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Biomedical subjects

Y Takatsu

Publications and source records attributed to Y Takatsu.

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

Enhancement of coronary thrombolysis with plasminogen pro-activator by pretreatment with heparin.

The effect of pretreatment with heparin on coronary thrombolysis by plasminogen pro-activator was studied in 20 dogs with a 1-h old clot in the left anterior descending coronary artery. The clot was induced by placement of a copper coil and thrombolysis was confirmed angiographically. Intravenous administration of plasminogen pro-activator at a rate of 5 micrograms/kg/min (group 1; n = 5) and 20 micrograms/kg/min (group 2; n = 5) after pretreatment with heparin (300 IU/kg) induced thrombolysis in 31 +/- 4 min and 14 +/- 2 min, respectively. When plasminogen pro-activator was administrated intravenously at a rate of 20 micrograms/kg/min without heparin pretreatment (group 3; n = 5), the infusion interval for successful thrombolysis was prolonged to 45 +/- 6 min, which was significantly longer than that in groups 1 and 2 (p less than 0.001). In these three treatment groups, thrombolysis was not associated with severe alteration in plasma hemostatic factors (fibrinogen and alpha 2-antiplasmin). An evaluation of plasma urokinase activities using a chromogenic substrate S-2444 did not show that heparin increased the plasma urokinase activities. By increasing the dose of plasminogen pro-activities. By increasing the dose of plasminogen pro-activator to 80 micrograms/kg/min, successful reperfusion was rapidly obtained in 25 +/- 5 min without heparin pretreatment (group 4; n = 5); this was significantly faster than the results seen in group 3 (p less than 0.001). An analysis of urokinase activities showed that plasminogen pro-activator was fully converted to urokinase, which induced complete depletion of fibrinogen and alpha 2-antiplasmin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Early estimation of acute myocardial infarct size soon after coronary reperfusion using emission computed tomography with technetium-99m pyrophosphate.

Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acute positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Thromboxane A2 analogue induced coronary artery vasoconstriction in the rabbit.

Diffuse coronary artery vasoconstriction was provoked in the rabbit by a stable thromboxane A2 analogue, STA2 (9,11-epithio-11,12-methano thromboxane A2). Injection of 25 micrograms.kg-1 STA2 into the left main trunk caused complete occlusion of the left anterior descending artery and narrowing of the left circumflex artery. Two minutes after injection, however, the diameter of the coronary artery returned to the control value (n = 10). The right coronary artery was also temporarily occluded by an injection of 25 micrograms.kg-1 STA2. Left ventricular end diastolic pressure increased significantly, and ST segment elevation of the electrocardiogram occurred during vasoconstriction. The angiographic findings showed that the vasoconstriction in the coronary artery induced by STA2 was similar to the diffuse vasoconstriction seen clinically. Induction of the vasoconstriction by STA2 was prevented by the preadministration of 25 micrograms.kg-1 of either a calcium antagonist, diltiazem, or a thromboxane A2 receptor antagonist, ONO 3708 (n = 10). The relation of the calcium movement to this vasoconstriction was studied in vitro using the isolated left circumflex artery in the rabbit. STA2 (50 micrograms.litre-1 to 0.5 mg.litre-1) produced a concentration dependent contraction of helical strips of left circumflex artery. Diltiazem (50-100 g.litre-1) suppressed this contraction dose dependently. ONO 3708 (10 micrograms.litre-1 to 1 mg.litre-1) caused a significant rightward and downward shift of the dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Heparin requirement in tissue-type plasminogen activator-induced experimental coronary thrombolysis: comparison with urokinase-induced coronary thrombolysis.

The requirement of heparin in experimental coronary thrombolysis induced by tissue-type plasminogen activator (t-PA) was studied in closed-chest dogs with one hour old coronary thrombi and compared with that in urokinase (UK)-induced coronary thrombolysis. Animals were divided into 5 treatment groups as follows: group 1 received intracoronary t-PA alone (1,000 IU/kg/min; n = 5), and if thrombolysis was not induced within 40 to 50 min, dogs then received an intravenous injection of heparin (300 U/kg) plus intracoronary t-PA; group 2 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary t-PA (n = 5); group 3 also received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received t-PA but intravenously, as compared with the groups administered by the intracoronary route (n = 6); group 4 received intracoronary UK alone (1,000 IU/kg/min; n = 6); group 5 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary UK (n = 5). Thrombolysis was confirmed angiographically. In group I, coronary thrombolysis could not be induced within 44 +/- 4 min by intracoronary t-PA alone, but it occurred in 8 +/- 4 min when administered in combination with heparin in all dogs. Heparin alone failed to elicit reperfusion within 10 min in group 2, 3 and 5. t-PA, however, induced successful reperfusion in 16 +/- 5 min (group 2) and in 23 +/- 6 min (group 3), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Serum PGI2-regulating factors in acute myocardial infarction.

