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Biomedical subjects

A Kitabatake

Publications and source records attributed to A Kitabatake.

At least 217 records · Page 12Linked to original sources
PubMed1990

Increased intracardiovascular clotting in patients with chronic atrial fibrillation.

To clarify whether the formation of thrombi could be induced by atrial fibrillation itself or by factors predisposing to atrial fibrillation such as mitral stenosis, plasma D-dimer levels (cross-linked fibrin degradation products) were measured in 73 patients without atrial fibrillation (Group 2). In Group 1, 49 of the 73 patients had factors predisposing to atrial fibrillation such as valvular heart disease, and the remaining 24 had lone atrial fibrillation. In Group 2, 16 patients had organic heart disease and the remaining 5 had a chest pain syndrome. The plasma D-dimer level was significantly higher in Group 1 (150 +/- 19 ng/ml) than in Group 2 (61 +/- 3 ng/ml) (p less than 0.01, mean +/- standard error of the mean). In both groups, there were no significant differences in plasma D-dimer level between patients with and without organic heart disease (146 +/- 18 versus 156 +/- 46 ng/ml in Group 1; 61 +/- 4 versus 59 +/- 10 ng/ml in Group 2). These findings indicate that atrial fibrillation itself may be more important than factors predisposing to atrial fibrillation in the development of intracardiovascular clotting.

Atrial Fibrillation↗
PubMed1990

Doppler echocardiographic quantitation of cross-sectional area under various hemodynamic conditions: an experimental validation in a canine model of supravalvular aortic stenosis.

The hemodynamic effects on cross-sectional area calculated with the continuity equation were assessed in canine experiments. In 13 open chest dogs, 46 supravalvular aortic stenoses were created by aortic root banding. The cross-sectional area of the stenosis was calculated by Doppler echocardiography with application of the continuity equation before and after the following hemodynamic interventions: protocol 1, atrial pacing at 90, 120, 150 and 180 beats/min after sinus node crush; protocol 2, preload reduction by mild and severe clamping of the inferior vena cava; and protocol 3, afterload augmentation by mild and severe clamping of the descending aorta. In each observation, a dimension of the stenosis was directly measured by two-dimensional echocardiography, and the cross-sectional area was determined as a reference standard. As a result of the hemodynamic interventions, significant changes were observed in stroke volume and pressure gradient (protocol 1), in cardiac output, stroke volume and pressure gradient (protocol 2) and in heart rate, cardiac output and pressure gradient (protocol 3). Despite these changes in hemodynamic variables, the Doppler-derived cross-sectional area showed no significant change for a given stenosis. In addition, areas calculated with the continuity equation (x) agreed well with those determined by two-dimensional echocardiography (y) (r = 0.96, p less than 0.001, y = 0.97x + 0.02, SEE = +/- 0.06 cm2). Thus, it is concluded that Doppler echocardiography with application of the continuity equation accurately predicts the stenotic cross-sectional area over a wide range of hemodynamic conditions in supravalvular aortic stenosis.

Animals↗
PubMed1990

Polymorphonuclear leukocytes induced vasoconstriction in isolated canine coronary arteries.

To assess how polymorphonuclear leukocytes (PMNs) act on coronary vasoactivity, we measured the changes in isometric tension of isolated rings of canine coronary arteries upon addition of autologous PMNs to organ chambers in which the rings were suspended. When PMNs isolated by the colloidal polyvinylpyrrolidone-coated silica (Percoll) gradient method were added to the chambers, ring preparations of left circumflex coronary arteries developed isometric tension. The increase in tension was dependent on the amount of PMNs (1 X 10(4) to 5 X 10(6) cells/ml). Maximal tension obtained by an optimal amount of PMNs (5 X 10(5) cells/ml) was almost comparable to that produced by prostaglandin F2 alpha (5 microM). Integrity of endothelial cells was not disrupted after the addition of PMNs because the developed tension could be reversed by the addition of acetylcholine in an endothelium-dependent manner. Mechanical rubbing of endothelium abolished the PMN-induced vasoconstriction, which was regained by placing an endothelium-unrubbed ring inside a rubbed ring ("sandwich preparation"). When PMN suspensions were pretreated with 5-lipoxygenase inhibitors of arachidonate, PMN-induced vasoconstriction was greatly suppressed, although the pretreatment of vascular preparations did not alter the development of isometric tension. These findings indicate that PMNs induce the contraction of coronary arterial rings in the presence of intact endothelial cells. The mechanism by which PMNs induce the contraction is the release of vasoconstrictive substances by metabolic interaction between PMNs and endothelial cells. Vasoconstrictive substances produced by the PMN-endothelial system, such as 5-lipoxygenase metabolites through a "leukotriene A4 steal" mechanism, may contribute to the contraction of vascular smooth muscle.

