[Enteroinsular axis and neuroregulatory mechanism (author's transl)].
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Biomedical subjects
Publications and source records attributed to N Sakamoto.
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Effects of pH and urine flow on urinary excretion of nicotine were examined in 11 smokers after they had smoked 3 cigarettes during water diuresis. Plasma nicotine showed a slight but nonsignificant rise after smoking. Urinary excretion of nicotine increased significantly from the pre-smoking levels of 258 +/- 76 and 252 +/- 147 (mean +/- SEM) ng/15 min to the peaks of 2,587 +/- 1,224 and 2.561 +/- 584 ng/15 min 30 and 45 min after the start of smoking. Thereafter, urinary nicotine tended to decrease and rise with changes in urinary flow. There was a correlation between urinary nicotine and urinary flow after smoking (r = 0.26, p less than 0.05). Eleven subjects were grouped based on the mean urinary pH throughout the experiment. No significant amount of nicotine was excreted in the group with pH above 7.5 while groups with pH below 7.4 excreted substantial nicotine after smoking. There was a negative correlation between urinary pH and nicotine excretion (r = -0.58, p less than 0.001). Urinary excretion of nicotine cannot be used as an index of smoking unless pH and urine flow are controlled.
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Right heart catheterization was carried out on 14 patients with pulmonic regurgitation using intracardiac phonocardiography. All the patients showed pulmonic regurgitant murmur in the right ventricular outflow tract. In addition, seven out of the 14 patients showed mid-diastolic and presystolic murmurs maximally in the outflow tract of the right ventricle. Furthermore, inspiration increased the loudness of these diastolic murmurs in four patients. These findings were compatible with those of right-sided Austin Flint murmur due to functional tricuspid stenosis in pulmonic incompetence. Ten out of the 14 patients had pulmonary hypertension and all the subjects with a rightsided Austin Flint murmur showed elevated pulmonary arterial pressure. Thus, pulmonic regurgitation with pulmonary hypertension is thought to be closely related to the right-sided Austin Flint murmur and the turbulence resulting from antegrade flow across a closing tricuspid valve may be responsible for the genesis of the murmur.
There have been many reports about ventricular arrhythmias during acute coronary occlusion. Nevertheless, it is only recently that interest has been taken in the occurrence of ventricular arrhythmia after reperfusion following coronary occlusion. To investigate the mechanism of the latter kind of arrhythmia, we studied the effect of changing the duration of occlusion time on the recovery time courses of the VMRT (Ventricular Multiple Response Threshold), and of the A-V differences in the serum K+ concentration across the heart. The time course of delta K+ recovered soon after reperfusion, while changes in VMRT needed more time for recovery to the initial state. Concerning heart rate, blood pH, and the levels of Na+, Cl-, and Ca++, no significant changes were detected. There was no relation between the time courses of VMRT and those of the A-V differences in serum K+. Consequently, time courses in VMRT were dependent upon the duration of coronary occlusion time. A possible explanation for these results may be that the longer the duration of the preceding occlusion time, the more severe the myocardial damage due to myocardial ischemia.
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Bovine, rabbit and human dental pulp glycosaminoglycans were analyzed qualitatively and quantitatively using two-dimensional electrophoresis. The major components of bovine and rabbit dental pulp were chondroitin 4-sulphate and hyaluronic acid, while in the human dental pulp dermatan sulphate and chondroitin 4-sulphate were the major components.
The effects of intravenous pindolol on the electrophysiologic properties of the atrioventricular conduction system was studied in intact dog, using His bundle electrogram and the extrastimulus method. Pindolol was administered intravenously in a dose range of 4 to 40 micrograms/Kg. The latter dosage of pindolol is above those used clinically. Significant effects of intravenous pindolol were observed on sinus cycle length, the A-V nodal conduction time, the ERP of the atrium, the ERP and FRP of the A-V node, and the ERP of the ventricle. Sinus cycle length was prolonged during sinus rhythm. Intraatrial conduction time was not altered by pindolol, while the ERP of the atrium was slightly increased. The A-H interval was generally prolonged by pindolol without Wenckebach type A-V block, but the H-V interval was unchanged. Both ERP and FRP of the A-V node was prolonged. The ERP and RRP of the His-Purkinje system were not statistically evaluated, because no block within the His-Purkinje system were not statistically evaluated, because no block with the His-Purkinje system or prolongation of H-V interval was produced and only a few QRS complexes by extrastimulus showed aberrant configration in the intact canine heart. In addition, pindolol prolonged the ERP of the ventricle.
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Serum mitochondrial glutamic-oxaloacetic transaminase activity was determined in 83 patients with various liver diseases and 10 healthy adults. 1) The average of mitochondrial glutamic-oxaloacetic transaminase value was 1.2 mU in healthy adults, 8.3 mU in patients with acute hepatitis, 13.7 mU in patients with post-transfusion hepatitis, 5.0 mU in patients with persistent hepatitis, 4.5 mU in patients with chronic inactive hepatitis, 9.6 mU in patients with chronic active hepatitis, 5.6 mU in liver cirrhosis, and 295 mU in a patient with fulminant hepatitis. 2) While one patient with acute hepatitis showed the highest value in the group of 29 mU, one patient with fulminant hepatitis showed an extremely high value of 295 mU, revealing an obvious difference between them. 3) One patient with fresh myocardial infarction also showed an extremely high value of 110 mU.
In order to study the origin of the basal systolic murmurs in mitral stenosis, left and right heart catheterization was performed in 18 patients with mitral stenosis using intracardiac phonocardiography. Our data revealed that the basal systolic murmurs originated in the aorta, the pulmonary artery, and the outflow tract of the right ventricle. In 14 cases, we noted the maximal ejection systolic murmur in the aorta near the aortic valve. However, in two cases, there was a loud systolic murmur in the pulmonary artery. These murmurs occurred in early to mild-systole and were crescendo-decrescendo in configuration. The pitch of the murmur ranged from low to medium frequency in the majority of cases. They are produced by the turbulence of blood flow in the aorta and the pulmonary artery. A late systolic murmur was also recorded in the outflow tract of the right ventricle in two patients. This is thought to occur due to functional or relative infundibular stenosis of the right ventricle. It differs in location and timing from those in the aorta and the pulmonary artery. The outflow tract of the right ventricle is regarded as the third origin of the basal systolic murmur in mitral stenosis.