Search

The structure of the three-body $nn��$ system, which has been observed recently by the HypHI collaboration, is investigated taking $��N-��N$ coupling explicitly into account. The $YN$ and $NN$ interactions employed in this work reproduce the binding energies of $^3_��$H, $^4_��$H and $^4_��$He. We do not find any $^3_��n$ bound state, which contradicts the interpretation of the data reported by the HypHI collaboration., To be publsihed in PRC as a Rapid communication

The structure of the three-body $nn\Lambda$ system, which has been observed recently by the HypHI collaboration, is investigated taking $\Lambda N-\Sigma N$ coupling explicitly into account. The $YN$ and $NN$ interactions employed in this work reproduce the binding energies of $^3_{\Lambda}$H, $^4_{\Lambda}$H and $^4_{\Lambda}$He. We do not find any $^3_{\Lambda}n$ bound state, which contradicts the interpretation of the data reported by the HypHI collaboration., Comment: To be publsihed in PRC as a Rapid communication

The structure of heavy hyperhydrogen $^6_��$H is studied within the framework of a $tnn��$ four-body cluster model. Interactions among the constituent subunits are determined so as to reproduce reasonably well the observed low-energy properties of the $tn, t��$ and $tnn$ subsystems. As long as we reproduce the energy and width of $^5$H within the error bar, the ground state of $^6_��$H is obtained as a resonant state., 16 Pages, 3 figures, To be published in Nuclear Physics A

There is some controversy regarding the mechanisms of an upward shift in the left ventricular diastolic pressure-volume curve during ischemia. The effects of handgrip exercise on the pressure-volume curve were examined in 21 patients with coronary artery disease and in 6 control subjects. Pressure-volume curves were constructed from digitized left ventricular pressure and volume derived from biplane left ventriculogram. Diastolic pressure-volume curve shifted upward in 12 patients with coronary artery disease during handgrip exercise (Group 1), but not in the other 9 patients who were similarly afflicted (Group 2). The upward shift did not occur in any control subject. No difference was observed in rate-pressure product gain during exercise. In Group 1, left ventricular end-diastolic pressure increased (p less than 0.01) and ejection fraction was reduced (p less than 0.01), although it did not change in Group 2. In Group 1, the time constant was prolonged (p less than 0.01) with no change in the coefficient for elastic modulus. In Group 2, these parameters remained unchanged. Group 1 was accompanied by more extensive asynergy than Group 2. Thus, isometric handgrip exercise resulted in an upward shift in the diastolic pressure-volume curve in patients with coronary artery disease. Incomplete relaxation and/or the viscoelastic properties of the left ventricle associated with ischemia could be responsible for this phenomenon.

The case of a patient with right coronary artery-right atrial fistula was reported, with special reference to the noninvasive evaluation. On two-dimensional echocardiography in the short axis view, it was observed that the fistula had an entrance from the right coronary cusp, with the body of fistula sigmoid-like appearance running along the tricuspid ring and atrioventricular groove. In the subxyphoidal approach the exit of fistula into the right atrium was demonstrated. Intrafistular blood flow and drainage flow into the right atrium were identified by color flow mapping. The potential usefulness of the combination of two-dimensional, pulsed Doppler echocardiography and color flow mapping were discussed.

二重指示薬希釈法により肺血管外水分量を心疾患32例,すなわち冠動脈疾患20例,僧帽弁疾患11例,拡張型心筋症1例において測定した.さらに肺血管外水分量に対する硝酸薬の影響も検討した.肺血管外水分量は熱とICG平均循環時間の差と,心拍出量の積により求めた.肺うつ血群の肺血管外水分量は12.6±3.3ml/kgと正常肺血行動態群6.6±2.2ml/kgに比し大であつた(p

To investigate the value of the 12-lead ECG and two-dimensional echocardiography (2DE) in the distinction of left circumflex (LCX) from right coronary artery (RCA) disease, we analyzed the location of Q waves, infarct lesions, and coronary artery narrowings in 26 patients with angiographically documented single-vessel disease. Q waves in leads II, III, and aVF were associated with the posterior wall (PW) lesions at the papillary muscle level. Extensive lesions from the PW to the posterior septum (PS) identified RCA disease, while extension to the lateral wall (LW) identified LCX disease. Eleven of 12 patients with high posterior infarction (tall R wave in V1) were found to have extensive LW lesions and 10 of these had coronary narrowings in or proximal to the obtuse marginal branch of LCX. All 6 patients with high posterior infarction and high lateral infarction (Q in I or aVL) had infarct lesions extending from the LW to the anterior wall (AW) and were associated with LCX disease with a large obtuse marginal branch. Of 10 patients with Q waves in V6, the apical LW and PW were involved in 7 and either segment in 3. Nine of these 10 patients had LCX disease. It is concluded that the location of Q waves in inferior infarction could aid in recognizing infarct extension and underlying coronary artery disease.

The aim of this study was to clarify the combined effects of propranolol and nifedipine on the regional wall motion and haemodynamic variables of the heart in dogs with chronic ischaemia. After an injection of propranolol the heart rate and stroke volume significantly decreased (from 128(18) beats X min-1 to 113(12) beats X min-1 and from 15.1(3.1) ml to 12.2(2.6) ml respectively) and the left ventricular end diastolic pressure and systemic vascular resistance in systole increased significantly (from 7.3(1.5) mmHg to 10.0(1.8) mmHg and from 8.61(1.42) kPa X litre-1 X min-1 to 11.80(1.59) kPa X litre-1 X min-1 respectively). In the regional myocardium the end diastolic length increased significantly in both border and normal zones (7(3)% and 4(2)% respectively) and the percentage systolic shortening in the normal zone decreased significantly from 18.0(3.1)% to 15.1(2.9)%. In the border and infarcted zones the percentage systolic shortening or systolic lengthening did not change. The administration of nifedipine resulted in significant decreases in left ventricular systolic pressure and in systemic vascular resistance (from 122(17) mmHg to 105(14) mmHg and from 11.80(1.59) kPa X litre-1 X min-1 to 6.63(1.24) kPa X litre-1 X min-1 respectively) and stroke volume increased to 18.2(4.4) ml. The percentage systolic shortening in the border and normal zones improved significantly to 9.8(3.2)% and 19.2(3.7)% respectively without any change in end diastolic length and left ventricular end diastolic pressure. In the infarcted zone no significant change in systolic lengthening or end diastolic length was seen. Thus impaired left ventricular pump function induced by propranolol was reversed by nifedipine.