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Biomedical subjects

T Yamakado

Publications and source records attributed to T Yamakado.

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

[Effects of contrast media on left ventricular function. Comparison with iohexol and diatrizoate].

To investigate the effects of a low-osmolar nonionic (Iohexol: I) and a high osmolar ionic contrast media (Diatrizoate: D) on left ventricular (LV) function after left ventriculography (LVG), we studied 19 patients with coronary artery disease (I: 9 cases, D: 10 cases) during diagnostic cardiac catheterization. The first LVG was performed by injecting 40 ml of I or D at a rate of 12 ml/sec, measuring simultaneous LV pressure with a catheter tip manometer (Millar instruments). At 4 minutes after the first LVG, we repeated hemodynamic measurements and LVG. Single-plane volumes (RAO 30 degrees) were calculated every 20 msec (50 frame/sec) using the area-length method. LV systolic function was estimated by ejection fraction (EF), ratio of end-systolic pressure to end-systolic volume (ESP/ESV) and maximal (+)dP/dt. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV diastolic compliance was evaluated by the diastolic pressure-volume (PV) relationship. Results. 1. LV end-diastolic pressure and volume were augmented more significantly in D than in I group, probably due to the difference of their osmolarity. 2. EF increased in D group with increase of LV preload after the first LVG, but didn't change in I group. ESP/ESV and maximal(+)dP/dt were not changed after the first LVG in both groups. 3. LV isovolumic relaxation remained unchanged with I and D. 4. LV diastolic PV relation curve shifted upward more in D than I group. We conclude that Iohexol has less influences on LV function than Diatrizoate and may be used in high risk patients.

Contrast Media↗
PubMed1989

S-100 antigen and calmodulin in human leukemic cells.

Both S-100 antigen and calmodulin were shown in normal lymphocytes with S-100 being decreased in lymphocytic leukemia cells. Although small amounts of S-100 antigen and calmodulin were shown in acute myeloblastic leukemia cells, they could not be detected in normal granulocytes. In lymphoblastic leukemia, S-100 antigen levels in T-cell leukemia cells were higher than in B-cell leukemia cells, while calmodulin was decreased in chronic leukemia cells. In mitogen-stimulated lymphocytes, the levels of S-100 antigen were decreased, while those of calmodulin were either increased or unchanged. Calcium-dependent cyclic nucleotide phosphodiesterase was highest in acute lymphoblastic leukemia. These data suggest, therefore, that calcium ions may play a role in the proliferation, differentiation or leukemic change in lymphocytes and, hence, that measurement of calcium binding proteins may be useful in the investigation of leukemia cells or lymphocytes.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1989

[Coronary angiography in patients with U wave inversion during coronary artery spasm].

During ergonovine-induced vasospastic angina, U wave inversion without significant ST segment deviation on the precordial electrocardiograms was documented in four patients. Coronary angiography revealed incomplete spastic obstruction of the left anterior descending artery without delayed filling and runoff in three patients. In the remaining patient, the proximal left anterior descending artery was totally occluded and there were well-developed collaterals from the non-spastic artery. Thus, ergonovine-induced U wave inversion was related to the presence of coronary vasospasm, and angiography demonstrated less severe myocardial ischemia in such patients than in cases with ST segment elevation or depression, which is usually associated with subtotal or total obstruction of a major coronary artery without adequate collaterals. In their clinical courses, two patients had episodes of angina with ST segment elevations or depressions. It was suggested that vasospastic angina with U wave inversion alone is one aspect of a continuous spectrum of vasospastic myocardial ischemia.

Adult↗
PubMed1989

[Clinical significance of exercise induced ST segment depression after successful percutaneous transluminal coronary angioplasty--assessment by thallium-201 SPECT].

