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Biomedical subjects

Y Nimura

Publications and source records attributed to Y Nimura.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Experimental studies on fistula formation after percutaneous trans-hepatic cholangiodrainage].

The process of intra- and extra-hepatic fistula formation after percutaneous transhepatic cholangiodrainage (PTCD) was investigated. Furthermore, effects of such 4 materials of catheter as vinyl chloride, silicon, polyethylene and poly-urethane on this formation process were compared in order to clarify factors influencing the process. Fistula formation began 2 weeks after PTCD, and nearly completed after 4 weeks. A drainage fistula most markedly formed in the use of vinyl chloride, as the fistula wall was thick and its collagen fibers were microscopically observed to be dense and regularly arranged. On the other hand, fistula walls were thin, and their connective tissues consisted of immature cells and sporadically observed, when the other materials were used. However, degeneration of the liver cells around the intrahepatic fistula was most markedly seen in the use of vinyl chloride. In addition, the fistula formation tended to be more facilitated at early stage when the extrahepatic bile duct was occluded. These results suggested that vinyl chloride is the most suitable material if the drainage is applied for the fistula formation.

Animals↗
PubMed1988

[Anterolateral papillary muscle motion before and after septal myotomy in hypertrophic obstructive cardiomyopathy].

The left ventricular outflow pressure gradient in hypertrophic cardiomyopathy results from systolic anterior motion of the mitral valve (SAM). This abnormal orientation of the valve was previously proposed to be caused by inappropriately hypertrophied papillary muscles which protrude to the interventricular septum (IVS). Septal myotomy can alter the orientation of the papillary muscles and resolve the pressure gradient, without myectomy. Recently, we have experienced two instructive cases to prove our previously advocated hypothesis. Case 1: This 54-year-old man complained of effort dyspnea, and his echocardiogram disclosed marked SAM, and a thickened IVS (28 mm) and left ventricular posterior wall (16 mm). The intraventricular pressure gradient was 134 mmHg, and there was mitral regurgitation of grade 2/4. A longitudinal incision via the aorta on the anterior portion of the IVS, toward the base of the anterolateral papillary muscle, resolved the pressure gradient and mitral regurgitation, and two-dimensional echocardiography demonstrated that the SAM resolved at the lateral aspect of the valve, but it remained on the medial side. Case 2: This 57-year-old man complained of dyspnea during effort. He had marked SAM. The intraventricular pressure gradient was 65 mmHg, and there was grade 3/4 mitral regurgitation. Longitudinal incisions on the anterior, medial and posterior parts of the IVS abolished the SAM and reduced mitral regurgitation to grade 1/4. In both cases, during systole, the anterolateral papillary muscle protruded into the left ventricular ontflow tract, causing SAM. After surgery, the direction of the muscle axis moved toward the mitral orifice during systole, resulting in alleviation of SAM on the same side of the location of septotomy. This further confirmed our concept that disoriented papillary muscles play essential roles in causing SAM. If the Venturi forces previously stressed by other investigators cause SAM, the latter should resolve on both the medial and lateral aspects, even by septotomy. Thus, the Venturi theory seems untenable.

Cardiomyopathy, Hypertrophic↗
PubMed1988

[A case of primary intrahepatic cholesterol gallstones difficult to manage by percutaneous transhepatic cholangioscopy].

A case of a 60-year-old man with primary intrahepatic cholesterol gallstone was reported. Several stones, each size 3mm in diameter, were packed in the diverticulum-like dilated part of the posterior-inferior-ventral bile duct branch of the right lobe and 3 stones, each size 3-4mm in diameter, were scattered separately in the lateral segment of the left lobe of which the bile duct branches were diffusely tortuous and with mildly irregular dilatation. Morphologic appearance of the biliary system except in these 2 areas was normal. All stones including a large gallbladder stone consisted of cholesterol. Intraluminal approach, not only ERC but also PTCS, can hardly detect intrahepatic stones of more peripheral areas, although combination of US and enhanced CT may be useful even though bile duct branches are not dilated. We failed in PTCS lithotomy in this case for the first time in our experience with more than seventy cases of intrahepatic stones. However, by PTCS it was possible to investigate the morphology of the biliary system in detail and consequently, to make the diagnosis of primary intrahepatic stones. This patient has cured by cholecystectomy and minimum hepatectomy.

