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Biomedical subjects

D Saito

Publications and source records attributed to D Saito.

At least 145 records · Page 8Linked to original sources

Simple technique for measuring regional contractility by a modified strain guage arch.

A simple modification of a commercially available gauge arch, namely the addition of pins to effect mechanical couplings to heart muscle rather than suturing, results in an isometric myocardial force sensor which is easy to insert, stable and relatively atraumatic to the myocardium. Compressing the pins by means of a machinist's vernier caliper which is removed after the sensor is implanted, insures controlled muscle stretch. Tests in open-chest dogs show that force sensed by this gauge is little affected by changes in heart rate, left ventricular end-diastolic pressure or aortic pressure, but faithfully reflects the inotropic effects of isoproterenol or propranolol. Thus, the modified strain gauge arch is sensitive to changes in contractility but not to changes in preload or afterload.

Animals↗

[A case of two-chambered left ventricle with echoes of an abnormal floating mass].

A case of a two-chambered left ventricle with an abnormal floating mass was reported. A 13-year-old boy was admitted to our hospital because of a grade III/VI transsystolic apical murmur. Chest radiography showed mild cardiomegaly. The electrocardiogram showed QS patterns in leads V1-V3, and left ventricular high voltage with wide QRS complexes. A two-dimensional echocardiogram revealed two chambers divided by the septum in the left ventricle, and a mass floating in the apical chamber. A levogram showed the double chambered left ventricle incompatible with the findings of echocardiography. The walls of the accessory chamber and the septum were hypokinetic, but not dyskinetic. Coronary arteriograms were unremarkable. At surgery, tangled trabeculae carneae and chordae tendineae were observed on the apical surface of the septum. The accessory chamber communicated freely with the main chamber through an orifice with a diameter of 1.5 cm. No other congenital malformations were found. Microscopic examination of the accessory chamber wall showed the thickened endocardium and hypertrophic myocardial fibers, and there was no area of fibrosis.

Adolescent↗

Diagnosis of early gastric cancer seen as less malignant endoscopically.

In order to make the endoscopic diagnosis of early gastric cancer more accurate, we determined the endoscopic and clinicopathological characteristics of the 129 cases of early gastric cancer with less malignant appearance among the 978 cases of the disease with a solitary lesion detected at the National Cancer Center Hospital during the period between 1962 and 1981. According to findings required to make a differential diagnosis, the endoscopic appearance of the 978 cases were divided into the following four groups: 170 cases of polypoid, 587 of ulcerative, 119 of gastritis-like and 102 of advanced cancer-like. Among the four groups, the frequency of cases with less malignant appearance was quite high in the gastritis-like group. The lesion in this group was defined as the cancerous lesion which shows only superficial mucosal abnormality, not associated with any polypoid or ulcerative components. Chronologically, it has been rapidly increasing in recent years. These two paradoxical phenomena in the gastritis-like group, that is, "high frequency of less malignant appearance" and "increase in number of cases" not only indicate the inadequacy of the conventional criteria for the recent cases but also show that the gastritis-like malignancy is detectable. New additional endoscopic criteria for the gastritis-like malignancy, for example, irregular margin of the shallow mucosal depression, disproportion of the mucosal granularity, irregularity on the erythematous change and discoloration are essential in order to detect much more cases with less malignant appearance.

Aged↗

Changes in stenosis resistance and myocardial blood flow after a brief coronary occlusion in the dog.

Stress-induced changes in the resistance due to coronary arterial stenosis of a fixed diameter and in the myocardial blood flow distal to the stenosis were investigated in the open-chest dog. Myocardial blood flow in the inner and outer third of the left ventricular wall was continuously measured with heated cross-thermocouples. The circumflex coronary artery was constricted with a thick string so that myocardial reactive hyperemia was nearly eliminated. Without constriction, a 15-second occlusion of the artery produced no significant changes in the resistance of large coronary arteries. On the contrary, in the presence of coronary constriction, a brief coronary occlusion caused a sustained decrease in distal coronary pressure and subendocardial myocardial flow during reactive hyperemia, while coronary flow returned quickly to the pre-occlusion level with significant reactive hyperemia of subepicardial flow. This change resulted in a long-lasting increase in the stenosis resistance. These results suggest that stenosis resistance changes dynamically, resulting in additional myocardial ischemia especially in the subendocardial myocardial layers.