To evaluate the clinical significance of ST segment depression during repeated Treadmill exercise after successful PTCA, Thallium-201 SPECT was performed. The Thallium-201 SPECT was performed before, one week after and 3-6 months after PTCA. All thirty-five patients had one vessel disease and positive Thallium-201 exercise test. During follow-up period for 3-6 months, 11 of 35 patients had persistent ST segment depression. Restenosis of dilated coronary lesion was demonstrated in 6 of 11 patients. In another 3 of 35 patients, exercise induced ST segment depression was disappeared during follow-up Treadmill exercise. In 14 patients with persistent or transient ST segment depression after PTCA, Thallium-201 SPECT demonstrated transient ischemia in 5 of 6 patients with restenosis. In other 8 patients without restenosis, SPECT images did not demonstrate myocardial ischemia and coronary arteriographic findings could not verify side branch stenosis or intimal dissection which might cause myocardial ischemia. The etiology of ST segment depression after successful PTCA in one vessel disease is not produced by exercise induced myocardial ischemia but still unknown mechanisms may be present.

Adult↗
PubMed1988

Echocardiographic findings in nine patients with cardiac amyloidosis: their correlation with necropsy findings.

The echocardiographic abnormalities of nine patients with cardiac amyloidosis were correlated with their postmortem findings. All had congestive heart failure and autopsy-proven amyloidosis. M-mode echocardiographic features included (1) small or normal left ventricular (LV) dimensions; (2) thickened interventricular septa and posterior LV walls (89%); (3) left atrial enlargement (89%); and (4) reduced LV distensibility (78%, 100%) and contractility (22%, 44%). Serial M-mode echocardiography revealed that cardiac amyloidosis was initially manifested as diastolic LV dysfunction rather than systolic dysfunction. The final stage of this disease was characterized by severe impairment of both systolic and diastolic LV functions. Two-dimensional echocardiography provided additional features: (1) a more accurate diagnosis of pericardial effusion (67%) and (2) a characteristic "granular sparkling" appearance of the ventricular wall (55%). In four of five cases, these hyperrefractile myocardial echoes corresponded to scattered amyloid deposits histopathologically. There was no correlation between the types of amyloid deposits and the hyperrefractile myocardial echoes. Thus, cardiac involvement in systemic amyloidosis could be non-invasively assessed by M-mode and two-dimensional echocardiography.

Adult↗
PubMed1987

[Left ventricular systolic and diastolic functions in hypertrophic cardiomyopathy: with special reference to clinical symptom and the effects of calcium blocking agent (nifedipine)].

To assess left ventricular (LV) diastolic function in hypertrophic non-obstructive cardiomyopathy (HCM), biplane angiograms and pressures (catheter-tip manometer) were analyzed in 23 patients with HCM and 10 normal subjects (N). The effects of calcium antagonist on LV diastolic function was also evaluated by sublingual administration of 20 mg of nifedipine in 17 patients with HCM. Frame-by-frame (20 msec) analysis of angiograms was performed. LV relaxation was assessed by the time constant (T) of isovolumic LV pressure decline. 1. As compared with N, HCM showed greater increase in LV end-diastolic pressure and time constant (T). There was a significant prolongation of time from end-systole to the peak filling rate (PFR) during rapid filling period in HCM, while PFR did not differ between N and HCM. Left and upward shifts of LV diastolic pressure-volume relations were noted in HCM. Thus, abnormal LV diastolic function in HCM was characterized by impaired relaxation, delayed early diastolic filling and decreased LV compliance. 2. Clinical symptom of chest pain in HCM was associated with a decreased normalized PFR (PFR/SV and PFR/EDV). This finding suggested that an abnormal LV diastolic filling may be one of the contributing factors of chest pain in HCM. 3. Sublingual nifedipine (20 mg) did not always improve impaired relaxation and diminished LV compliance in HCM. Further study will be needed in the treatment of abnormal LV diastolic function in HCM with calcium blocking agents.

Administration, Sublingual↗
PubMed1986

The beneficial effects of 40% and 100% O2 inhalations on acutely-induced myocardial ischemia in dogs.

The effectiveness of O2 inhalation on the acutely-induced ischemic myocardium in dogs was investigated. In 22 open-chest mongrel dogs, the left anterior descending coronary artery was partially occluded to reduce coronary flow. The regional coronary vein accompanying the artery was cannulated to obtain coronary venous blood. Switching of inspiratory gas from room air to 40% O2 produced an elevation of coronary venous O2 saturation from 35.8 +/- 12.7 (S.D.) to 41.1 +/- 11.9% and shifting of myocardial lactate production to utilization (from -0.9 +/- 36.9 to 5.0 +/- 36.7%), indicating that 40% O2 inhalation ameliorated ischemia. Application of 100% O2 inhalation caused even more beneficial effects; coronary venous O2 saturation was elevated to 50.6 +/- 12.6% and myocardial lactate extraction was improved to 7.8 +/- 40.5%. The present study indicated that 40% O2 inhalation was effective and 100% O2 inhalation even more effective in ameliorating acutely-induced myocardial ischemia. Decreases in myocardial contractile force and left ventricular size and suppression of sympathoadrenal activity might be possible mechanisms for these beneficial effects.

