[A case of acute myocardial infarction without significant stenosis which was operated because of cardiac tamponade].
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Biomedical subjects
Publications and source records attributed to K Yanagihara.
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Both murine and human cell lines transformed by the v-Ki-ras gene have been shown to be much more sensitive to the toxic effects of the cardiac glycoside ouabain than their respective controls. This differential toxicity has previously been used in the isolation of flat revertant clones from populations of Kirsten murine sarcoma virus transformed NIH/3T3 cells. Here, we have undertaken a further characterization of this phenomenon in murine and human tumor cells. Two different techniques, a 51Cr-release assay and a quantitative Crystal violet elution assay, have been employed to compare the sensitivities to ouabain of normal and v-Ki-ras-transformed NIH/3T3 cells. In each assay, ras-transformed NIH/3T3 cell lines displayed an increased sensitivity to ouabain as compared to the parental NIH/3T3 cell line, both in dose-response and in time-course experiments. In a separate study, ouabain was also able to inhibit the growth in semi-solid medium of 2 v-Ki-ras-transformed NIH/3T3 cell lines (DT and K-NIH) in a dose-dependent fashion. The same concentrations of ouabain were effective in both the 51Cr-release and Crystal violet assays. To address the question of whether increased sensitivity to ouabain is a specific result of transformation with the ras oncogene or is a common event which accompanies transformation by other oncogenes, we have screened a variety of transformed NIH/3T3 derivatives. All of these lines displayed an increased sensitivity to ouabain when compared to the parental NIH/3T3 cell line.
Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.
Spontaneous echocardiographic contrast is caused by increased ultrasonic density in the cardiac chambers or great vessels, or both, with the characteristic flow pattern of blood, but in the absence of any intravascular injections. This study demonstrated the clinical features and characteristics of the echocardiographic findings of eight patients with spontaneous contrast echoes. Spontaneous contrast echoes were observed in the right heart in five patients, and in the left heart in two. In one patient spontaneous contrast echoes were observed in the right and left heart. All six patients with spontaneous contrast echoes in the right heart had impaired liver function. In these patients, we observed that spontaneous contrast reaching the heart via the hepatic vein on two-dimensional echocardiography. In one patient with atrial septal defect, these contrast echoes were also recognized in the superior mesenteric vein and portal vein. Since capillary beds normally remove ultrasound contrast, the failure of this function suggests porta-systemic shunting in or around the liver. All three patients with spontaneous contrast echoes in the left heart had prosthetic valve dysfunction including paravalvular or transvalvular regurgitation, and consequent hemolysis. Under these conditions, water-vapor bubbles may be formed because of an exhaust pressure decrease due to the Bernoulli effect, or gases may be released from erythrocytes during hemolysis. These water-vapor bubbles or gases could be the cause of spontaneous contrast echoes in the left heart. In conclusion, spontaneous contrast echoes in the right heart are produced by gas absorbed from the intestine because of porta-systemic shunting. The cause of spontaneous left-sided heart echo contrast may be related to prosthetic valve regurgitation, and consequently to hemolysis.
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To assess the incidence of valvular regurgitation, 180 patients more than 40 years of age without cardiac symptoms were studied by pulsed Doppler echocardiography. The 180 patients were categorized by age as group 1, 40 to 49 years; group 2, 50 to 59 years; group 3, 60 to 69 years; group 4, 70 to 79 years; and group 5, more than 80 years of age. The incidence of valvular regurgitant flow signals increased significantly with age. Multivalvular regurgitation were often detected in groups 4 and 5. Furthermore, acoustically silent regurgitation at each valve was frequently noted (71 of 85 cases with valvular regurgitant flow signal: 84%). Mitral valve prolapse was diagnosed by two-dimensional echocardiography in 27 patients, but a mid-systolic click or pansystolic murmur with late-systolic accentuation was not noted. In conclusion, valvular regurgitations were common in the aged who lacked auscultatory findings.