Human serum or plasma contains two factors which regulate PGI2 metabolism. The one is "PGI2-synthesis stimulating factor" which stimulates PGI2 synthesis in the vessel wall. The other is "PGI2-stabilizing factor" which stabilizes PGI2 in the blood. In the very early phase of acute myocardial infarction, the serum levels of these two factors were significantly reduced, which may be related to the thrombus formation in the coronary artery in acute myocardial infarction.

Blood Proteins↗
PubMed1987

Hemodynamic effect of oral TA-064 after dobutamine in congestive heart failure.

The hemodynamic effect of oral TA-064 (20 mg), a newly synthesized inotropic agent, was compared with that of intravenous dobutamine (5 micrograms/kg/min) in eight patients with congestive heart failure who had been treated with intravenous dobutamine, digitalis, diuretics, and prazosin. Hemodynamics was measured using a Swan-Ganz catheter during the pre-dobutamine control period, during dobutamine infusion period, during the pre-TA-064 control period and at 90 minutes after oral administration of TA-064. Stroke work index was increased and mean pulmonary capillary wedge pressure was decreased with TA-064 or dobutamine. Cardiac index and stroke index was increased by each drug, and pulmonary and systemic vascular resistances were decreased. Mean systemic arterial pressure, heart rate and pressure-rate product did not significantly change in comparison with the control level. In conclusion, TA-064 has a hemodynamic effect similar to that of dobutamine and may be useful as an oral substitute for dobutamine in patients with congestive heart failure after temporary management with dobutamine.

Administration, Oral↗
PubMed1987

Diffuse triple-vessel coronary artery spasm complicated by idioventricular rhythm and syncope.

A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. Atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.

Aged↗
PubMed1986

Vasodilator therapy with a new stable prostacyclin analog, OP-41483, for congestive heart failure due to coronary artery disease and comparison of hemodynamic effects and platelet aggregation with nitroprusside.

A new stable prostacyclin analog, OP-41483, was used in patients with severe congestive heart failure (CHF) due to coronary artery disease and compared with nitroprusside. During infusion of both drugs, mean brachial arterial pressure, total pulmonary resistance, pulmonary artery wedge pressure and systemic vascular resistance decreased significantly. Cardiac index and stroke index also increased significantly. Platelet aggregation did not change significantly during nitroprusside but decreased significantly with OP-41483 infusion. Thus, this analog may be useful for treatment of patients with CHF due to coronary artery disease.

Aged↗
PubMed1986

Selective thromboxane A2 synthetase inhibition in vasospastic angina pectoris.

To investigate whether thromboxane A2 is responsible for the initiation of vasospastic angina pectoris, thromboxane B2 levels were measured in the great cardiac vein and the arterial blood of 12 patients with clinically and angiographically proved vasospastic angina and therapeutic trials were performed with selective thromboxane A2 synthetase inhibitor OKY-046, an imidazole derivative. During ergonovine-provoked (11 cases) and spontaneous (1 case) anginal attacks, great cardiac vein thromboxane B2 increased from 121 +/- 27 to 430 +/- 382 pg/ml (p less than 0.05, n = 12), arterial thromboxane B2 increased from 93 +/- 18 to 122 +/- 33 pg/ml (NS, n = 12) and thromboxane B2 production increased from 3.18 +/- 1.88 to 25.16 +/- 22.32 ng/min (p less than 0.05, n = 6). Subsequently, OKY-046, 400 mg/day orally, was administered to 7 of the 12 patients, while a continuous electrocardiogram was recorded on a dual channel Holter monitor during a 3 day placebo period and the 3 day OKY-046 regimen. Although peripheral plasma thromboxane B2 levels decreased significantly from 98 +/- 15 to 12 +/- 8 and 28 +/- 10 pg/ml (1 and 6 hours after ingestion, respectively) (p less than 0.05 for both), 6-keto-prostaglandin F1 alpha production in serum increased significantly from 0.48 +/- 0.22 to 2.3 +/- 0.72 (1 hour) and 1.8 +/- 0.46 ng/ml (6 hours) (p less than 0.05 for both) during OKY-046 administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylates↗
PubMed1986

Altered platelet alpha 2 adrenoreceptor in acute myocardial infarction and its relation to plasma catecholamine concentrations.