Animals↗

Increase in the resistance of stenotic coronary segment by intravenous infusion of isoproterenol.

The effects of intravenous infusion of isoproterenol on stenosis resistance were studied in the anesthetized open-chest dog. The circumflex coronary artery (LCx) was isolated near its origin and an electromagnetic flow transducer was placed around the vessel for measuring coronary flow. A polyethylene catheter was inserted into the small branch of LCx for monitoring distal coronary pressure. LCx was constricted with a thick cotton string to a degree of obstruction that eliminated reactive hyperemia following a 20-second coronary occlusion. The coronary resistance across the stenotic segment (RL) was calculated as the pressure gradient across the stenosis divided by coronary flow. Isoproterenol was infused intravenously in a dose to keep the heart rate at a level 25-30% above the control with and without coronary constriction. For maintaining the ascending aortic pressure at the pre-isoproterenol level, the descending thoracic aorta was constricted with a tape. In the absence of coronary constriction, the vascular resistance of large coronary arteries was not affected by isoproterenol with a significant increase in coronary flow. In the presence of coronary stenosis, isoproterenol markedly increased RI regardless of additional aortic constriction. The magnitude of the increase in RL during aortic constriction varied directly with the percent increase in the pressure gradient across the coronary stenosis. Pacing-tachycardia essentially did not affect RL. These results suggest that isoproterenol increased the vascular resistance of the stenotic segment with fixed caliber.

Animals↗

Decrease in myocardial oxygen extraction with aortic constriction in the dog.

In the open-chest dog constriction of the descending thoracic aorta, which raises central aortic pressure by 30-80 mmHg, increases cardiac oxygen usage (MVO2) and coronary blood flow (CBF) but reduces heart rate and myocardial oxygen extraction [(A-V)O2]. Pacing tachycardia superimposed on aortic constriction further increases MVO2 and CBF but does not alter (A-V)O2. Atropine or vagotomy abolishes the effect of aortic constriction on (A-V)O2, whereas vagal stimulation in the presence of alpha- and beta-adrenergic blockade reduces (A-V)O2. L-propranolol and phenoxybenzamine fail to modify the effect of aortic constriction on (A-V)O2. These results indicate that aortic constriction reduces (A-V)O2 by eliciting parasympathetically-mediated coronary vasodilation.

Animals↗

Right and left ventricular oxygen metabolism in open-chest dogs.

A comparison of blood flow and myocardial O2 consumption (MVO2) in the right and left ventricles was made in 21 open-chest dogs. Simultaneous measurements were made of left anterior descending (LAD) and right coronary arterial blood flow and of O2 saturation in the coronary sinus and in from one to four anterior cardiac veins. Blood flow was greater in the LAD than in the right coronary artery, 87 +/- 5 vs. 46 +/- 3 ml.min-1.100 g-1. Similarly, the O2 saturation was 51 +/- 3% in the anterior cardiac veins and 40 +/- 1% in the coronary sinus. In a subset of seven dogs, the O2 saturation in blood from anterior cardiac veins varied substantially from vein to vein. The mean MVO2 was greater for the left than for the right ventricle, 8.6 +/- 1.4 vs. 4.0 +/- 0.3 ml O2.min-1,100 g-1. Increases in LAD flow with no increase in O2 extraction accounted for enhanced MVO2 of the left ventricle due to pacing, isoproterenol, or methoxamine. In contrast, pacing, isoproterenol, or constriction of the pulmonary artery increased MVO2 of the right ventricle by both augmented O2 extraction and a rise in right coronary blood flow. We conclude that right coronary arterial blood flow is lower per 100 g tissue and is less dependent on MVO2 than is LAD blood flow. The heterogeneity of O2 saturation in anterior cardiac veins suggests that regional differences in MVO2 may exist.

