Search PubMed⌕ Search

Biomedical subjects

R Katori

Publications and source records attributed to R Katori.

At least 73 records · Page 4Linked to original sources
PubMed1985

Effects of long use of a beta-blocker, carteolol, on exercise hemodynamics in hypertensives.

The symptom limited maximal exercise was performed by a supine bicycle ergometer before and 12 weeks after oral carteolol therapy in 10 patients with essential hypertension of WHO Stage 1 and 2. At rest, arterial blood pressure (BP) and venous pressure (VP) significantly declined after therapy, while heart rate (HR), cardiac index (CI), stroke index (SI) and systemic vascular resistance (SVR) were not significantly changed. The maximal exercise work of post-therapy was similar to that of pre-therapy in 9 patients and increased in one. When compared with the pre-therapy values at each work load of exercise, carteolol caused significant decreases in systolic BP, mean BP, HR and CI, and a significant increase in SVR, while SI and VP were not significantly changed. Plasma levels of renin activity, aldosterone, and catecholamines were not altered by carteolol throughout the study at rest and with exercise. It may be concluded that the inhibition of HR increase by carteolol results in a reduced cardiac output during moderate and severe exercise and then suppresses the elevation of BP, so that carteolol makes it possible to achieve more exercise with less cardiac work.

Administration, Oral↗
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

[Early relaxation of the left ventricular wall in coronary artery disease].

A mechanism for the genesis of early relaxation of the left ventricle was assessed. For 18 patients with coronary artery disease, biplane left coronary cineangiography was performed and the coordinates (x, y, z) of the points of the artery were measured by frame to frame basis throughout one cardiac cycle. The spatial distance (segment length) between any two points was calculated on each frame as (Formula: See text) to investigate shortening and relaxation characteristics of the ischemic and nonischemic segments. Coronary angiography was repeated during right atrial pacing to aggravate ischemia, and following nitroglycerin administration to ameliorate ischemia. From data of six normal subjects, 43 segments were calculated. All showed shortening during systole and lengthening in diastole. Right atrial pacing caused early relaxation in only two of the 43. Two hundred and fifteen segments were calculated for 18 patients with coronary artery disease. All but eight segments showed normal relaxation on control angiography. Following pacing, 115 segments showed early relaxation, and in 107 of the 115, normal relaxation were restored after nitroglycerin. Among the 107 segments, 44 were ischemic and 63 were normal. For 34 segments with early relaxation by pacing, pacing was repeated after administering nitroglycerin, and 15 did not reproduce early relaxation. The present study showed that early relaxation was observed in patients with coronary artery disease, which was effectively ameliorated by nitroglycerin, suggesting this phenomenon is closely related to the development of myocardial ischemia. The decreased active tension, reduced duration of tension, development and delay in electrical depolarization in the ischemic segment can be a reasonable inducement to early relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cineangiography↗
PubMed1984

[Intrathoracic movement of the normal and hypertrophied hearts measured by biplane coronary cineangiography].

The shift of the heart during systole within the thorax was measured using bifurcations of the left coronary artery as cineangiographic markers. Biplane coronary cineangiography was performed in 13 normal subjects and 6 patients with non-obstructive hypertrophic cardiomyopathy (HCM). The spatial coordinates (X, Y, Z) of the bifurcations on the cineangiograms were measured using a motion analizer-digitizer-computer system. The systolic excursion of the motion of a bifurcation located at the anterior-basal point of the heart was 1.4 +/- 0.1 (+/-SD) cm leftward, 3.0 +/- 0.3 cm caudally and 2.5 +/- 0.1 cm anteriorly in normal subjects. In the cases with HCM, on the other hand, the bifurcation moved 2.2 +/- 1.1, 2.7 +/- 1.2 and 2.2 +/- 0.6 cm during systole, respectively. The movement at the apex in the normal subjects was 1.7 +/- 0.2 cm rightward, 1.5 +/- 0.2 cm caudally and 1.5 +/- 0.2 cm posteriorly, although the direction was reversed as compared to that of the anterior wall of the cardiac base. The amplitude of the excursion was also reduced at the apex, suggesting the systolic twist of the ventricular wall. The excursion of the apex in HCM was 0.6 +/- 1.7, 1.5 +/- 1.8 and 2.5 +/- 1.4 cm, respectively, toward the base of the heart as in the normal subjects. The maximum speeds of these motions were 34.0 +/- 9.2 cm/sec leftward, caudally and anteriory at the anterior-basal point and 36.2 +/- 7.3 cm/sec rightward, caudally and posteriorly in the normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1983

Regional differences in shortening and relaxation characteristics of the left ventricular wall of normal subjects as studied by biplane coronary cineangiograms.