Changes in platelet alpha 2 adrenoreceptors and their relation to plasma catecholamine concentrations were studied in 11 patients with acute transmural myocardial infarction. A radiolabelled alpha 2 adrenoreceptor antagonist, [3H]-yohimbine, was used to assay alpha 2 adrenoreceptors on platelet membranes, and plasma catecholamine concentrations were measured by high performance liquid chromatography. The number of platelet alpha 2 adrenoreceptors, the dissociation constant, and plasma noradrenaline and adrenaline concentrations were studied 6.6 (3.3) (mean (SD)) hours after the onset of acute myocardial infarction and one month later. The mean (SD) number of adrenoreceptors increased significantly from 94.5 (50.5) fmol/mg protein immediately after infarction to 157.0 (65.7) fmol/mg protein one month later. The dissociation constant, however, did not change significantly (4.33 (1.40) nmol/l vs 4.37 (1.22) nmol/l). Raised noradrenaline (5.60 (4.37) nmol/l) and adrenaline (0.28 (0.14) nmol/l) concentrations had fallen significantly to normal values (1.21 (0.67) and 0.09 (0.05) nmol/l respectively) a month after infarction. The decrease in the number of alpha 2 adrenoreceptors soon after infarction may be beneficial because such a change will reduce the strength of various reactions to catecholamines, such as vasoconstriction.

Aged↗
PubMed1985

Lactate metabolism in acute myocardial infarction and its relation to regional ventricular performance.

Myocardial metabolism was assessed in 20 patients with acute anterior myocardial infarction using lactate uptake (defined as (aortic lactate - great cardiac venous lactate)/aortic lactate X 100) as an index. The regional ejection fraction of the anterior wall was obtained from left ventriculography. There was a linear relation between lactate uptake and regional ejection fraction (r = 0.79, p less than 0.001). Four patients without total occlusion in the infarct vessel had a higher lactate uptake (19.6 +/- 6.7 versus 4.2 +/- 13.4%, p less than 0.05) and regional ejection fraction (26.3 +/- 7.9 versus 14.9 +/- 7.0%, p less than 0.05) than did 16 patients with total occlusion. The latter group of patients underwent intracoronary infusion of urokinase, which resulted in reperfusion in 13 patients. Lactate uptake before urokinase infusion (sample I), just after reperfusion (sample II), 30 minutes after reperfusion (sample III) and 4 weeks after reperfusion (sample IV) was 5.7 +/- 13.2, -13.9 +/- 14.7, 2.9 +/- 15.2 and 20.2 +/- 11.0%, respectively (sample I versus II and II versus III, p less than 0.01; sample I versus IV and III versus IV, p less than 0.05). The decrease in lactate uptake immediately after reperfusion, which was accompanied by an increase in creatine kinase-MB isoenzyme release into the blood, was considered to be the result of a "washout" effect. Lactate uptake was ameliorated 4 weeks later, accompanied by an improvement (from 15.1 +/- 7.1 to 23.4 +/- 7.2%, p less than 0.01) in the regional ejection fraction. It is concluded that the degree of asynergy was closely related to the extent of metabolic deterioration in myocardial infarction.

Acute Disease↗
PubMed1985

A new stable prostacyclin analogue OP41483 (15-cyclopentyl-omega-pentanor-5(E)-carbacyclin).

Effects of a new stable prostacyclin analogue OP41483 (15-cyclopentyl-omega-pentanor-5(E)-carbacyclin) on platelet aggregation, plasma thromboxane B2 levels, hemodynamic parameters, and clinical safety were studied. Normal volunteers received intravenous infusions of OP41483 at doses of 2.5 (n = 3), 5.0 (n = 3), 10 (n = 3), and 20 (n = 5) ng/kg/min for one hour. During infusion, ADP (adenosine diphosphate)-induced platelet aggregation decreased significantly, and blood pressure decreased slightly, but plasma thromboxane B2 levels did not change significantly. The intravenous infusion of OP41483 at the dose of 10 ng/kg/min for one hour over three successive days was performed. During the each infusion, platelet aggregation and mean blood pressure decreased significantly.

