subjects. There was a significant inverse correlation between plasma beta-TG and creatinine clearance. Nephrotic patients showed significantly smaller platelet volume and markedly elevated plasma beta-TG levels when compared to the controls. Plasma beta-TG decreased remarkably in 3 out of 4 patients with markedly increased beta-TG levels when they were given antiplatelet drugs. The results suggest that platelet aggregation and the release reaction were increased in patients with CGN. Activated platelets may be an important factor in the genesis of the thrombotic tendency in the nephrotic syndrome.

Adolescent↗
PubMed1981

Effect of alpha-tocopherol on sodium arachidonate-induced pulmonary embolism with platelet aggregates.

The effect of vitamin E (VE) on arachidonate-induced respiratory distress and sudden death in rats was examined. Fourteen VE deficient rats (VEDR), 11 normal control rats (NCR) and 12 VE supplemented rats (VESR) were injected with sodium arachidonate into the central vein, VEDR developed various arrhythmias, respiratory distress, apnea, hypotension, and 11 out of 14 VEDR (79%) died shortly after the injection. Many of these rats demonstrated obstruction of the small pulmonary vasculature with platelet aggregates. On the other hand, NCR and VESR developed much attenuated respiratory insufficiency and 5 out of 11 (45%) and 2 out of 12 (17%) died respectively. Twenty-six VEDR, 16 NCR and 25 VESR were used for an in vitro study of the platelet and vessel wall. VEDR demonstrated increases in platelet counts and aggregation as compared with NCR and VESR. Lipid peroxide in platelets, plasma and the aorta was significantly increased in VEDR. Prostacyclin-like activity in the aorta was not different among VEDR, NCR and VESR. The above results indicate that the pronounced respiratory distress, high mortality rate and pulmonary microembolism with platelet aggregates in VEDR may be attributed to the increase in platelet number and aggregability. The increased platelet aggregability was suggested to be the result of increased prostaglandin biosynthesis in platelets. The increased lipid peroxidation in vessel wall and plasma might also contribute to the enhanced respiratory distress. The respiratory distress and mortality as well as in vitro laboratory results were not different between NCR and VESR. This study indicates that vitamin E supplementation does not protect against the development of respiratory distress and sudden death induced by arachidonic acid over the normal control rats.

Animals↗
PubMed1981

Vascular smooth muscle reactivity to rabbit aorta contracting substance (RCS) and production of prostacyclin-like substance in normotensive and hypertensive rats.

Male SHR of young prehypertensive (5-6 weeks) and mature hypertensive (24-28 weeks) ages and age and sex matched control normotensive Wistar rats (NWR) were studied for aortic smooth muscle contractility in response to rabbit aorta contracting substance (RCS), serotonin, norepinephrine and potassium. Production of prostacyclin (PGI2) in SHR and NWR aortae of these two age groups was also compared. The contractility of young SHR in response to the agonists was all depressed as compared with the matched NWR. With age advances to 24-28 weeks, aortic responsiveness of NWR to all agonists were reduced and the contractility became the same for SHR and NWR except for the response to RCS which was now greater in SHR than in NWR. The PGI2-like substance released from young SHR aortae was the same as that from the matched NWR. The PGI2-like substance in mature aged rat aortae was much higher than that in young rat aortae and the activity in mature SHR was 1.8 times higher than that of the age matched NWR. The increased production of PGI2-like substance in aorta walls of the mature aged SHR may be a compensatory mechanism to reduce the elevated blood pressure.

Animals↗
PubMed1980

The increase of the electrophoretic mobility of platelets after laparotomy.

A fully automatic instrument for the determination of electrophoretic mobility of colloidal particles was applied to human platelets. A significant increase in platelet electrophoretic mobility was observed one day after a laparotomy. This suggests that a selective consumption of platelets with smaller surface negative charge may occur during postoperative hemostatic plug formation or under surgical stress. In addition, the difference in electrophoretic mobility observed between males and females suggests an effect of estrogen on platelets.

Adolescent↗
PubMed1980

Platelet release reaction in vivo in patients with ischaemic heart disease after isometric exercise and its prevention with dipyridamole.

In 20 patients with ischaemic heart disease (IHD), platelet sensitivity to ADP-aggregation, plasma von Willebrand factor (vWF) and plasma beta-thromoboglobulin (beta-TG) were measured before and after isometric exercise. Effect of dipyridamole on these determinants was studied in a crossover fashion. To assess plasma vWF level, a new simple method was employed which has the advantage of not requiring an optical aggregometer and was proved to be reproducible. No significant difference was seen in platelet sensitivity to ADP-aggregation, vWF and beta-TG among healthy controls, IHD patients on placebo and on dipyridamole at rest. After exercise, platelet sensitivity to aggregation, plasma vWF and beta-TG increased significantly in IHD patients on placebo. In healthy controls, no significant changes were seen. On dipyridamole, above changes seen in IHD patients were not seen. The results suggests that isometric exercise may induce platelet release reaction in vivo and may produce hypercoagulable state in IHD patients. These phenomena may be prevented by pretreatment with dipyridamole.

Adult↗
PubMed1980

Inhibitory effect of Urografin 76 on platelet function and thrombus formation in vascular catheters.

The effect of Urografin 76 on platelet aggregation and thrombus formation in vascular catheter was studied. In vitro experiments revealed that ADP-, epinephrine-, and collagen-induced platelet aggregation was significantly inhibited by Urografin 76 in concentrations greater than 0.3, 1, and 5% respectively. Rabbits that received 10 ml of Urografin 76 demonstrated a transient decrease in platelet aggregation for at least 3 minutes. Urografin 76 was apparently more effective than saline in preventing blood clot formation.

Animals↗