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Biomedical subjects

G Osakada

Publications and source records attributed to G Osakada.

At least 37 records · Page 2Linked to original sources
PubMed1984

[Dynamics of the interventricular septum in mechanical overload].

To assess wall thickness dynamics of the interventricular septum, ultrasonomicrometry was directly applied to measure wall thickness of the septum as well as the left ventricular free wall thickness in open chest dogs. In the control resting state, the end-diastolic wall thickness and magnitude of the systolic thickening of the septum were essentially equal to those of the left ventricular free wall. Acute interventions, such as pressure or volume overloading on the right or left ventricle, induced the same dynamic changes in the septum as in the left ventricular free wall. To evaluate the chronic changes in wall thickness dynamics of the interventricular septum, echocardiographic studies were conducted in patients with chronic pressure or volume overload in the right or left ventricle. While sustained pressure or volume overload in the left ventricle resulted in an increase in wall thickness of both the septum and left ventricular free wall, chronic pressure overload of the right ventricle induced the hypertrophy only in the septum but not in the left ventricular free wall. Thus, the interventricular septum can be regarded as a functional part of the left ventricle, and the mechanical loading on the left ventricle will ultimately induce proportional changes in the septum and the left ventricular free wall. Although the septal function is largely independent of acute changes in right ventricular loading, a chronic effect cannot be ignored.

Animals↗
PubMed1983

End-systolic dimension-wall thickness relations during myocardial ischemia in conscious dogs. A new approach for defining regional function.

Overall and regional left ventricular (LV) function was studied during progressive coronary stenosis in conscious dogs by determining the relations at end-systole between LV pressure, chamber dimensions, and regional LV wall thickness. An index of regional wall stress was also analyzed. Using ultrasonic dimension gauges, measurements were made of LV wall thickness in control and ischemic regions, and the external long- and short-axis LV diameters were determined; an implanted micromanometer measured LV pressure. Internal LV diameters were obtained from the external diameters by subtraction of wall thickness, and the index of regional wall stress employed a thick-walled ellipsoidal model. During regional ischemia, the LV long axis at end-systole did not change, whereas the short-axis diameter progressively increased (from 24 +/- 7 mm [standard deviation] to 30 +/- 9 mm, p less than 0.001, indicating a more spherical LV shape during ischemia). The end-systolic pressure did not change, and therefore the end-systolic pressure-diameter relation shifted progressively, suggesting a global decrease in LV contactility. The end-systolic points relating LV wall thickness in the ischemic region to the end-systolic LV pressure revealed the regional nature of the abnormality, showing a progressive displacement to the left, whereas there was no significant displacement of this relation in the control region. The application of this index over a range of loading conditions during partial vena caval occlusion was illustrated. Thus, the regional end-systolic wall thickness-pressure relation provides a new index for defining the regional contractile state of the LV myocardium which is potentially load-independent and offers the possibility for echocardiographic application.

Animals↗
PubMed1983

Effect of exercise on the relationship between myocardial blood flow and systolic wall thickening in dogs with acute coronary stenosis.

Relationships between regional myocardial perfusion and transmural function, both during treadmill exercise and at rest, were examined in conscious dogs with varying degrees of coronary stenosis produced by a hydraulic occluder. In 13 dogs we measured myocardial blood flow with microspheres (10-12 microns in diameter) and regional systolic wall thickening (%). During exercise with coronary stenosis, myocardial blood flow was characterized by nonuniform distribution, and associated with regional dysfunction. The relationships between normalized myocardial blood flow and normalized %wall thickening during exercise with coronary stenosis were linear, with significantly different slopes (mean myocardial blood flow: y = 1.23x - 0.16, r = 0.93; subendocardial myocardial blood flow: y = 1.50x - 0.02, r = 0.86; subepicardial myocardial blood flow: y = 0.83x - 0.18, r = 0.87). To fill the gap between available subendocardial and subepicardial data during exercise with coronary stenosis and control points, however, would require nonlinear components. In 10 of the dogs, coronary stenosis at rest was also produced to compare regional myocardial blood flow - %wall thickening relations at rest with those during steady state exercise. The absolute mean myocardial blood flow - %wall thickening relation during exercise with coronary stenosis (y = 11.6x - 1.9, r = 0.90) was significantly shifted rightward from the resting relation (y = 25.3x -2.1, r = 0.80). However, when changes in %wall thickening were plotted vs. myocardial blood flow per beat, the relationships at rest and exercise were nearly superimposable. Likewise, relations between normalized myocardial blood flow and changes in %wall thickening at rest and exercise were not significantly different. We conclude: %wall thickening during exercise is directly related to changes in mean myocardial blood flow but is related in nonlinear fashion to changes in subepicardial and subendocardial myocardial blood flow; %wall thickening may provide a reliable index of the relative transmural flow distribution during exercise as well as at rest; during brief bouts (5-8 minutes) of exercise with coronary stenosis, the relationship between stabilized regional contractile dysfunction and level of myocardial blood flow per beat is the same as that during coronary stenosis at rest.