Animals↗
PubMed1990

Detection of oxygen-derived free radical generation in the canine postischemic heart during late phase of reperfusion.

To define the relation between oxygen-derived free radical (oxy-radical) generation in the reperfused ischemic myocardium and the progression of myocardial damage, we measured oxy-radical generation in the ischemic myocardium and the propagating infarct size in a model of canine coronary occlusion (90 minutes) and reperfusion. We used electron paramagnetic resonance spin-trapping techniques (5,5-dimethyl-1-pyrroline N-oxide [DMPO]) to detect oxy-radicals in the rapidly frozen myocardial samples taken by needle biopsy. There was no detectable generation of DMPO adducts in the normal myocardium before or after reperfusion. In the reperfused ischemic myocardium, electron paramagnetic resonance signals of DMPO-OOH (superoxide anion) and DMPO-OH (hydroxyl radical) were detected, with peak concentrations at 1 hour after reperfusion for DMPO-OOH and at 3 hours after reperfusion for DMPO-OH, respectively. These DMPO adducts were also detected during the early phase (15 seconds) of reperfusion, but the concentrations of these signals were much less than those during the late phase of reperfusion. Treatment with human recombinant superoxide dismutase (2.5 mg/kg/hr) and catalase (2.5 mg/kg/hr) during the course of experiments abolished DMPO-OOH formation but had little effect on DMPO-OH formation. Infarct size (percent of risk area infarcted), quantified by a dual staining method with Evans blue dye and triphenyltetrazolium chloride, was 18.3 +/- 4.8% (mean +/- SEM) at 90 minutes of occlusion. After 5 hours of reperfusion, infarct size increased to 43.6 +/- 7.2%. These results indicate that a greater magnitude of oxy-radical generation was sustained in the ischemic myocardial tissue during the late phase (1-3 hours) of reperfusion, associated with the progression of myocardial infarction. The concurrent appearance of oxy-radicals and progressive infarction may support the view that a chain reaction of oxy-radicals contributes to the propagation of myocardial cell damage in the postischemic heart.

Animals↗
PubMed1990

Disruption of microtubules as an early sign of irreversible ischemic injury. Immunohistochemical study of in situ canine hearts.

Structural disruption of the cytoskeleton may be involved in irreversible ischemic injury. In the present study, ischemic changes in microtubules during various periods of myocardial ischemia were studied with an immunohistochemical technique in open-chest dogs. In intact myocardium, microtubules were stained as a filamentous network throughout cytoplasm and a circular network around the nucleus, which disappeared with colchicine treatment. In brief ischemia of less than 15 minutes, microtubule patterns were unaltered. After 20 minutes, however, characteristic microtubule stains were partly lost in patchy lesions. As an increase in ischemic period, lesions of loss of microtubule stains were increased in number and size. After 120 minutes of reperfusion following 60 minutes of ischemia, the lesions with intact actin filaments but with disrupted microtubules were replaced by the severely injured cells in which the regular myofibrillar registrations were distinctly disrupted. After 24 hours of reperfusion following 40 minutes of occlusion of the left circumflex artery, the percent area of disrupted microtubules at 40 minutes of ischemia was replaced by that of irreversibly injured lesions in the posterior papillary muscle. These results indicate that disruption of microtubules during ischemia heralds irreversible ischemic injury. However, in in vitro study, the myocardium incubated in hypoxic solution for 60-120 minutes demonstrated earlier disruption of the microtubules than the vinculin. Electron microscopic study also showed minimal irreversible changes in the lesions with disrupted microtubules. Thus, taken together, we conclude that microtubules that support the structural integration of myofibrils and other organelles are disrupted in severe myocardial ischemia before the irreversible injury, promoting the irreversible change after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Quantitative color flow imaging to measure the two-dimensional distribution of blood flow velocity and the flow rate.