Bile Ducts, Intrahepatic↗
PubMed1988

[Studies on the radiographic anatomy of the biliary tree of the caudate lobe].

The cholangiograms obtained through percutaneous transhepatic cholangioscopy (PTCS) were studied for the purpose of clarifying radiographic anatomy of confluence of the bile ducts of the caudate lobe and the main trunks at the hepatic hilum. PTCS was performed on a total of 112 patients at our department, January, 1979 through December, 1984. Among them 60 cases without lesions in the hepatic hilum were used for this study. Four types of the bile duct of the caudate lobe were distinguished by cholangiography in the 60 cases: 1) A duct ran from the cranial portion of the right caudate lobe along the inferior vena cava to the hepatic hilum in 53 (Blr); 2) A duct ran from the cranial portion of the left caudate lobe to the hepatic hilum in 50 (Blls); 3) A duct ran from the left lateral part of the left caudate lobe to the hepatic hilum in 59 (Blli) and 4) A duct from the caudate process to the hepatic hilum in 42 (Blc). We found that cholangiogram following percutaneous transhepatic biliary drainage or selective cholangiogram using the PTCS make an accurate identification of the bile duct of the caudate lobe possible.

Adult↗
PubMed1987

Chronic pancreatitis at early age of onset presenting interesting findings through endoscopic retrograde pancreatography and chemical analysis of nonopaque pancreatic concretion.

This case concerns a 20-year-old male patient with an approximate 10-year history of recurrent and severe abdominal pain radiating to the back. Endoscopic retrograde cholangiopancreatography revealed a short obstructing stenosis of the main pancreatic duct in the head of the pancreas, marked and tortuous dilatation of the prestenotic portion of the main pancreatic duct and its side branches, and a filling defect in the side branch in the body of the gland. Pancreaticojejunostomy was performed to induce decompression of the pancreatic duct. Histology of the pancreas showed advanced chronic pancreatitis. Three nonopaque concretions were obtained at operation. The largest one, which was milky white in appearance and elastic and soft in consistency, proved to be made up of protein. The concretion was rich in acidic amino acids, but poor in basic or aromatic residues. The molar composition of amino acids in the concretion was, in decreasing order, aspartic acid, serine, valine, glycine, and glutamic acid. Powder x-ray diffractometry revealed no crystalline structures.

Adult↗
PubMed1987

Histopathological study of hypertrophic cardiomyopathy with progression to left ventricular dilatation.

The heart of seven cases of fatal congestive heart failure with dilated left ventricle, developing in 5 patients with symptomatic hypertrophic cardiomyopathy (HCM) and 2 patients with histologically widespread disarray of both ventricles, was morphologically investigated. These 7 cases showed myocardial widespread disarray and massive fibrosis, the mean percent area of fibrosis was 40.6% and 59.4% at upper and lower levels of left ventricles, respectively. Fibrosis was most extensive in the lateral wall, and followed by anterior, posterior and interventricular walls. The severity of cell infiltration in left ventricle was completely matched to that of fibrosis and was most extensive in subepicardial area followed by middle and subendocardial areas of left ventricle. The intima and medial thickness of intramural small arteries in the fibrotic areas was significantly larger (p less than 0.05) than that of nonfibrotic areas, which suggested that the effect of intramural small artery was not essential for pathogenesis of massive fibrosis.

Adolescent↗
PubMed1987

Uhl's anomaly as a result of progression to ventricular dilation from hypertrophic cardiomyopathy.

A 17-year-old female with clinically diagnosed Uhl's anomaly died of intractable congestive heart failure, liver cirrhosis, and protein losing gastroenteropathy. Cardiac catheterization, echocardiography and nuclear angiography proved to be valuable in making the diagnosis. At autopsy, there was widespread myocardial disarray and extensive fibrosis of both ventricles which led to, in particular, almost total absence of the myocardium of the right ventricle. The present case implicated that certain case of Uhl's anomaly might be related to widespread myocardial disarray and extensive fibrosis, which is known as idiopathic cardiomyopathy.

Adolescent↗
PubMed1987

Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography.