Acute Disease↗
PubMed1983

A diastolic mid-echo in torn chordae tendineae of the mitral valve.

Echocardiographic studies were performed on 3 patients with torn chordae tendineae of the mitral valve proven by open heart surgery or during autopsy. Mitral regurgitation was noted after episodes of bacterial endocarditis in 3 patients; one had had rheumatic valvular disease before the episode. Conventional M-mode echocardiograms showed coarse diastolic fluttering of the mitral valve, multiple mitral valve echoes in systole, and diastolic mid-echoes between both anterior and posterior leaflets. The last pattern was found in all 3 patients. There was only one patient with an unusual systolic echo in the left atrium. Two-dimensional echocardiograms from 2 patients revealed an abnormal echo in the left ventricle in diastole which moved into the left atrium in systole, slightly beyond the closure line of the mitral valve. This moving abnormal echo observed in two-dimensional echograms presumably originated from torn chordae tendineae and was consistent with the diastolic mid-echo noted in M-mode echograms. Thus, the diastolic mid-echo of the mitral valve by M-mode echocardiography is an important finding in the diagnosis of torn chordae tendineae of the mitral valve, and two-dimensional echocardiography can identify the movement of torn chorda itself.

Adult↗
PubMed1983

[New approach for quantifying left ventricular regional wall motion in ischemic heart disease: motion vector analysis of endocardial surface by two-dimensional echocardiography].

To quantify regional wall motion of the left ventricle with two-dimensional echocardiography, the motion of an endocardial surface point in echocardiograms was analyzed throughout systole on frame by frame using video motion analyzer. With a fixed external reference system and in the "69% point (C)" by Ingels et al, the motion vector (M) of a point was expressed in two components; the contracting component (Y) directed toward the point C, and the component vertical to it, the shearing component (X). In the control group, the magnitude of M and its contracting component were widely varied with the location along the endocardial surface (5.6 +/- 1.6, 5.0 +/- 1.5 mm in the apex, 10.9 +/- 2.2, 10.4 +/- 2.0 mm in the inferior base, p less than 0.001 and p less than 0.001, respectively). The shearing component and the angle theta at which M and Y meet, showed narrow normal ranges (1.9 +/- 1.4 mm, 15.1 +/- 1.4 mm, 15.1 +/- 11.2 degrees), and were independent of their locations. In the ischemic group, however, the points of non-ischemic regions showed low values of theta (14.9 +/- 8.9 degrees), which were not significantly different from those of the control group, while the points of ischemic regions showed high values of theta (over 2SD of the control group). The distribution of these points with abnormal theta values was well correlated to that of the segments with asynergic motion evaluated by both real-time two-dimensional echocardiography and left ventriculography (p less than 0.001 and p less than 0.001, respectively). These results suggest that this new approach with quantitative echocardiography is sensitive and specific for the assessment of regional wall motion of the left ventricle and may provide accurate clinical information for the evaluation of ischemic heart disease.

Adolescent↗
PubMed1982

Left ventricular geometry during partial and complete coronary occlusion in the conscious dog.

Seven dogs were instrumented with a left ventricular micromanometer and pairs of ultrasonic crystals to measure left ventricular wall thicknesses (control and ischemic regions) and short and long left ventricular axes; cuff occluders were placed around the left circumflex coronary artery and the inferior vena cava. Measurements were performed at rest, after 2 min of partial and complete coronary occlusion, and 1 and 10 min after release of partial and complete coronary occlusion. Left ventricular wall thickness in the ischemic region showed reduced systolic thickening during partial coronary occlusion and systolic thinning during complete coronary occlusion. During diastole, at zero pressure (inferior vena cava obstruction) the left ventricular short axis was unchanged during partial coronary occlusion but significantly increased (creep) during complete coronary occlusion (P less than 0.05), whereas after release of both partial and complete coronary occlusion the short axis at zero pressure decreased significantly (P less than 0.025). Left ventricular wall thickness at zero diastolic pressure in the ischemic region was significantly thinner during complete coronary occlusion than during control and significantly thicker (reactive hyperemia) 1 min after release of both partial and complete coronary occlusion. The long left ventricular axis remained unchanged during the entire experiment. At end-diastole, the long/short axis ratio was normal during partial (1.72; control 1.68; NS) and complete coronary occlusion (1.69; NS), but it decreased significantly from control of 2.10 to 1.99 with partial coronary occlusion and 1.85 with complete coronary occlusion (P less than 0.01). The changes in the L/S ratio during partial and complete coronary occlusion were proportional to changes in left ventricular chamber volume (correlation coefficient 0.94). Our data show that left ventricular shape remains normal at end-diastole during partial and complete coronary occlusion but becomes significantly more spherical at end-systole, with reduction of the normal tendency for the ventricle to become more elliptical during systole. These elliptical and spherical shape changes of the left ventricle during partial and complete coronary occlusion appear to be closely related to the chamber volume.