The coordinates of the ramifying points of the left coronary artery were measured using biplane coronary cineangiograms in 19 patients who were later diagnosed as normal. The spatial distances (segment length) between any two of these points were calculated and one cardiac cycle was plotted frame by frame in order to investigate shortening and relaxation characteristics of the segments. In most instances, the segments evidenced shortenings during systole and prolongations during diastole. The extent of shortening, as a percentage of maximum length ranged from 7.8 to 18.0%. The segments measured at the apex started shortening 77 msec sooner than those at the base, in other words, 90.3 +/- 6.2 msec before the R wave peak on the electrocardiograms. This indicates that the initial shortening at the apex contributes to the build up of left ventricular pressure. While at the base, since it begins to shorten after the completion of the build up in left ventricular pressure, it contributes more to the ejection of blood from the left ventricle. On the other hand, there is little systolic shortening at the atrioventricular groove and in some instances there is systolic expansion, suggesting that in comparison to the other portions of the left ventricle it is assigned an entirely different role.

Cineangiography↗
PubMed1983

The failure of oxygen breathing to decrease the myocardial contractile force in denervated dogs.

This study was done to discover whether or not the oxygen-induced depression of sympathoadrenal activity contributes to a reduction of myocardial contractile force during oxygen breathing. In 10 open-chest dogs, myocardial contractile force was measured using a myocardial strain gauge arch during air and oxygen breathing before denervation (intact heart) and after bilateral vagotomies, sympathectomies and adrenalectomies with the intravenous administration of propranolol, phenoxybenzamine and atropin (denervated heart). One hundred percent oxygen breathing caused similar increases in arterial pO2 in both the intact (from 94 +/- 10 to 442 +/- 25 mmHg) and the denervated dogs (from 113 +/- 11 to 456 +/- 15 mmHg). Coronary blood flow measured at the left anterior descending coronary artery was reduced by oxygen breathing from 28.4 +/- 3.4 to 21.7 +/- 2.3 ml/min in the intact dogs, and from 19.4 +/- 3.4 to 14.9 +/- 2.6 ml/min in the denervated dogs. Myocardial contractile force was significantly reduced by oxygen breathing in the intact dogs (a reduction of 5.8 +/- 1.4%). In the denervated dogs, on the other hand, no significant changes in myocardial contractile force was seen. This study suggests that the reduction in myocardial contractile force is mediated through sympathoadrenal activity, and thus, is abolished by sympathoadrenal blockade.

Adrenalectomy↗
PubMed1983

Decrease of urinary taurine in essential hypertension.

In order to evaluate how taurine relates to the pathogenesis of essential hypertension, the taurine content of plasma, whole blood and urine was measured in 18 normals and in 79 hypertensive patients. The patients included 32 untreated cases of essential hypertension, 32 treated cases and 15 cases with labile hypertension. There were no statistically significant differences between normals and essential hypertensives in either plasma or whole blood taurine content. However, in comparison to urinary taurine excretion in normals, 1594.0 +/- 143.7 mumol/day (mean +/- SE), that for untreated essential hypertensives, 708.1 +/- 57.1 mumol/day (p less than 0.001), and for treated essential hypertensives, 953.6 +/- 94.3 mumol/day (p less than 0.001), were significantly lower. Those with labile hypertension showed almost the same value, 1478.3 +/- 134.3 mumol/day, as normals. Taurine clearance and the taurine/creatinine ratio were also markedly decreased in essential hypertensives without treatment. For all subjects, taurine clearance had a positive correlation (r = 0.327, p less than 0.01) with creatinine clearance, but there were significant negative correlations between systolic blood pressure and daily urinary taurine excretion (r = -0.472, p less than 0.01) and between diastolic blood pressure and daily urinary taurine excretion (r = -0.382, p less than 0.01). There were also significant positive correlations between daily urinary taurine excretion and serum high-density lipoprotein cholesterol (r = 0.559, p less than 0.01) and between the former and cardiac index (r = 0.547, p less than 0.01). These results suggest that a deficiency of taurine plays an important role not only in elevating blood pressure in essential hypertension but also in atherogenesis as well.

Adult↗
PubMed1983

[Characteristics of left ventricular regional wall relaxation at the infarction site].