The aim of the present study was to elucidate the mechanisms of mitral regurgitation accompanying myocardial infarction. Severity and site of mitral regurgitation was evaluated by the real-time two-dimensional Doppler flow imaging technique in 81 patients with old myocardial infarction. The incidence of mitral regurgitation did not depend on the region of infarction. There was, however, a close relationship between the site of regurgitation and the region of infarction. In patients with mitral regurgitation spurting from the posteromedial area of the valve, the inferior wall was involved in infarction without exception and in some of these patients, the posteromedial papillary muscle was also found to be affected by myocardial infarction; in those with regurgitation spurting from the anterolateral area, the anterior wall showed asynergy. On the other hand in patients with mitral regurgitation spurting from the central area, the region of infarction varied. In these patients, however, the larger the diameter of the mitral anulus, the more severe the grade of regurgitation. The extent of asynergy was another factor related to the severity of mitral regurgitation. Both longitudinally and transversely, broad infarction leads to the enlargement of the mitral anulus. However, even if the mitral anulus is not so dilated, severe involvement of either commissural area results in severe mitral regurgitation from the same commissural side. Thus, there are two major causative factors of mitral regurgitation: (1) asynergy of the papillary muscle or the ventricle that results in mitral regurgitation located in the commissural area of the same side as asynergy, and (2) enlargement of mitral anulus, which results in regurgitation from the central area of the orifice.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Characterization of histamine H1-receptor on rat hepatocytes.

The binding sites for [3H]pyrilamine in isolated rat hepatocytes were characterized. Scatchard analysis revealed two kinds of binding sites in hepatocytes, a high-affinity site and a low-affinity one. The rates of binding of the radioligand with the high-affinity binding site and its dissociation were rapid. The specificity of the sites for various histamine antagonists indicated that the high-affinity [3H]pyrilamine binding site is representative of the histamine H1 receptor. Treatment of hepatocytes with protease or phospholipase A2 significantly decreased the maximum binding capacity of the high-affinity site without affecting its dissociation constant, suggesting that the binding site is proteinaceous and is sensitive to a change in the lipid moiety of the membrane. Hepatocytic cyclic AMP and cyclic GMP were not significantly modulated by incubating hepatocytes with histamine. Thus, the action of histamine on hepatocytes might not be mediated by the cyclic nucleotides.

Animals↗
PubMed1987

[Non-invasive assessment of the peak pressure gradient between the aorta and pulmonary artery in patent ductus arteriosus].

The validity of continuous wave Doppler ultrasound estimation of the peak pressure gradient between the aorta (Ao) and pulmonary artery (PA) in patients with patent ductus arteriosus (PDA) was evaluated. Ten patients, all without other anomalies, underwent cardiac catheterization and cine-angiography, and the peak pressure gradient between the Ao and PA (dP(C)) was measured during catheterization. In all cases the mean PA pressure was less than 35 mmHg. According to the angiographic findings, the patients were categorized as Group A, consisting of seven patients whose features of the ductus were wedge- or tube-like in configuration; Group B, consisting of two patients whose features were termed "orifice-like" stenosis including one with abrupt narrowing on the PA side of the ductus and the other with a short segmental ductus. Group C consisted of one patient who had a long curved segmental ductus. The maximum velocity of ductus flow was measured by continuous wave Doppler ultrasonography, and the estimated peak pressure gradient between the Ao and PA by Doppler (dP(D] was calculated using the simplified Bernoulli equation (dP = 4V2). In group A, dP(D) was overestimated compared to dP(C) in all patients by 19 to 51 mmHg (mean 34 mmHg). However, in group B, the difference between dP(D) and dP(C) was small, 5 mmHg and 7 mmHg, respectively. In group C, dP(D) was underestimated as opposed to dP(C). Thus, in the limited cases, the simplified Bernoulli equation could be used in estimating the peak pressure gradient between the Ao and PA. However, this equation leads to overestimation in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗
PubMed1987

[The physiological role of the pericardium: studies based on right heart inflow dynamics in cases of left-sided pericardial defect].