A quantitative Doppler color flow imaging was employed to measure the two-dimensional distribution of blood flow velocity and flow rate in a large vessel. Regional blood flow velocity was determined by converting the color intensity at the respective pixel into corresponding flow velocity and correcting the flow velocity for spatial ultrasound beam incident angle. Instantaneous flow rate was determined precisely from the image of velocity distribution on the cross-section of the flow tract in a steady flow model circuit. In clinical application, the differences in phasic changes in two-dimensional velocity distribution in the ascending aorta, between normal subjects and the patient with aortic regurgitation, were clearly depicted. The quantitative color flow imaging may have great potential to determine noninvasively and real-timely the two-dimensional distribution of flow velocity as well as flow rate in a large vessel.

Aortic Valve Insufficiency↗
PubMed1990

The role of Na+/H+ exchange in norepinephrine-induced protein synthesis in neonatal cultured rat cardiomyocytes.

It is reported that Na+ influx contributes to stretch-induced cardiac hypertrophy. Na+ influx may also be involved in cardiac hypertrophy induced by catecholamine. In the present study, to test whether Na+/H+ exchange plays an important role in norepinephrine-induced cardiac hypertrophy, the effect of Na+/H+ exchange inhibitor, amiloride on protein synthesis was studied in cultured neonatal rat cardiomyocytes in serum free medium. [3H]Phenylalanine uptake was determined 24 and 48 hours after administration of norepinephrine with and without amiloride. In the control, norepinephrine increased [3H]phenylalanine uptake in a dose dependent manner (10(-5)-10(-7) M). Prazosin (10(-7) M) and amiloride (10(-5)-10(-4) M) significantly attenuated the norepinephrine mediated protein synthesis. These results indicate that alpha 1-adrenergic stimulation enhances the protein synthesis through activation of Na+/H+ exchange. Therefore, Na+ influx and/or PH increase may play a key role in cardiac hypertrophy.

Amiloride↗
PubMed1990

Pathologic involvement of the left ventricle in chronic cor pulmonale.

To determine whether or not the left ventricle is pathologically involved in patients with chronic cor pulmonale, right and left ventricular weights, wall thickness, myocyte diameters, and percentage of fibrosis in 18 autopsied hearts were examined in patients with chronic pulmonary disease (CPD); ten had right ventricular hypertrophy on their electrocardiograms, and eight were without right ventricular hypertrophy. Five with extracardiopulmonary disease were used as controls. The weight of the right ventricle was significantly increased in CPD when compared to control subjects. Walls of both ventricles were significantly thicker in CPD. Myocyte diameters of both ventricles were significantly greater in CPD. The percentage of fibrosis in the right ventricle was significantly greater in CPD. The percentage of fibrosis in the left ventricle was significantly greater only in patients with right ventricular hypertrophy. We concluded that the left ventricle was also involved pathologically in patients with chronic cor pulmonale in the end stage of the disease.

Adult↗
PubMed1990

[Myocardial adrenergic derangement due to myocardial ischemia: decreased myocardial uptake of I-123 metaiodobenzylguanidine after PTCA in a patient with effort angina].

Regional denervation of adrenergic nerves has been clinically demonstrated in patients with myocardial infarction using I-123 metaiodobenzylguanidine (MIBG) scintigraphy. However, it is not clarified whether adrenergic denervation can be induced by prolonged myocardial ischemia as well as by myocardial infarction. This case with effort angina had 99% stenosis of right coronary artery and showed perfusion defects at inferior myocardial regions in the exercise thallium-201 study. However, inferior wall motion estimated by echocardiography and left ventriculography was normal indicating the absence of myocardial infarction. After percutaneous transluminal coronary angioplasty for the stenosis, I-123 metaiodobenzylguanidine (MIBG) and thallium-201 (Tl-201) myocardial scintigraphies were done to estimate the therapeutic effect of PTCA. Although the Tl-201 study during exercise showed normal findings indicating the success of PTCA, marked defects was detected at inferior myocardial regions in the I-123 MIBG studies just after and 4 hours after an intravenous injection of I-123 MIBG. These results suggest that adrenergic derangement may be induced by prolonged myocardial ischemia and may persist for periods even though myocardial perfusion is normalized.

3-Iodobenzylguanidine↗
PubMed1990

[Gallium-67 myocardial imaging for the detection of adriamycin cardiomyopathy].