Animals↗

Cough syncope due to atrio-ventricular conduction block.

A case of cough syncope due to A-V conduction block of the heart is reported in this paper. A-V conduction block and lightheadedness were induced by coughing but not by an Aschner test, carotid sinus massage, Valsalva maneuver, pharyngeal stimulation, and stimulation of systemic baroreceptors. Permanent right-ventricular pacing completely abolished the patient's symptoms. The results suggest that hypersensitivity of a broncho-pulmonary reflex to coughing was responsible for the A-V conduction block and resulting syncopes.

Aged↗

Increase in stenotic resistance following a brief coronary occlusion in the anesthetized open-chest dog.

Changes in the stenotic resistance of a coronary artery following brief coronary occlusion were studied in the anesthetized open-chest dog. A critical coronary stenosis was constructed by tying a thick string around the circumflex coronary artery (LCx) near its origin. The LCx was occluded for 5, 10, 15, 20 and 30 seconds with and without coronary stenosis then the reactive hyperemia was observed. In the absence of the stenosis, resistance of the segment of the large coronary artery remained unchanged during the reactive hyperemia independent of the duration of occlusion. In the presence of the stenosis, however, stenotic resistance increased for a certain time after the release of occlusion. This increased resistance lasted longer with more severe stenosis and with longer duration of coronary occlusion. These results suggest that stenotic resistance can increase dynamically, and that the duration of increased resistance may reflect the severity of the stenosis.

Anesthesia↗

Enhancement of myocardial reactive hyperemia and adenosine-induced coronary vasodilation by dilazep, a new adenosine potentiator.

The effect of N,N'-bis[3'-(3",4",5"-trimethoxybenzoyloxy)-propyl]hexahydro-1, 4-diazepine (dilazep) on myocardial reactive hyperemia and coronary vasodilatory potency of adenosine was studied in the anesthetized open-chest dog. Dilazep injected i.v. was detected in the pericardial effusate, suggesting that the drug could enter the interstitial space of the heart. A threshold dose of dilazep increased vasodilatory action of exogenous adenosine. The dose of dilazep enhanced compensation for flow debt during myocardial reactive hyperemia caused by 5-, 10-, 15-, 20- and 30-s coronary occlusions, respectively, whereas peak flow rate was increased in response to only 5- and 10-s occlusions by dilazep, respectively. The results obtained suggest that dilazep potentiates the effect of endogenous adenosine which is released during ischemia and also suggest that adenosine plays important role in myocardial reactive hyperemia.

Adenosine↗

[Clinical study of phase analysis by RI multigated method].

Phase analysis using RI multigated method was performed in 32 patients with various conditions including right and left bundle branch blocks (RBBB and LBBB), myocardial infarction, WPW syndrome, QT prolongation syndrome, atrioventricular (A-V) dissociation, valvular heart disease, and others. Pixel numbers were plotted into the histogram regarding the one cardiac cycle as 360 degrees. Standard deviation (S.D.) of a phase was calculated from the histogram in order to quantify asynchrony of the ventricles. Results were as follows: 1. Phase analysis was useful as a parameter of asynchrony. 2. There was a close negative correlation between left ventricular ejection fraction (LVEF) and S.D. of a phase. (r = -0.86, n = 32, p less than 0.001) 3. A marked time lag was observed in the infarcted area, and its value was mild in RBBB and LBBB. 4. A time lag between right and left ventricles was diminished or slightly reversed in the cases of RBBB with left anterior hemiblock compared to the cases of lone RBBB. 5. No significant changes were observed in other heart diseases with phase analysis.

Arrhythmias, Cardiac↗

Intracoronary adenosine deaminase reduces canine myocardial reactive hyperemia.