Using pulsed Doppler echocardiography, the effects of postural change on the blood flow pattern in the superior vena cava and in the right ventricular inflow tract were investigated to evaluate the physiological role of the pericardium. Eight cases of left-sided pericardial defect and eight healthy subjects were examined. 1. Suppressed inflow into the right atrium during systole in left-sided pericardial defect was manifested as a reduction of the systolic wave (S) in the superior caval vein and impairment of the systolic shift of the tricuspid annulus. This suppression suggested unsatisfactory volume expansion in the right atrium due to the absence of negative intrapericardial pressure. 2. In left-sided pericardial defect, the right ventricular inflow pattern differed from the normal, most distinctly in the right lateral recumbent position, though the cardiac motion was nearly identical with that of the normal in this position. In this position, the ratio of the peak velocity of presystolic filling to that of rapid filling was increased, and the deceleration half time of rapid filling was prolonged. These findings indicated that the right ventricular rapid filling was retarded, and was compensated by the filling due to atrial contraction. It is assumed that right ventricular filling is influenced by hydrostatic pressure due to changes in posture in the absence of restriction by the pericardium. 3. It is concluded that the pericardium maintains negative intrapericardial pressure, so that each cardiac chamber is uniformly expanded for its filling, and that this function minimizes the influence of posture on cardiac hemodynamics.

Adult↗
PubMed1987

[Noninvasive measurement of cardiac output using two-dimensional Doppler echocardiography and analysis of sources of error].

The purpose of this study was (1) to analyze the factors responsible for errors in the two-dimensional Doppler echographic measurements of cardiac output (C.O.) and (2) to establish a noninvasive method for measuring C.O. The subjects were 50 cardiac patients who had neither aortic valve disease nor intracardiac shunts. The C.O. was calculated using the following formula: C.O. (l/min) = mean flow velocity (cm/sec) x pi(aortic ring diameter/2)2 (cm2) x 60/10(3) Left ventricular ejection flow velocity was recorded in the center of the aortic ring from the apical approach. Mean velocity was calculated by integration of instantaneous mean velocity in the ejection phase divided by the cardiac cycle length, and was corrected by the Doppler incident angle. The inner diameter of the aortic ring was measured in the parasternal long-axis view at the time of the maximum ejection flow velocity. The following results were obtained: 1. Sources of error in the measurement of cardiac output. 1) Accuracy of instantaneous mean velocity calculating circuit: This calculating circuit was accurate in model experiments using pulsatile flow. 2) Effect of high-pass filter: In model circuits, application of high-pass filter overestimated flow velocity. The higher the cut-off frequency of the high-pass filter, the larger the overestimation. This was probably due to the parabolic flow velocity profile in the circuit. 3) Flow velocity profile in the aortic ring: The flow velocity profile seemed to be flat in the aortic ring except near the anterior aortic wall. Therefore, the effect of the high-pass filter was considered to be negligible in case of clinical application. 4) The effects of shift and size of sample volume: The location of sample volume relative to the aortic valve ring shifted about 7 mm during systole. However, the shift and size of sample volume seemed to have little effect on the measured C.O., because the flow velocity profile was nearly flat in the aortic ring. 5) Ultrasound beam incident angle: From a practical viewpoint, it was necessary to set an incident angle of less than 50 degrees for minimizing the error. We were able to set the angle within 50 degrees in all but one of patients. 6) Diameter of the aortic ring: Two-dimensional echographic measurement of the aortic ring diameter was not so accurate; it seemed to become a major source of error in the calculation of C.O.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

[Optimum time for surgical intervention in pure mitral regurgitation: serial echocardiographic evaluations].

To determine the optimum time for surgical intervention in pure mitral regurgitation, 39 patients were studied by echocardiography before and after surgery. Pure mitral regurgitation included mitral valve prolapse with or without ruptured chordae tendineae. Twenty-two patients had mitral valve replacement and 17 had mitral valve reconstruction. Serial echocardiograms were obtained from all 39 patients (average follow-up: 40 months). Two of the 39 patients died suddenly at home on 26 and 62 months after surgery. One of the 39 patients now suffers from congestive heart failure. These three patients had preoperative left ventricular end-diastolic dimensions greater than 70 mm and left ventricular end-systolic dimension greater than 50 mm. Operation is recommended for patients with end-diastolic dimension less than 70 mm and end-systolic dimension less than 50 mm.

Echocardiography↗
PubMed1987

[Relationship of two-dimensional echocardiographic mitral valve prolapse to mitral regurgitation assessed by color Doppler flow imaging].