In order to investigate relaxation characteristics of the infarcted wall, segment lengths of the left ventricular wall were calculated in 6 patients with anterior myocardial infarction and in 9 angiographically normal subjects. The biplane left coronary cineangiography was performed and coordinates of ramifying points of the left coronary artery on the infarcted or non-infarcted wall were measured and the spatial lengths (segment lengths) on each wall were calculated. If the two points are on the left anterior descending artery (LAD) in infarcted patients, a calculated length is regarded as a segment length in the infarcted portion, while if the length is calculated between the two points located on the coronary artery other than LAD, it is a non-infarcted segment. Each segment length was calculated in frame by frame covering one cardiac cycle. The maximum length (Lmax), minimum length (Lmin) and the length at the beginning of P wave of the electrocardiogram (LECG P) were calculated. The extent of relaxation of the segment caused by atrial kick was calculated as (Lmax--LECG P)/Lmax X 100, (% delta Lla). This value was 2.8 +/- 1.5 and 3.5 +/- 1.4% on anterior and inferior walls, respectively, in 9 normal subjects and 3.6 +/- 1.2 and 4.0 +/- 0.9% in 6 patients with anterior infarction, revealing no significant difference among 4 values. This indicates that the amount of lengthening of the segment by atrial kick remains unchanged even if the wall is infarcted. The extent of diastolic lengthening of the segment by rapid and slow fillings, which excludes atrial filling, was calculated as (LECG P--Lmin)/Lmax X 100, (% delta L1-la).(ABSTRACT TRUNCATED AT 250 WORDS)

Cineangiography↗
PubMed1982

Reduction of left ventricular epicardial segment length by 100% oxygen breathing in open-chest dogs.

We conducted this study in order to learn whether or nt oxygen inhalation reduces left ventricular size, one of the major determinants of myocardial oxygen demand. In 11 open-chest dogs, a Mercury-in-Silastic gauge was applied to measure left ventricular circumferential length while the dogs were being ventilated with either room air or 100% oxygen. Four characteristic notches were identified on the resulting length curve: L1, length at the beginning of ejection; L2, length at the end of ejection; L3, length in early diastole; and L4, length at end diastole, L1 was shortened from 24.9 +/- 10.5 to 24.4 +/- 9.9 mm (a decrease of 1.4 +/- 2.1%) by oxygen breathing, L2 was also shortened from 26.8 +/- 11.5 to 26.2 +/- 10.7 mm (a decrease of 1.5 +/- 2.9%), L3 from 17.5 +/- 4.4 to 17.4 +/- 4.3 mm (a decrease of 0.7 +/- 2.7%) and L4 from 17.7 +/- 4.8 to 17.5 +/- 4.7 mm (a decrease o 1.3 +/- 2.4%). These changes all disappeared when the inspiratory gas was changed from oxygen back to air. Heart rate and left ventricular end-diastolic pressure showed no significant changes but were accompanied by a slight reduction in aortic pressure and myocardial contractile force. This study demonstrated a small but consistent reduction in left ventricular circumferential length by oxygen breathing. This reduction in left ventricular size will reduce left ventricular tension and thus result in reduction of left ventricular myocardial oxygen demand when oxygen inhalation is applied to patients with ischemic heart disease.

Animals↗
PubMed1982

[Effect of nitroglycerin on epicardial and endocardial shortening characteristics in dogs].

In 8 dogs, several paired lead beads as radiopaque markers were implanted in the subepicardial and subendocardial regions, and biplane cineradiograms were obtained after closure of the chest. The spatial distance (segment length) between the two markers in the outer and inner sides of the myocardium was calculated using a digitizer-computer-plotter system, and the effect of nitroglycerin on regional left ventricular geometry was assessed. Segment length at the R wave of the electrocardiogram (LECG R) was reduced from 39.7 +/- 11.8 (mean +/- SD) to 38.8 +/- 12.1 mm at the subepicardium and from 31.9 +/- 9.5 to 29.5 +/- 10.4 mm at the subendocardium 3 minutes after intravenous injection of 0.5 mg of nitroglycerin. Segment length at endsystole (LES) was also reduced from 38.9 +/- 11.7 to 38.2 +/- 11.8 mm at the subepicardium and from 29.6 +/- 9.2 to 27.9 +/- 9.9 mm at the subendocardium by nitroglycerin. Systolic shortening [(LECG R--LES)/LECG R] x 100) showed a slight reduction after nitroglycerin. Left ventricular wall thickness measured as a distance between subepicardial and correspondent subendocardial markers showed a slight but significant increase by nitroglycerin: Maximal thickness was increased from 10.9 +/- 3.2 to 11.4 +/- 3.3 mm, and thickness at the R wave of the electrocardiogram was also increased from 10.9 +/- 3.1 to 10.5 +/- 3.2 mm. Thickening of the wall was markedly increased at the anterior mid portion of the left ventricle but not at the base, suggesting nitroglycerin has larger effect on the former position than the latter.