To detect Adriamycin cardiomyopathy, radionuclide myocardial imagings with Tl-201, Tc-99m pyrophosphate, I-123 metaiodobenzylguanidine and Ga-67 were performed in a 49 year-old-woman receiving Adriamycin (a total dose of 230 mg/m2) for the treatment of breast cancer. This patient demonstrated symptoms of congestive heart failure 2 months after the last intravenous administration. At the period of performing the radionuclide studies, echocardiographic LV ejection fraction (EF) was 22%. Despite severe deterioration of cardiac function, Tl-201 SPECT demonstrated no defect and Tc-99m pyrophosphate (PYP) SPECT demonstrated no positive finding. I-123 metaiodobenzylguanidine (MIBG) scintigraphy demonstrated no regional defect. However, I-123 MIBG washout rate during 4 hours was markedly enhanced, probably reflecting abnormalities of norepinephrine kinetics due to the progression of heart failure. Compared to these pharmaceuticals, Ga-67 was diffusely accumulated in the heart. Then, 5 months after the first study, when LV EF improved to 30% and congestive symptoms disappeared probably owing to beta-blockade therapy, myocardial accumulation of Ga-67 markedly reduced. It has been reported that Ga-67 accumulates in malignant tumor cells and leukocytes. Since, in Adriamycin cardiomyopathy, myocardial accumulation of leukocytes with myocardial fibrotic changes have been histologically demonstrated, the results of Ga-67 scintigraphy may reflect the accumulation of leukocytes. Thus, this case indicates that Ga-67 scintigraphy is advantageous for detecting Adriamycin cardiomyopathy and may be more useful than Tl-201 and Tc-99m PYP scintigraphies.

Doxorubicin↗
PubMed1989

Attenuation of neutrophil function by inhibitors of arachidonate metabolism reduces the extent of canine myocardial infarction.

To assess the role of neutrophils and arachidonate metabolites in evolving myocardial infarction, the effect of inhibitors of arachidonate metabolism on the extent of myocardial damage and neutrophil function was examined in a 90-minute occlusion/5-hour reperfusion model of canine myocardial infarction. A thromboxane A2 synthetase inhibitor, CV-4151, and a lipoxygenase inhibitor, AA-861, greatly reduced the infarct size. They also attenuated the production of chemoattractant leukotriene B4 and chemotactic activity of neutrophils isolated from peripheral circulation. Under these conditions, both the increases in peripheral leukocyte count and neutrophil infiltration in ischemic myocardium were inhibited. These results indicate that the inhibition of 2 pathways of arachidonate metabolism may decrease infiltration of activated neutrophils in ischemic myocardium by attenuating chemotactic function of neutrophils, resulting in reduction of the extent of myocardial infarction.

Animals↗
PubMed1989

Limited atrial compensation to reduced early diastolic filling in hypertensive patients with advanced left ventricular hypertrophy: a Doppler echocardiographic study.

To assess atrial contribution to left ventricular (LV) filling in hypertension, we studied, using pulsed Doppler echocardiography, 22 hypertensive patients without apparent LV hypertrophy (LVH), 12 hypertensive patients with LVH, and 24 age-matched normal subjects. From mitral flow velocity waveform, we determined peak velocity of early diastolic filling flow (peak E), peak velocity of late diastolic filling flow (peak A), and the peak A/peak E ratio (peak A/peak E). Peak E decreased in hypertensives without apparent LVH and showed a further decrease in hypertensives with LVH compared with normal subjects (57 +/- 8 [mean +/- SD]; P less than 0.001, 46 +/- 7; P less than 0.0001, vs 65 +/- 10 cm/s). On the other hand, peak A/peak E increased in hypertensives without apparent LVH, and greatly increased in hypertensives with LVH (1.06 +/- 0.14; P less than 0.001, 1.40 +/- 0.29; P less than 0.0001, vs 0.79 +/- 0.21). However, increased peak A was not significantly different between the hypertensive groups (60 +/- 8 vs 64 +/- 8; NS, both; P less than 0.001 vs 50 +/- 10 cm/s for normal subjects). In hypertensives, we found no significant correlation between peak A and the wall thickness index (WTI, determined as mean LV wall thickness normalized by LV diastolic dimension), whereas peak E was significantly correlated with WTI (r = -0.65; P less than 0.001). Our findings indicate that atrial contraction can not fully compensate the decrease in early diastolic filling caused by advanced LVH. We conclude that atrial compensation for reduced early diastolic filling is limited in hypertensive patients with advanced left ventricular hypertrophy.

Adult↗
PubMed1989

Semiquantitative evaluation of aortic regurgitation by Doppler echocardiography: effects of associated mitral stenosis.