Although two-dimensional echocardiography is a standard for diagnosing mitral valve prolapse, the diagnostic criteria are controversial. Regardless of valve ballooning we have used our criteria which are based on the dislocation of the mitral valve coaptation. The purpose of this study was to clarify the relationship between the location and the degree of mitral valve prolapse assessed by two-dimensional echocardiography and those of mitral regurgitation evaluated by color Doppler flow imaging, which enables us detailed analysis of regurgitation. Twenty-three patients with idiopathic mitral valve prolapse diagnosed by our criteria were studied. They were 14 men and nine women, ranging in age from 19 to 72 years (mean 44.7). In any patients, prolapse of either the anterior or posterior leaflet does not satisfy the Gilbert's criteria. Twenty of the 23 patients had mitral regurgitation by color Doppler flow imaging, and the grade was II, III or IV in 16 of these 20 patients. In 19 of 20 patients, the localization of the regurgitant jet flow from the mitral orifice coincided with the two-dimensional echocardiographic site of dislocation of mitral valve coaptation. Therefore, it was concluded that the dislocation of mitral leaflet coaptation detected by two-dimensional echocardiography is an abnormal finding regardless of the protrusion of the valve beyond the mitral ring.

Adult↗
PubMed1987

[Papillary muscle infarction: echocardiographic features and genetic factors].

To study the pathogenesis of papillary muscle infarction, its echocardiographic features were examined in 60 patients with old inferior infarction. Sixty-three healthy elderly persons served as the controls. 1. The papillary muscles were echocardiographically classified as fingerlike and non-fingerlike in configuration whose frequencies were 43% and 57%, respectively. In healthy subjects, the papillary muscles were less echogenic than the left ventricular wall. 2. In five patients, the posteromedial papillary muscle exhibited enhanced echo intensity and no contraction. The papillary muscles in two of these five patients were histologically examined and the diagnosis of papillary muscle infarction was verified. In these five patients, the papillary muscles were echocardiographically classified as fingerlike, and left ventricular infarction was observed to involve the attachment of the posteromedial papillary muscle. All five patients had mitral valve prolapse; posterior in four and anterior in one. Inferior infarction extended to the region just beneath the mitral annulus in the former four patients, but not in the latter one. 3. The echocardiographic features of papillary muscle infarction consisted of enhanced echo intensity of the papillary muscle and mitral valve prolapse, especially that of the posterior leaflet at the posteromedial commissural side, and extension of the asynergy region to the attachment portion of the papillary muscle. The fingerlike morphology of the papillary muscle and involvement of the attachment within the infarcted region are predispositions to the development of papillary muscle infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Effect of brain death on hemodynamics and cardiac function: an experimental study].

An experimental model was designed to study hemodynamic and left ventricular functional changes in the course of and after brain death in 13 mongrel dogs. Brain death was induced by creating intracranial hypertension by inflating a balloon inserted into the subdural space. Hemodynamic parameters and left ventricular systolic function as assessed by echocardiography were measured before and during intracranial hypertension and 30 min and 1, 2, 3, 5 and 8 hrs after brain death. During intracranial hypertension, heart rate, systemic and pulmonary blood pressures, cardiac output and systemic vascular resistance raised significantly. After brain death, all parameters decreased rapidly and significantly, and then stabilized. On comparison with values obtained before intracranial hypertension, systemic blood pressure decreased markedly following brain death, while no marked change was noted in cardiac output. This result is attributable to a marked reduction in peripheral vascular resistance following the induction of intracranial hypertension. The left ventricular end-diastolic and end-systolic diameters did not change; consequently, fractional shortening did not change, either. The Weissler's index improved after brain death, reflecting a marked reduction in systemic vascular resistance. This indicates limited usefulness of afterload-dependent cardiac indices. At the agonal period of brain death, three of 13 dogs died because of ventricular fibrillation or a marked decline in systemic blood pressure. Within five to eight hours after brain death, seven dogs died because of intractable acidosis. These results represent the specific hemodynamic features occurring after brain death. It is thought that recognition of these features is useful in managing cases of brain death and in selecting donors for heart transplants.

Animals↗
PubMed1987

Predominance of prostaglandin D2 and I2 in the rat gastric mucosa--analysis by high-performance liquid chromatography.

We have developed a method for measuring prostaglandins (PGs) in rat gastric mucosa by high-performance liquid chromatography (HPLC). The levels of PGD2 and 6-keto-PGF1 alpha, a degradation product of PGI2, were five times higher than those of PGE2 and PGF2 alpha. Oral administration of indomethacin (6 mg/kg body weight) completely abolished the synthesis of all detectable PGs uniformly. These results suggest that endogenous PGs, especially PGD2 and I2, play some roles in the function of the gastric mucosa.

6-Ketoprostaglandin F1 alpha↗