[Clinical studies of the reconstruction of right ventricular outflow tract in tetralogy of Fallot; including criteria for use of transannular patching (author's transl)].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Tabayashi.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The relation of pulmonary hemodynamics to pathological change in the pulmonary vasculature was examined in a model of unilateral pulmonary venous (PV) obstruction. The left upper pulmonary vein (A group, n=6) or both the left upper and left lower pulmonary veins (B group, n=6) of two-week-old piglets were banded; the control group (n=6) was sham operated. At eight weeks after PV banding, mean pulmonary arterial pressure was highest in the B group, intermediate in the A group and lowest in the control group. In all groups, the media of the pulmonary artery was equally thickened in both lungs, whereas the media of the pulmonary vein was thickened only in those lung lobes having stenotic pulmonary veins. For all animals from three groups, left pulmonary arterial wedge pressure (PAWP) correlated with medial thickness of the pulmonary arteries of the right lung (r=0.76, p=0.003), the left upper lobe (r=0.54, p<0.03), the left lower lobe (r=0.49, p=0.04). This finding suggests that the pathogenesis of PAWP-related medial thickening of the bilateral lung pulmonary artery begins with the sensing by the bilateral lung of PV pressure buildup in the unilateral lung.
Hemodynamic changes induced by hypoxia and cold stress were examined on the model of pulmonary venous obstruction (PVO) to investigate the mechanism of pulmonary hypertensive crisis. Bilateral pulmonary venous stenosis was surgically created in 7 newborn piglets of the PVO group. Sham operations were performed on 6 piglets of the control group. Following the baseline hemodynamic measurement (FiO2 = 0.3) at 8 weeks after the operation, the piglets were exposed to hypoxia (FiO2 = 0.14) for 10 minutes, and were also exposed to cold stress for 20 minutes. Hypoxia significantly increased mean pulmonary arterial pressure in the PVO group. Hypoxia increased not only pulmonary arterial resistance, but also pulmonary venous resistance in the PVO group. Cold stress did not change pulmonary arterial resistance or pulmonary venous resistance in each group. In the lungs of the PVO group, the medial muscular layer of the pulmonary arteries and pulmonary veins were thickened. This probably accelerates hypoxia-induced vasoconstriction, which in turn increases pulmonary arterial and venous resistances.
To drive an artificial heart system optimally, information from the autonomic nervous system may be needed; however, it is very difficult to monitor autonomic nerve discharges continuously. In this study, we propose a new automatic control algorithm for a total artificial heart (TAH) using fluctuations in the circulatory system. It was reported that fluctuations in hemodynamics reflect ongoing information from the autonomic nervous system. A Mayer wave at 0.1 Hz was reported to reflect sympathetic information. We observed fluctuations in vascular resistance, which can be measured during use of an artificial heart. Four adult goats were used for the experiments. Through a left thoracotomy, hemodynamic parameters were measured during chronic animal experiments. All time series data were recorded on magnetic tape. Quantitative analysis, statistics, and spectral analysis were carried out on a computer through an analog-digital (AD) converter. A Mayer wave peak was clearly recognized in all goats in the spectrum of vascular resistance. A band pass filter was used to convert this information to automatic control. Time series curves of the Mayer wave of vascular resistance were provided, and compared with the time series curve of the cardiac output. After a change in the Mayer wave, increase in cardiac output was observed. This phenomenon may be interpreted as sympathetic nervous control of changes in cardiac output. These results suggest that an artificial heart may be controlled by the measurement of the Mayer wave of vascular resistance, making it possible to control an artificial heart with neural information.
To develop the optimal automatic control algorithm for an in vivo artificial heart system, investigation of the basic characteristics of the cardiovascular system may be important. The clinical significance of chaotic dynamics in the cardiovascular system has attracted attention. The circulation is a so-called complex system with many feedback circuits, making it very difficult to investigate the origin of chaos within the system. In this study, we investigated the origin of chaos by open loop analysis with an artificial heart (which has no fluctuation in pumping rate or contraction power) in chronic animal experiments with healthy adult goats. As a result, in the artificial heart circulatory time series data, low dimensional deterministic chaos was discovered by nonlinear mathematical analysis, suggesting the importance of blood vessels in the chaotic dynamics of the cardiovascular system. To investigate the origin of chaos further, sympathetic activity was directly measured in animals with artificial hearts. Chaotic dynamics was also recognized in sympathetic action potentials, even during artificial heart circulation. Coupling of the nonlinear information between blood vessels and sympathetic activity was suggested by analysis of mutual information. In chaotic dynamics, the central nervous system (CNS) played an important role through sympathetic activity. These findings may be useful for the development of an automatic control algorithm for an artificial heart.