The accuracy of pulsed and continuous wave (CW) Doppler methods for evaluating aortic regurgitation (AR) was compared in patients with and without mitral stenosis (MS), with aortic root angiography as a gold standard. AR was diagnosed with pulsed Doppler echocardiography, by the detection of broad frequency spectral patterns in the isovolumic relaxation time. If these indications were present, AR was graded by examining the extent of diastolic turbulence in the left ventricular cavity (flow mapping method). With CW Doppler echocardiography, AR was diagnosed by the detection of a peak velocity of greater than 2 m/s; if this velocity was attained, AR was graded by measuring the time from the peak velocity to half the peak velocity (half-time method). The angiographic grade corresponded to that determined by the pulsed and CW Doppler methods in 37 and 37 of 46 patients without MS, respectively. Angiographic grade corresponded to the grade determined by the pulsed and CW Doppler methods in 13 and 17 of the 23 patients with MS, respectively. Eight of 10 discrepancies between pulsed Doppler and angiographic grades were due to overestimation of AR by the flow mapping method, apparently because the transmitral jet produces diastolic turbulence in the left ventricular cavity independent of AR. On the other hand, three of six discrepancies between CW Doppler and angiographic grades were due to the incapability of detecting signals of AR by CW Doppler echocardiography. Thus both the pulsed and the CW Doppler methods are useful to evaluate AR in patients without MS. In patients with MS, however, AR is most accurately diagnosed by the detection of AR signals in the isovolumic relaxation time by pulsed Doppler echocardiography, and the degree of AR is more accurately assessed by the CW Doppler half-time method.

Adult↗
PubMed1989

Right coronary artery occlusion: its role in the mechanism of precordial ST segment depression.

To investigate the mechanism of precordial ST segment depression during right coronary artery occlusion, precordial ST segment shifts and myocardial lactate metabolism were evaluated during coronary angioplasty in 10 patients with (group A) and 7 patients without (group B) precordial ST segment depression during balloon occlusion of the right coronary artery, and in 17 patients with precordial ST segment depression during balloon occlusion of the left anterior descending artery (group C). A 12 lead electrocardiogram was continuously recorded in each patient. Blood lactate in the aorta and great cardiac vein was measured during the procedure, and the lactate extraction ratio in the anterior wall was determined both before and during balloon occlusion. Eight of the 10 patients in group A and 1 of the 7 patients in group B had a dominant large right coronary artery. There were no significant differences in summed ST segment elevation in leads II, III and a VF between group A (0.56 +/- 0.26 mV) and group B (0.46 +/- 0.19 mV) during balloon occlusion of the right coronary artery, and no significant differences in summed ST segment depression in leads V1 to V6 during balloon occlusion between group A (0.44 +/- 0.26 mV) and group C (0.38 +/- 0.14 mV). Lactate extraction ratio before balloon occlusion was similar among the three groups. Patients in group A had a higher lactate extraction ratio during (38 +/- 11%) compared with before (30 +/- 11%) (p less than 0.05) balloon occlusion despite precordial ST segment depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1989

Effects of atrioventricular interval on left ventricular diastolic filling assessed with pulsed Doppler echocardiography.

Effects of changes in atrioventricular interval on left ventricular diastolic filling were studied using pulsed Doppler echocardiography in 14 patients with programmable dual chamber pacemakers. Peak early diastolic filling velocity (E) and peak atrial filling velocity (A) were measured from the transmitral flow velocity pattern at three different atrioventricular intervals under the same pacing rate of 80 beats.min-1 in each patient. When the atrioventricular interval was switched from intermediate [148(SD10) ms] to short [68(11) ms], stroke volume did not change significantly [60(14) to 58(13) ml], but E increased from 39(12) to 44(11) cm.s-1 (p less than 0.05), and A decreased from 48(8) to 38(9) cm.s-1 (p less than 0.05). At the short atrioventricular interval, incomplete atrial emptying by the atrial contraction seemed to cause a reciprocal increase in the early diastolic filling. When the atrioventricular interval was switched from intermediate to long [234(16) ms], stroke volume, E and A did not change significantly [57(14) ml, 37(13) cm.s-1, 51(8) cm.s-1 respectively]. At the short and long atrioventricular intervals, atrial filling always changed in the direction opposite to that of early diastolic filling. Changes in stroke volume as well as peak early diastolic filling velocity caused by altering atrioventricular interval were pronounced in aged patients and patients with decreased early diastolic filling. In conclusion, left ventricular diastolic filling patterns can be affected by atrioventricular interval even without any concomitant pathological changes in the left atrial or ventricular function. These effects should not be taken lightly, especially in patients with decreased left ventricular early diastolic filling.

Adolescent↗