Animals↗
PubMed1985

Effects of nifedipine and diltiazem on hemodynamic responses at rest and during exercise in hypertensive patients.

Twelve patients with uncomplicated systemic hypertension were treated with nifedipine (30 mg/day) and diltiazem (180 mg/day) for 1 month each, and performed two stage (50 watt and 100 watt) of bicycle ergometer exercise before and after each period of administration. Both drugs produced significant reduction in systolic and diastolic blood pressure at rest and during exercise, while the mean values of systolic blood pressure tended to be less with nifedipine than with diltiazem. Nifedipine caused a nonsignificant increase in heart rate at rest and during exercise, but diltiazem significantly decreased it at rest and during exercise. Cardiac output was significantly increased at rest and during mild exercise (50 watt), but not during more strenuous exercise (100 watt) with both drugs. Thus, different actions in arterial vasodilation and chronotropism between nifedipine and diltiazem in usual clinical doses were noted. However, nifedipine and diltiazem may be effective in hypertensive patients, probably with left ventricular dysfunction, because both drugs reduced systemic blood pressure even during exercise with simultaneous increase in cardiac output at rest and during mild exercise.

Adult↗
PubMed1985

[Effects of nitroglycerin on left ventricular systolic, diastolic and regional myocardial function in patients with coronary artery disease].

To investigate the actions of nitroglycerin on left ventricular (LV) systolic and diastolic functions in coronary artery disease, high-fidelity LV pressures and LV biplane cineventriculograms were simultaneously made for 16 patients with old myocardial infarction before and 5-10 minutes after the sublingual administration of 0.6 mg of nitroglycerin. Before and after the nitroglycerin administration, heart rates were maintained constant at an average of 73 beats/min by right atrial pacing. LV volume and segmental wall shortening were derived from frame by frame (20 msec) analysis of LV biplane angiograms. The results were as follows: There were significant decreases in LV end-diastolic pressures (-44%) and volumes (-10%), mean arterial pressures (-12%) and LV systolic pressures (-16%), suggesting preload and afterload reductions. Global ejection fraction was significantly increased from 0.41 to 0.45, while cardiac output decreased significantly (-8%) because of a decrease in preload. Augmented ejection fraction was associated with increased shortening of the normal and hypokinetic segments. The dyskinetic segment remained unchanged. Thus, the degree of nitroglycerin-induced potentiation of LV regional contraction seemed related to the degree of regional myocardial ischemia and fibrosis. The time constant (T) of the LV pressure decay was slightly but significantly decreased, which may imply the possibility of improving LV relaxation using nitroglycerin. LV early filling significantly decreased as evidence by a fall in the peak filling rate (PFR) and the normalized PFR. The decrease of the PFR, however, may be related mainly to preload reduction by nitroglycerin. In 11 of 16 patients, there was a displacement of LV diastolic pressure-volume curves downward and to the left. The shift of the curves may be caused by the effects of ventricular interaction and/or the pericardium.

Cardiac Output↗
PubMed1984

Mepacrine-induced inhibition of human platelet cyclic-GMP phosphodiesterase.