We employed intracoronary infusions of calf intestine adenosine deaminase (ADA) to test the hypothesis that adenosine regulates coronary blood flow during myocardial reactive hyperemia (RH). Infusions of 4.5 U ADA/min per kg body weight into the left circumflex coronary artery of 10 open-chest dogs reversibly reduced repayment of flow debt by 30-39% (P less than 0.05) following 5-, 10-, 15-, 20-, and 30-second coronary occlusions, the percentage reduction being independent of occlusion length. ADA reduced peak RH flow rate (17%, P less than 0.05) only after 5-second occlusions. Intracoronary infusions of [131]ADA in seven dogs produced interstitial ADA concentrations between 1.2 and 13.1 U/ml in perfused myocardium and, in five of these dogs, 131I activity in the cardiac node was 1.8-35 times that of contiguous mediastinal tissue. Theophylline, a specific adenosine antagonist, reduced repayment of flow debt by 27-36% (P less than 0.02) in eight dogs, an effect similar to that of ADA. In six other dogs, ADA plus theophylline did not reduce RH flow debt repayment below that produced by ADA alone. This experiment confirms the contribution of adenosine to myocardial RH but shows that this nucleoside accounts for but a third of volume flow. Other, as yet unidentified, factors are collectively more important.

Adenosine Deaminase↗

Comparative effects of heart rate and aortic blood pressure on MVO in the anesthetized open-chest dog.

Comparative effects of heart rate and aortic blood pressure on myocardial oxygen consumption (MVO2) were studied in anesthetized open-chest dogs. The left coronary artery was perfused through the external shunt with blood from the left common carotid artery. Heart rate was changed with the left atrial pacing and the constriction of the descending thoracic aorta was utilized to elevate the proximal aortic blood pressure (BP). The left ventricular enddiastolic pressure was insignificantly changed with the atrial pacing and with the aortic constriction. With the constant BP (100 +/- 5 mmHg), and unit increase in heart rate per minute augmented MVO2 by 0.027 ml/min/100 Gm of left ventricular muscle, while one mmHg elevation of BP caused 0.15 ml increment in MVO2 per minute per 100 Gm of left ventricular muscle under the constant heart rate (115 +/- 5 beats/min). Therefore an unit change in BP caused five- to six-fold greater increase in MVO2 compared with that in heart rate, indicating extremely important roles of BP in MVO2.

Animals↗

[Echocardiographic and non-gated computed tomographic findings of intrapericardial tumor and mediastinal tumor adjacent to the heart (author's transl)].

UNLABELLED: Echocardiographic and computed tomographic findings of a case of intrapericardial tumor are reported, and two other cases of mediastinal tumor are presented in a discussion of the differential diagnosis of intrapericardial from mediastinal tumors. CASE REPORT: A 7-year-old male complained of cough and dyspnea. Cardiomegaly had been pointed out at a mass X-ray examination about a month prior to the admission. Two-dimensional echocardiography revealed a massive anterior pericardial effusion and a fist-sized tumor with cystic structure. The tumor pushed the heart backward at the level of the aortic root. Non-gated computed tomography of the chest disclosed the size and location of the tumor, but failed to clarify the internal structure. The patient underwent successful removal of a tumor, 12 x 10 x 8 cm in size and 350 g in weight, originating from the left atrial wall. Histologically, the tumor was a fibrosarcomatous mesothelioma. Usually, an intrapericardial tumor is easily suspected by echocardiography by the presence of pericardial effusion, although there have been a few reports of intrapericardial tumors without pericardial effusion. Echocardiographic diagnosis of the intrapericardial tumor is difficult in such cases. Identification of the pericardium is necessary to diagnose whether a tumor is intra- or extrapericardial. This identification, however, is not always easy by echocardiography when the ultrasonic beams become tangent to the pericardium. The pericardium between the tumor and the heart could not be identified by echocardiography in our two cases of mediastinal tumor. Computed tomography is helpful in diagnosing the size and location of a mediastinal tumor.

Adult↗