Highly lymphomagenic mouse type-C viruses were generated from radiation- or chemically-induced T-cell lymphoma cell lines of NFS/N mouse origin infected with a non-oncogenic ecotropic virus E4. By analysis of these progeny viruses, the following results were obtained. 1) The viruses were lymphomagenic in neonatally inoculated NFS/N and C3H/He mice and W/Fu rats but not in Balb/c and C57BL/6N mice, indicating that they possess the Fv-1n tropism of exogenously infected parent virus. 2) Lymphomagenic viruses consisted of plural viral subpopulations. Recombinant mink cell focus-inducing (MCF) and ecotropic viruses were cloned from them. Inoculation of either MCF or ecotropic virus alone or both viruses together did not cause lymphoma in NFS/N mice and there was no evidence of viral replication in the recipients. 3) Inoculation of either MCF- or ecotropic virus-infected NFS-ME cells alone did not cause lymphoma development in pre-irradiated NFS/N mice, while transplantation of both MCF- and ecotropic virus-infected NFS-ME cells resulted in the development of lymphomas of host origin. These results show that lymphomagenic MCF virus was generated through the recombination of E4 viral genome and a modified proviral DNA of endogenous viruses present in radiation- or chemically-induced lymphomas, and that an interaction or synergism of MCF and ecotropic viruses is required for MCF virus to exert lymphomagenic activity.
It is well known that a small amount of regurgitation occurs through Björk-Shiley valves. Obviously, this functional regurgitation is related to the construction of the Björk-Shiley valve, wherein the disc does not overlap the ring, but fits within its orifice, leaving a minimal space between the edge of the disc and the ring. The aim of this study was to evaluate the clinical significance of regurgitation in patients having Björk-Shiley valves in the aortic position by pulsed Doppler echocardiography. The study group consisted of 46 patients with normally functioning valves and five patients with malfunctioning valves. Valve dysfunction resulted from paravalvular regurgitation in three, and thrombosed valves in two (confirmed by surgery and angiography). Using pulsed Doppler echocardiography, aortic regurgitation was observed in 29 of the 46 normally functioning Björk-Shiley aortic valves. Among these, regurgitant flow signals were constantly located in the vicinity of the valve ring in the left ventricular outflow tract. Therefore, these regurgitant flow signals were considered to represent functional regurgitation of the Björk-Shiley valve. Aortography was performed for 11 of the 46 normally functioning Björk-Shiley valves, and there was minimal transvalvular regurgitation in all. In all of the five malfunctioning Björk-Shiley aortic valves, aortic regurgitant flow signals were detected by pulsed Doppler echocardiography, and the maximal distance of the regurgitant flow signals from the Björk-Shiley valve ring was more than 0.5 cm. However, it was difficult to differentiate transvalvular regurgitation from paravalvular regurgitation using pulsed Doppler technique alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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Hepatic vein flow can be reliably measured because Doppler sampling volumes are easily oriented parallel with the course of the hepatic vein. In this study, the relationship between the Doppler signal in the hepatic vein and the external jugular vein pulse was evaluated, and the contribution of the Doppler echocardiography to the quantitative diagnosis of tricuspid regurgitation was also assessed. The subjects consisted of five healthy persons, four patients with lone atrial fibrillation, 27 patients who underwent cardiac surgery, and 34 patients with tricuspid regurgitation. The severity of the regurgitation was judged by right ventriculography and inferior caval angiography. The pattern of the Doppler hepatic vein flow mimicked that of the jugular phlebogram in each patient. The normal hepatic vein flow consisted of two forward flows toward the heart; one in systole; the other, in diastole, and one retrograde flow toward the liver during atrial contraction. In patients with lone atrial fibrillation, a systolic backward flow toward the liver or a decrease in the systolic forward flow was observed, though there was no tricuspid regurgitation. In patients who had cardiac surgery, a systolic backward flow toward the liver or a decrease in the systolic forward flow was usual. However, a prominent systolic backward flow toward the liver was observed in patients with severe tricuspid regurgitation, and a decreased systolic forward flow toward the heart was observed in patients with moderate tricuspid regurgitation in sinus rhythm. We concluded that Doppler measurement of hepatic vein flow does not contribute to the diagnosis of tricuspid regurgitation in the presence of atrial fibrillation or in postoperative conditions, but that it is useful in identifying severe tricuspid regurgitation.