The effect of mepacrine (DL-quinacrine-HCI), a specific inhibitor of phospholipase C, on cyclic-GMP levels in human platelets was investigated. The concentrations of mepacrine producing 50% inhibition of human platelet aggregation induced by 5 microM ADP and 3 micrograms/ml of collagen were 50 +/- 8 and 70 +/- 15 microM, respectively. Addition of mepacrine to human platelet suspension resulted in increases in cyclic GMP. In contrast to cyclic-GMP levels, cyclic-AMP content was not affected by mepacrine. Mepacrine did not stimulate guanylate cyclase, but did specifically inhibit human platelet cyclic-GMP phosphodiesterase, separated from cyclic-AMP phosphodiesterase or other forms of phosphodiesterase on DEAE-cellulose columns. Stimulation by cyclic GMP of human platelet cyclic-GMP-stimulated cyclic-AMP phosphodiesterase activity was not inhibited by mepacrine. The IC50 value of the drug for cyclic-GMP phosphodiesterase was 40 microM, and IC50 for cyclic-AMP phosphodiesterase was 1.2 mM. Mepacrine was 30-times more potent as an inhibitor of human platelet cyclic GMP than of cyclic-AMP phosphodiesterase. Mepacrine blocks arachidonate release from human platelets by inhibiting phosphatidylinositol-specific phospholipase C. The increase in cyclic-GMP levels produced by addition of mepacrine will explain part of the pharmacological action of this drug.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1984

Reduction of left ventricular size following oxygen inhalation in patients with coronary artery disease as measured by biplane coronary cineangiograms.

Left ventricular size is one of the major determinants of myocardial oxygen consumption, therefore if oxygen inhalation reduces myocardial oxygen demand, such might be beneficial in the treatment of acute myocardial infarction. Routine diagnostic biplane left coronary cineangiograms were obtained during air or oxygen breathing in 11 patients with old myocardial infarction or angina pectoris. Coordinates of the points on the left coronary artery were measured and throughout one cardiac cycle frame by frame. The spatial distance (segment length: L) between any two of these points was calculated. Segment length at R wave on the electrocardiogram (LECG R) and minimum value (Lmin) for each segment were calculated. Arterial pO2 was elevated by oxygen breathing from 91 +/- 4 (+/- SE) to 427 +/- 18 mmHg. Left ventricular segment length was significantly reduced by oxygen breathing: LECG R being reduced following oxygen breathing from 62.3 +/- 3.0 to 60.6 +/- 3.0 mm (a decrease of 3.3 +/- 0.8%) and Lmin also being reduced from 55.9 +/- 2.8 to 54.4 +/- 2.8 mm (a decrease of 3.1 +/- 1.0%). These figures indicate that left ventricular size was reduced. Reduction in left ventricular size through oxygen inhalation, by reducing myocardial oxygen demand, should therefore be beneficial in coronary artery disease.

Adult↗
PubMed1984

Potentiation of antiaggregating activity of adenosine by a phosphodiesterase inhibitor, EG626 (oxagrelate), in human platelets in vitro.

EG626 (oxagrelate), a specific inhibitor of cyclic AMP phosphodiesterase, produced in vitro a concentration-dependent inhibition of platelet aggregation induced by collagen and ADP in human platelets. When adenosine was added to the platelet rich plasma (PRP) in the presence of a threshold concentration of EG626, the potency of adenosine in inhibiting platelet aggregation was markedly potentiated. This potentiating effect of EG626 proved to be synergistic, but not additive and was accompanied by a marked accumulation of cyclic AMP in the platelets. The antiaggregating and cyclic AMP increasing activities of adenosine were little affected by S-(p-nitrobenzyl)-6-thioguanosine (6TG), an uptake inhibitor of adenosine, or 2'-deoxycoformycin, an inhibitor of adenosine deaminase. The incorporation of adenosine into platelets was abolished by 6TG. These observations indicate that incorporation of adenosine into platelets is not required for inhibition of aggregation or an increase in cyclic AMP and that the site of action of adenosine is probably extracellular. It also appears that the synergistic action by EG626 is not the result of an inhibition of adenosine uptake and/or adenosine deaminase. This speculation is supported in part by the finding that EG626 also potentiates the antiaggregating activity of 2-chloroadenosine. Antiaggregating activity of prostaglandin E1, an activator of adenylate cyclase, was markedly potentiated in combination with EG626. Dibutyryl cyclic AMP showed a time-dependent inhibition of the platelet aggregation, and the inhibitory action was markedly potentiated by EG626. Qualitatively similar results were obtained with another phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX). All these data suggest that the synergistic potentiation of the antiaggregating activity of adenosine by EG626 might be due to the synergistic accumulation of cyclic AMP in the platelets. This action is mediated through activation of adenylate cyclase by adenosine in combination with the inhibition of cyclic AMP phosphodiesterase by EG626.

1-Methyl-3-isobutylxanthine↗