Animals↗
PubMed1982

Myocardial blood flow and function with critical coronary stenosis in exercising dogs.

Critical stenosis of coronary arteries does not alter myocardial blood flow (MBF) at rest, but eliminates hyperemia and corresponds to a degree of arterial narrowing that expends subendocardial vasodilator reserve. Because subepicardial vasodilator reserve remains with critical stenosis at rest, we tested the significance of this reserve in six exercising dogs chronically instrumented to measure MBF (microspheres), regional function (systolic wall thickening with sonomicrometers), and coronary blood flow velocity (CBFV, pulsed Doppler). Critical stenosis produced with a hydraulic occluder limited CBFV and mean MBF to the resting level during treadmill exercise, but MBF was maldistributed. Subendocardial MBF decreased 50% (P less than 0.05) and subepicardial MBF increased 104% (P less than 0.01) compared with resting control conditions, suggesting that a transmural "steal" phenomenon had occurred, with augmented MBF in the subepicardial region at the expense of subendocardial MBF. Systolic wall thickening decreased markedly from 31.5 +/- 6.8 to 9.4 +/- 2.0% (P less than 0.01) during exercise, indicating that use of subepicardial vasodilator reserve with critical stenosis had little sustaining effect on regional contractile performance. Rather, subepicardial vasodilator reserve is potentially deleterious, inasmuch as a steal effect could contribute to reduced subendocardial perfusion, the primary determinant of systolic wall thickening.

Animals↗
PubMed1982

Primary chylopericardium.

In a 23-year-old man with massive chylous pericardial effusion, oral administration of Sudan III and radio-active 131iodine-labelled triolein revealed an abnormal communication between the lymphatic system and the pericardial sac. Despite partial pericardiectomy and resection of the thoracic duct, the fluid reaccumulated, and a postoperative lymphangiogram showed an obstructed left thoracic duct. Resection of this left thoracic duct resulted in full recovery. This is the first reported case of this disease with a duplicate thoracic duct. Careful attention must be paid to the possibility of this variation before and during surgery.

Adult↗
PubMed1981

[Determinants of the diastolic pressure-volume relationship of the left ventricle: significance of myocardial ischemia and vena cava occlusion].

Diastolic pressure-volume relations of the left ventricle were studied in 7 dogs during partial and complete coronary occlusion. The pericardium was widely opened and the dogs were instrumented with a left ventricular micromanometer, cuff occluders around the left circumflex coronary artery and inferior vena cava, and ultrasonic crystals to measure control and ischemic wall thickness as well as both left ventricular long and short axes. Measurements were performed at rest and after 2 minutes of partial and complete coronary occlusion. The first experiment was performed without caval occlusion and a second experiment was carried out a few days later with caval occlusion. During partial coronary occlusion, no shift of the diastolic pressure-volume relationship was observed. However, during complete coronary occlusion the pressure-volume curve was shifted significantly upwards but no shift was observed when occlusion of the inferior vena cava was carried out. These findings suggest that the shift of the diastolic pressure-volume relationship during coronary occlusions (1) depends on the extent of myocardial ischemia and (2) is related to ventricular interaction since the shift was prevented by caval occlusion.

Animals↗
PubMed1980

Modification of regional function of ischaemic myocardium by the alteration of arterial pressure in dogs.