Animals↗
PubMed1982

[Left ventricular outer wall motion in hypertrophic cardiomyopathy assessed by biplane coronary cineangiograms].

Left ventricular wall motion in patients with hypertrophic cardiomyopathy may show a characteristic movement since this condition is characterized by a disproportionate thickening of the wall and disorientation of myocardial muscle fibers. Biplane coronary cineangiograms were performed in 5 patients with hypertrophic cardiomyopathy and the spatial distance between the bifurcation of the left coronary artery was calculated using a digitizer-computer-plotter system as a measure of epicardial chord segment length. Systolic shortening of the segment was calculated as (LECG R--LES)/ECG R x 100 (%), where LECG R and LES represent segment lengths at the R wave of the electrocardiogram and at the end of systole, respectively. The value amounted 6.9 +/- 5.1 (+/- SD)% on the average which was significantly lower than the previously described values (9.0 +/- 4.1%) in 19 normal subjects. In all of 3 segments at the apex, systolic shortening showed nearly zero or negative indicating systolic expansion. Reduced shortening in patients with hypertrophic cardiomyopathy observed at the epicardial segment in the present study might be a reflection of geometrical difference between endocardial and epicardial segments because shortening of the epicardium will be reduced even the endocardium shortens considerably if the thickness of the wall is markedly increased. Anterior surface of the interventricular septum might be unable to shorten freely along the long axis since it is a junction of trifurcation among right and left ventricular free walls and the interventricular septum if these three walls are thickened. The present study indicated that shortening characteristics in the outer myocardium in patients with hypertrophic cardiomyopathy is markedly impaired possibly due to geometrical difference between endocardial and epicardial segments caused by marked thickening of the wall and also due to the degeneration or disorientation of myocardial fibers.

Cardiomyopathy, Hypertrophic↗
PubMed1982

[Difference of the shortening characteristics between left ventricular endocardium and epicardium as measured by radiopaque markers in experimental dogs].

This study was performed to clarify the difference of shortening characteristics between left ventricular epicardium and endocardium. Four to five pairs of radiopaque markers (lead beads, phi 0.3- 0.8 mm) were implanted just beneath the epicardium and endocardium, respectively in eight open-chest dogs. After the pericardium and thorax were closed, biplane cine-roentgenograms were obtained. The spatial distance (segment length) between any two of the markers was calculated using a digitizer-computer-plotter system. Left ventricular wall thickness (Th) was measured as a distance between epicardial and endocardial markers. The maximum left ventricular thickness (Thmax) was 9.4 +/- 3.4 mm (mean +/- SD), the minimum (THmin) 8.4 +/- 3.1 mm, and a percent increase of wall thickness [(Thmax-Thmin)/Thmin] was 12.7 +/- 6.5%. The value of epicardial segment length divided by endocardial segment length as normalized by each length at R wave of ECG was 1.088 +/- 0.071 at the end of systole and 0.979 +/- 0.016 at end diastole, indicating that endocardial segment shortened and distended more than epicardial segment during systole and diastole, respectively. Epicardial segment began to shorten 3 +/- 26 msec earlier and distend 4 +/- 50 msec earlier than endocardial one. This study revealed a small but consistent difference in the amount of shortening and its initiation and termination between the epicardium and endocardium.

Angiocardiography↗
PubMed1981

Myocardial contractile force at high coronary arterial oxygen tension in dogs.

In 34 mongrel dogs, the left anterior descending coronary artery was perfused with the dog's own femoral arterial blood at a constant flow rate and the myocardial contractile force was measured using a myocardial strain gauge arch. When the femoral arterial blood was oxygenated (pO2 61.7 kPa (463 mmHg)) using an artificial lung, so that the perfused myocardium became hyperoxic, the myocardial contractile force was increased by 11.1 +/- 2.3%. When the perfusion rate was reduced by approximately 20%, there was a smaller increase in myocardial contractile force, 8.0 +/- 2.3%. If, in addition, oxygen inhalation was performed the myocardial contractile force decreased by 4.1 +/- 2.1%. In 10 mongrel dogs, the carotid arteries were perfused at a constant flow rate with femoral arterial blood from a donor dog. Oxygen inhalation by the donor dog caused a reduction in the myocardial contractile force of the experimental dog of 5.9 +/- 1.6%. It is suggested that oxygen has a direct effect in increasing myocardial contractile force. This increase is counteracted by oxygen-induced coronary vasoconstriction in some part and by a neurohumoral effect or suppression of chemoreceptor activity.

Animals↗