[Rupture of a papillary muscle after annuloplasty with successful early treatment by mitral valve prosthesis (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Sakamoto.
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Athough it has been generally believed that it is extremely difficult to prepare an experimental model of cerebral infarction in the dog with the use of temporary vascular occlusion, the procedure recently developed by one of the authors fascilitates the production of a localized infarction in the thalamus with a noticeably high rate of success. To obtain more reliability of this method, techniques of electroencephalography induced from depth electrode to the thalamus were applied in this experiment. Following a temporary vascular occlusion, a significant diminution of fast wave component of about 10 Hz occurred with attenuation of voltage in the ipsilateral thalamic depth electrode. In cases of 2 hour vascular occlusion done by this method, an obvious infarction in the thalamus was confirmed histologically 7 days later. The authors emphasised that when the experimental model of thalamic infarction in the dog are combined with EEG, not only can cerebral infarction be producted with more certainly but also the EEG changes can be followed. This analysis is important since it provides information on the chronological changes in the ischemic region or infarction lesion.
One day during an aneurysm surgery under the preoperative administration of mannitol, the feeding artery was accidentally occluded temporarily. Since then, investigation on whether or not mannitol can prevent infarctions in ischemic brain tissues have been carried out utilizing the thalamus infarction model in dogs. Twenty dogs were divided into equal groups, the control and the mannitol group. Temporary clipping for sixty minutes was adopted as a standard for both groups. The only difference between the groups was the administration of 2 g/kg of mannitol before the arterial occlusions. In the control, six of ten dogs showed infarctions verified as histological changes on the seventh post-ischemic day. In the mannitol group only one of ten showed infarction. Each of the difference is statistically significant (P less than 0.03).
Sixty four multiple intracranial aneurysm cases have been analysed for the purpose of identifying the relation between aneurysm rupture and aneurysmal features, mass signs, vasospasms and locations of the aneurysms. 1) 85% of the larger and largest aneurysm in each case were the ruptured aneurysm. 2) Aneurysms with a greater ratio of length to width showed a high frequency of rupturing. 3) Irregularities of the aneurysmal wall and the existence of a daughter aneurysm attached to the main aneurysm have a tendency to rupture. 4) Evidence of mass signs, associated with intracerebral, subarachnoid and subdural hematoma or a cerebral edema is also useful for the identification of the ruptured aneurysm. 5) Anterior communicating artery aneurysms have a relatively high frequency of being the ruptured aneurysm in cases of multiple aneurysm. 6) By utilizing all the investigated factors of the angiogram, the ruptured aneurysm might be identified in about 90% of the cases of multiple aneurysms.
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Twenty-eight cases after subarachnoid hemorrhage due to ruptured intracranial aneurysms was undergone third ventriculostomies as the reason that the development of postoperative CSF disturbances was determined to be highly probable. The indication and value of third ventriculostomy was discussed considering various clinical and operative findings. Postoperatively, six of the 28 cases required ventriculoperitoneal shunt operation. Although temporary disturbances of serum electrolytes was noted in three cases, no other side effects was attributed to third ventriculostomy. During hospitalization, no fatalities occured following third ventriculostomy. The addition of third ventriculostomy to surgery for ruptured intracranial aneurysms in highly recommended, especially in cases strongly indicating the possible occurrance of postoperative CSF flow disturbances.
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Dobutamine, a new synthetic inotropic agent, was administered by intravenous infusion to 22 patients following open heart surgery. The dosage of dobutamine started from 2 mug/kg/min and was increased stepwise to 4, 6, and 8 mug/kg/min. Cardiac index increased from 2.54 +/- 0.13 to 3.11 +/- 0.19 and 3.50 +/- 0.22 L/min/m2 with 4 and 8 mug/kg/min, respectively. Heart rate increased from 87.6 +/- 2.9 to 96.4 +/- 2.3 and 108.9 +/- 3.2 beats/min with 4 and 8 mug/kg/min, respectively. Systolic and mean aortic pressure and systolic pulmonary arterial pressure were elevated from 126.0 +/- 3.8 to 144.6 +/- 6.0 mm Hg, from 91.8 +/- 2.7 to 96.2 +/- 3.2 mm Hg, and from 33.4 +/- 2.3 to 37.1 +/- 2.5 mm Hg with 8 mug/kg/min, while other pressures were unchanged. Mean left atrial pressure fell significantly from 15.9 +/- 0.6 to 14.8 +/- 0.7 mm Hg. Stroke volume index, stroke work index, and left ventricular work also increased. Premature ventricular beats were observed in only one patient during dobutamine infusion, but no other side effect was observed. We conclude that dobutamine is a potent inotropic agent which increases cardiac output without causing significant tachycardia or arrhythmias, and is useful for the treatment of patients following open heart surgery.
In order to examine the variability of the pattern due to the location and direction of the ultrasonic transducer, echocardiograms of the pulmonary valve were obtained from different precordial areas in 28 patients with various diseases and in 3 normal subjects. By higher positioning of the transducer, the diastolic slope became slower or upward and the 'a' wave became indiscernible, giving the pattern of pulmonary hypertension even in the normotensives. The anterior cusp was also detected by tilting of the transducer in some cases. Systolic time intervals (STI) of the right ventricle, however, were not influenced by the beam angle. The present data strongly suggests that the echocardiogram of the pulmonary valve should be carefully evaluated in the light of the spatial relationship of the echo beam and the valve in order to give the diagnostic importance.
Experiments were carried out to examine whether the lung acts as a depot for circulating lipid, especially that absorbed from the intestine. When 0.5 ml of triolein was administered orally to rats, the triglyceride content of the lung increased 2-3 hr later, but its increase in the lungs 2-3 hr later was only of about 1/10 of that in the liver. In the fed state the triglyceride content of the lung was only about 1/8 of that of the liver. When [3H]palmitic acid was administered orally to mice its uptake by the lung 1 and 2 hr later was 1/25-40 of that by the liver. In the lung, it was incorporated into phospholipid more than into triglyceride, but in the liver it was predominatly incorporated into triglyceride. Most of the lipase activity in both the microsomal and soluble fractions of rat lung appeared to be due to lipoprotein lipase. Fasting did not decrease the lipoprotein lipase activity in either fraction. It was concluded that the lung is not important in removal of triglyceride from the blood, even during fat absorption from the intestine, and that the lung takes up circulating lipid for its own metabolism rather than for storage.
Immediately after mitral commissurotomy, we measured pulmonary blood volume by dye-dilution method and investigated the relationships between pulmonary blood volume and other hemodynamic parameters. Pulmonary blood volume correlated directly to pulmonary mean transit time, cardiac index, stroke volume index, and mean left atrial pressure. Pulmonary blood volume increased with mean pulmonary arterial pressures up to 35 mm. Hg but decreased with elevation above this level. The same patterns were observed in the correlations between pulmonary blood volume and both pulmonary distending pressure and pulmonary vascular resistance. These observations suggest that the changes of the pulmonary vessels begin with the elevation of mean pulmonary arterial pressure above 35 mm. Hg, pulmonary distending pressure above 25 mm. Hg or pulmonary vascular resistance above 5 units. Therefore, it is desirable to maintain mean pulmonary arterial pressure below 35 mm. Hg in patients immediately after mitral commissurotomy.
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