The effects of alterations of arterial pressure by nitroprusside and methoxamine on regional myocardial function were studied during total coronary occlusion and during partial coronary constriction in open chest dogs. Animals were instrumented with a left ventricular micromanometer, an electromagnetic flow probe around the left circumflex coronary artery, and three pairs of ultrasonic crystals in a control, marginally ischaemic, and ischaemic segments. In nine dogs, when the coronary artery was totally occluded by a hydraulic cuff placed distal to the flow probe, the end-diastolic length of all three segments was increased, and shortening was rapidly replaced by systolic expansion in the ischaemic segment. Active shortening decreased by 68% in the marginal segment, while it increased by 21% in the control segment. With nitroprusside infusion, peak systolic pressure was reduced from 15.2 to 11.3 kPa and hypokinesis of the marginal segment was improved to 45% of control value with a concomitant decrease in end-diastolic length by 5%. With methoxamine, left ventricular systolic pressure was elevated to 18.5 kPa, and marginal segment shortening further deteriorated to 19% of control with chamber enlargement. In 6 dogs, coronary flow was limited by a screw-driven metal clamp. When mean coronary flow was reduced by 50% of control value, stable hypokinesis was produced in the ischaemic segment. Nitroprusside infusion induced the same haemodynamic changes, however, shortening of the ischaemic segment deteriorated further and a passive bulge appeared. Methoxamine improved the percentage shortening from 1.2 to 6.4%. Thus, interventions with an agent which changes afterload in left ventricular ejection have multiple and complex effects on the contractile function of the ischaemic myocardium and, depending on the magnitude of coronary blood flow reduction, a potentially beneficial drug can be determined to an ischaemic myocardium.

Animals↗
PubMed1979

Effects of intraaortic balloon counterpulsation on regional myocardial function during acute coronary occlusion in the dog.

The effects of intraaortic counterpulsation on regional myocardial function were studied using ultrasonic dimension gauges in 24 open chest dogs. Pairs of ultrasonic crystals were implanted in the subendocardium of the left ventricle in control, marginally ischemic and ischemic segments. After coronary arterial occlusion, the end-diastolic length of all three segments was increased. Segment shortening was rapidly replaced by systolic expansion in the ischemic segment. In the marginal segment, active shortening decreased by 53% and, in the control segment, shortening was augmented by compensatory operation of the Frank-Starling mechanism. Balloon pumping initiated 10 minutes after coronary occlusion resulted in an increase in mean aortic diastolic pressure from 103 to 115 mm Hg without any significant change in peak systolic pressure. In the marginal segment, end-diastolic length decreased by 3%, and previously reduced shortening increased to 82% of control value, deteriorating again with discontinuation of counterpulsation. Balloon pumping produced no change in the dyskinetic motion of the ischemic segment but caused compensatory augmentation of shortening of the control segment. Thus, counterpulsation selectively improved segment function of the marginally ischemic segment, presumably as a result of a regional increase in myocardial blood flow and in availability of oxygen due to augmented perfusion pressure. The systolic unloading effect was counterbalanced by improved cardiac performance.

Acute Disease↗
PubMed1979

Dynamic geometry of the left atrium and left ventricle in acute mitral regurgitation.

The instantaneous transverse diameter of the left atrium, left ventricular free wall segment length (SEG), and the long axis of the anterior papillary muscle (APM) length were measured throughout the cardiac cycle, using ultrasonic dimension gauges together with left atrial and left ventricular pressures in 12 open-chest dogs. During atrial contraction, left atrial diameter decreased from 19.7 to 18.7 mm, while left ventricular dimensions increased simultaneously. During ventricular ejection, percent shortening was 26% in SEG and 10% in APM, while atrial diameter increased continuously to 20.5 mm, with a concomitant rise in the v wave of left atrial pressure. After normal mitral valve opening, left atrial diameter decreased rapidly simultaneously with the y descent of atrial pressure. Graded mitral regurgitation was then produced by sectioning the chordae tendineae. With moderate mitral regurgitation, end-diastolic length of the SEG increased by 27%, while extent of shortening (delta L) was augmented by 96%. End-diastolic length of the APM increased by 7%, and delta L was augmented by 60%. Left atrial pressure was sharply elevated, with a distinct a wave followed by the more prominent v wave. End-diastolic diameter of the left atrium was enlarged to 22.9 mm with increased atrial shortening and expansion. As mitral regurgitation was increased to a severe degree by additional chordal rupture, end-diastolic length and delta L continued to increase both in SEG and APM. Left atrial pressure was further elevated (a wave 25 mm Hg and v wave 47 mm Hg). Left atrial end-diastolic diameter further increased in 24.9 mm. However, the amplitude of left atrial shortening and expansion decreased remarkably. In severe mitral regurgitation, isoproterenol and nitroprusside decreased left atrial pressure and diameter, restoring more forceful atrial shortening.

Acute Disease↗