The effect of a combined treatment with radiation and N-nitrosoethylurea (NEU), or a split administration of NEU in inducing lymphoma was studied in female C57BL/6N mice. A single intragastric administration of 5 mg of NEU was only slightly lymphomagenic, inducing thymic lymphomas in 20% of mice, while the incidence was elevated to 92% if the NEU treatment was preceded (by 5 days) by 400 rad of total-body X-irradiation, which alone is seldom lymphomagenic. A high yield of lymphoma (84-93%) was also obtained if 5 mg of NEU was delivered in two split doses of 4 mg and 1 mg with a 4 day interval. Drastic injury to both the thymus and bone marrow caused by either 400 rad total-body X-irradiation or the first dose of NEU (4 mg) was followed by a vigorous regeneration within a few days. The maximum induction rate of lymphoma was obtained when the subsequent dose of NEU (1 mg) was given at the peak of DNA synthesis in the bone marrow and thymus following the first treatment. The data indicate that the principal effect of the irradiation or the first dose of NEU was to provide a susceptible cell population, and that a high yield of lymphoma was brought about through the action of the subsequent dose of NEU on a sufficient number of target cells engaged in heightened DNA synthesis.
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An unusual mid-diastolic musical murmur developed soon after cardiac catheterization of a 55-year-old man with mitral stenosis. His physical findings consisted of an accentuated first heart sound, an opening snap and a grade 3/6 mid-diastolic rumbling murmur. No early diastolic murmur was audible. However, soon after cardiac catheterization, a mid-diastolic "cooing" murmur at a frequency of 200 cycles/sec developed. This murmur resolved with the patient in the sitting position, or by leg raising. With Valsalva or Müller maneuvers this murmur was abolished transiently, and it disappeared on administering either amyl nitrite or methoxamine. Echocardiography revealed early diastolic vibrations in the aortic valve. Pulsed Doppler echocardiograms revealed harmonic signals of the aortic cusp at a fundamental frequency of 200 cycles/sec. These harmonic signals could be recorded only in mid-diastole. The frequency patterns of the murmur and the Doppler signals were identical; therefore, the murmur was judged to be produced by aortic valve vibrations. Furthermore, resonance of cardiac structures which accentuate the murmur might be related to the occurrence of this murmur. Pulsed Doppler echocardiography is helpful in identifying the site of origin of this musical murmur.
The efficacy of two-dimensional echocardiography in diagnosing the localization of myocardial infarction (MI) was studied by comparing the echocardiographic and pathological findings of 28 patients having MI. The ventricular wall was divided into 18 segments including three segments of the right ventricular wall. The regional wall motion abnormalities for each of the 504 segments were diagnosed by visual assessment. The echocardiographic recordings were reviewed individually by four examiners using the same protocol to assess the interobserver's variation. The receiver operating characteristics (ROC) curves differed by examiners. However, when the subjects were limited to anterior MI patients, the ROC curves established by the echo-trained physicians did not differ significantly. It was concluded that the echocardiographic diagnosis of regional wall motion by visual assessment has universal validity. Individual differences are thought mainly to depend on the sites of infarction. Sensitivities for detecting transmural (TM), non-transmural (non-TM) infarcted segments and intact segments were 90, 70 and 70%, respectively. Most of the underestimated TM or overestimated intact segments corresponded to the sites adjacent to MI. As the unexpectedly misdiagnosed segments, the mimic inward motion of the inferior wall drawn by the intact anteroapical wall was observed in a inferior MI patient, or the mimic anterior motion of the anteroapical wall by a swinging motion of the heart, or the paradoxical motion of the interventricular septum was observed in a right ventricular MI case. In the two third of the overestimated non-TM segments, it was considered that the wall motion was affected by the myocardial ischemia, which was not revealed by pathological examination. The underestimated non-TM segments located adjacent to the intact segments or opposite to the severely ischemic segments. From the echocardiographic viewpoint, nearly 90% of segments showing akinetic or dyskinetic motion had MI. However, one third of segments diagnosed as normal were actually MI segments.