BACKGROUND: We compare the effects of angiotensin-converting enzyme (ACE) inhibitor or angiotensin II type 1 (AT(1)) receptor blocker on density of myocardial beta-adrenergic receptors (beta-ARs) in a heterotopic heart transplantation model. METHODS: Hearts of F344 rats were heterotopically transplanted into Lewis rat recipients immunosuppressed with cyclosporine (10 mg/kg/day). Recipients were treated orally with the AT(1) receptor blocker L-158809 (3 mg/kg/day, n = 6), enalapril (3 mg/kg/day, n = 6), or vehicle only (n = 6) for 90 days. Density of myocordial beta-ARs was determined with an autoradiographic technique using [(3)H]CGP-12177. RESULTS: Graft status, the sum of the functional score and the score for color, was preserved better in the L-158809-treated group (5.8 +/- 0.9) and in the enalapril-treated group (5.6 +/- 0.8) than in the vehicle-treated group (3.8 +/- 0.9, p < 0.05). The grades of graft coronary artery disease in the L-158809-treated group and in the enalapril-treated group were significantly less than that seen in the vehicle-treated group. The density of myocardial beta-AR (fmol/mg of protein) was 3.5 +/- 0.5 in the L-158809-treated group (p < 0.05 vs. vehicle-treated group) and 3.2 +/- 0.5 (p < 0.05) in the enalapril-treated group but was 2.2 +/- 0.4 in the vehicle-treated group. CONCLUSION: L-158809 is as effective as enalapril in restoring myocardial beta-AR density in immunosuppressed rat transplant model, and this efficacy, as well as the prevention of graft coronary arteriosclerosis, is probably associated with the preservation of graft status.
To study hemodynamics together with various aspects of rejection after experimental heart transplantation, we developed a technique to produce a working left heart model of heterotopic (abdominal) heart transplantation. The interatrial septum and tricuspid valve of the donor heart are removed. The pulmonary arterial trunk, pulmonary veins, and inferior vena cava are ligated, and the stumps of the donor aorta and superior vena cava are anastomosed in an end-to-side fashion to the recipient abdominal aorta and inferior vena cava, respectively. Arterial blood from the recipient abdominal aorta thus perfuses the donor myocardium through the coronary artery, and the donor left ventricle receives venous blood from the recipient inferior vena cava as preload. In this model, the donor left ventricle does not pump out enough venous blood to desaturate the recipient femoral arterial blood but does generate approximately the same pressure as the recipient's heart. This model is reproducible, easy to manage, and can be applied to heterotopic heart transplantation in various experimental animals including rats.
The purpose of this study was to evaluate left ventricular (LV) diastolic mechanical properties after induced global ischemia using reliable new methods. The diastolic function of nonoxygenated crystalloid solution (CC sO2) was compared with those of oxygenated crystalloid (CC cO2) and oxygenated fluorocarbon cardioplegic (FC cO2) solutions. Postischemic ventricular performance was studied in 3 equal (no. 7) groups of dogs subjected to 120 minutes of global ischemia induced at an average myocardial temperature of 18.5 +/- 1.4 degrees C. LV diastolic function (chamber and myocardial stiffness) and relaxation (the exponential fall in LV pressure) were evaluated by sonomicrometry and Millar micrometers before ischemia and at 45 and 60 minutes after ischemia. LV chamber and myocardial stiffness in the CC sO2 group was significantly (p less than 0.05) elevated after ischemia, while the CC cO2 and FC cO2 groups did not show increases in LV chamber and myocardial stiffness after ischemia. LV relaxation before and after ischemia was not changed in any group. The myocardial water content of the CC sO2 group was significantly higher than that of the CC cO2 and FC cO2 groups (p less than 0.05). We conclude that (1) the postischemic increase in LV chamber stiffness in the CC sO2 group was dependent not only on the increase in intrinsic myocardial stiffness but also due to an increase in myocardial edema, and (2) there was no correlation between the LV relaxation rate and the leftward shift of diastolic compliance curves in the CC sO2 group.
During the period between November 1986 and November 1988, 13 consecutive patients with Stanford type A aortic dissection (8 acute and 5 chronic) were treated as follows: (1) urgent operation for cases with pericardial tamponade or severe heart failure, (2) initial medical treatment followed by elective operation for acute but stable cases or chronic cases, and (3) routine use of open distal anastomosis or selective cerebral perfusion. One patient died during medical treatment: 5 patients were operated on emergently. The remaining 2 acute and 5 chronic cases were operated on electively. There were no operative deaths, neurological disturbances, or late deaths. It is suggested that acute dissection of the ascending aorta requires immediate surgical intervention, especially when the entry is in the ascending aorta. On the other hand, it is also suggested that one could avoid emergency operations in selected cases with retrograde extension of the aortic dissection.
BACKGROUND: A heterotopically transplanted rat heart model described by Ono and Lindsey in 1969 has been widely used as a fundamental animal model of heart transplantation. However this "nonworking" model is greatly different from the orthotopic heart in view of left ventricular work, in which the experimental results obtained may not always reflect the clinical setting with an orthotopic transplanted "working" heart. We herein propose a new "working" left heart model in rats using a heterotopic abdominal transplantation technique by modifying the method of Ono and Lindsey. METHODS: First, a donor heart graft and a recipient were prepared in the conventional fashion. Second, the donor heart was tailored by the ligation of main pulmonary artery and the removal of tricuspid valve and interatrial septum. Third, the ascending aorta and right atrium of the donor heart were anastomosed to the infrarenal abdominal aorta and to the inferior vena cava of the recipient, respectively. Consequently, the left atrium and ventricle of heart graft were loaded with the blood from the right atrium through the interatrial communication. RESULTS: This surgical procedure required an average of 58 minutes and had negligible operative risk. The donor left ventricle produced a systolic blood pressure almost equal to the recipient's aortic pressure and maintained vigorous beat. CONCLUSIONS: This model is easily reproducible and would be useful for various studies on heart transplantation.