Adult↗
PubMed1985

Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations.

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.

Adult↗
PubMed1985

Acute myocardial infarction associated with systemic lupus erythematosus documented by coronary arteriograms.

A 19-year-old man with untreated systemic lupus erythematosus had an acute myocardial infarction. A coronary arteriogram five hours after the onset of symptoms revealed total occlusion of the left anterior descending coronary artery. Reperfusion was achieved by coronary thrombolytic therapy with urokinase. Four weeks later, a coronary arteriogram showed only minimal luminal irregularities at the original site of occlusion, where significant reduction in diameter could be induced by ergonovine maleate. This case suggests that coronary arterial involvement in systemic lupus erythematosus may be related to coronary arterial spasm.

Adult↗
PubMed1984

Decreased serum levels of a factor stimulating prostacyclin synthesis in acute myocardial infarction.

To investigate the role of a factor in serum stimulating prostacyclin synthesis in acute myocardial infarction, we compared the activities of the factor among 7 patients with acute myocardial infarction (2.5 +/- 0.8 hrs and 80 +/- 17 hrs after the onset of symptoms), 12 patients with angina pectoris, and 7 normal subjects. In this study, we found that in patients with acute myocardial infarction, this activity is much lower immediately after infarction (2.5 +/- 0.8 hrs) than 80 +/- 17 hrs later, or in patients with stable angina pectoris, or in healthy volunteers. Since prostacyclin is antiaggregating and vasodilating, the deficiency in this ability during the very early phase of acute myocardial infarction may be related to the development of the thrombosis of acute myocardial infarction.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Unusual vasomotor coronary arterial responses after reversal of ergonovine induced spasm with glyceryl trinitrate.

Unusual vasomotor responses in the coronary arteries occurred in two patients after the administration of glyceryl trinitrate to relieve spasm induced by ergonovine maleate. In one patient after treatment with glyceryl trinitrate and despite dilatation of the adjoining segments a new severe reduction in diameter occurred distally to the segments of the right coronary artery where the ergonovine induced spasm developed. In the other patient the left anterior descending artery filled very slowly after the completely occlusive spasm of the right coronary artery had resolved with glyceryl trinitrate though the circumflex did not. These vasomotor changes were associated with chest discomfort and electrocardiographic abnormalities in both cases. These findings indicate that caution is needed when performing provocative tests even after the ergonovine induced spasm has been reversed with glyceryl trinitrate.

Adult↗
PubMed1984

Intravenous infusion of a selective inhibitor of thromboxane A2 synthetase in man: influence on thromboxane B2 and 6-keto-prostaglandin F1 alpha levels and platelet aggregation.

The effect of the selective thromboxane A2 synthetase inhibitor OKY-1581, a pyridine derivative [sodium (E)-3-(4-(3-pyridylmethyl)phenyl)-2-methyl-2-propenoate], on thromboxane B2 and 6-keto-prostaglandin F1 alpha levels and platelet aggregation was studied in human volunteers. To clarify its effectiveness as an enzyme inhibitor, OKY-1581, at doses of 17, 83, 167, 417, 833, and 1667 micrograms/kg (n = 5 for each group), was injected intravenously, or was infused (10 micrograms/kg/min; n = 5) over 3 hr on 3 successive days. OKY-1580 (OKY-1581 free acid) was rapidly converted to its main beta-oxidized product, OKY-1565, and its reduced form, OKY-1558. During the study, plasma thromboxane B2 levels, inhibition of thromboxane B2 production in serum, and inhibition of rabbit platelet thromboxane A2 synthetase were monitored continuously. Twenty-five minutes after the injection of the above doses, plasma thromboxane B2 levels decreased by 4 +/- 7%, 40 +/- 14%, 57 +/- 7%, 68 +/- 6%, 93 +/- 5%, and 96 +/- 5% (mean +/- SD), respectively. Thromboxane B2 production in serum was decreased by 2 +/- 8%, 70 +/- 10%, 75 +/- 8%, 81 +/- 10%, and 96 +/- 8%, respectively, and rabbit platelet thromboxane A2 synthetase by 2 +/- 7%, 52 +/- 8%, 79 +/- 10%, 80 +/- 9%, 96 +/- 8%, and 95 +/- 7%. These parameters returned to the control levels 24 hr after the injection.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