A patient with a double-chambered right ventricle and cor triatriatum dexter was presented. The non-invasive diagnosis of cor triatriatum dexter was stressed. A plate-like echo was imaged in the right atrium using two-dimensional echocardiography. It divided the atrium into two chambers. Contrast echocardiography revealed delayed filling of the lower portion of the atrium. Pulsed Doppler echocardiography demonstrated systolic turbulence in the lower portion of the atrium, indicating that the plate-like structure produced a stenosis in the right atrium. We conclude that non-invasive methods including contrast echocardiography and pulsed Doppler echocardiography, are effective in identifying stenoses in the right atrium.
The present study was undertaken to detect the spontaneous mammary tumor-associated antigen ( MTAA ), and to find the cross-reacting antigen in chemically-induced mammary tumor. The antisera against spontaneous mammary tumor were raised in the WAF1 rats of the same strain and tested for the detection of tumor-associated soluble antigen of mammary tumor induced by N-ethylnitrosourea (ENU) and N-butylnitrosourea ( BNU ). The MTAA was found in the extract of spontaneous mammary tumor by the double immunodiffusion test, while it was not found in the extract of normal and fetal tissues, hyperplastic mammary gland, spontaneous fibroadenoma, and chemically-induced mammary tumor. On the other hand, the MTAA was not detected in the other types of tumors induced by ENU or BNU , i.e. gastric cancer, intestinal tumor, brain tumor, kidney tumor, bladder tumor, hemangioma, rhabdomyosarcoma, or leukemia. The spontaneous MTAA could not be detected in the spontaneous mammary tumor of C3H mice or human breast cancer either. The MTAA was extracted effectively by 3 M KC1. Furthermore, the MTAA was found in the cytoplasm of continuous established mammary tumor cell line ( SpMT -1) by the immunofluorescence test.
Twenty-seven patients in cardiogenic shock or medically refractory left ventricular failure due to acute myocardial infarction were treated with intraaortic balloon counterpulsation. Twenty-one of them were treated with counterpulsation alone; the remaining six underwent surgery. Thirteen patients were benefited by counterpulsation alone. Three of the patients treated with counterpulsation and surgery survived and were discharged from the hospital. Thus, 16 of the 27 patients (59%) survived. Four patients in medically refractory left ventricular failure or shock due to acute myocarditis were treated with counterpulsation. All patients were weaned easily from circulatory assist and were discharged from the hospital. This study shows that intraaortic balloon counterpulsation is a very useful adjunct to currently existing medical measures for the treatment of cardiogenic shock or for medically refractory left ventricular failure in both myocardial infarction and myocarditis.
In a previous report, we showed that pericardium closure is responsible for post-operative abnormal septal motion. To elucidate this hypothesis, we performed additional clinical and experimental studies. Twenty-six patients were studied during cardiac surgery. We also studied five dogs during cardiopulmonary bypass using M-mode and two-dimensional echocardiography. M-mode echograms and short-axis views of the left ventricle were obtained before and after pericardiotomy, and before and after pericardium closure. In the clinical study, the patients were divided into three groups according to pre-operative septal motion: Group 1 included six patients with atrial septal defect showing paradoxical motion, Group 2 included thirteen patients with aortic or mitral regurgitation of hyperdynamic motion, and Group 3 consisted of seven patients with ventricular septal defects or mitral stenosis showing normal systolic motion. In Group 1, septal motion became normal after closure of atrial septal defect and then, became abnormal just after pericardium closure. Again in Group 2, septal motion became normal following surgical repair, but abnormal motion appeared immediately after pericardium closure. In Group 3, normal septal motion persisted until just prior to closure of the pericardium. Abnormal septal motion in all groups persisted following chest closure. In all dogs, paradoxical septal motion resulted from pericardium closure after cardio-pulmonary bypass. We conclude that both pericardium closure and cardio-pulmonary bypass are responsible for post-operative abnormal septal motion.