[Nonsuture small vessel replacement using microballoon catheter].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Iwabuchi.
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.
Our previous experimental and clinical studies yielded the following results: CSF flow around the subarachnoid vessels is often interrupted by subarachnoid clots; anaerobical incubation of CSF-blood mixture led to a marked fall in the pH value; the vasocontractility of anaerobically incubated CSF-blood mixtures was greater than that of aerobically incubated samples; vasocontraction induced by anaerobically incubated samples was inhibited to a far greater extent the prostaglandin synthesis inhibitor meclofenamic acid than by phenoxybenzamine; cases of asymptomatic marked angiographical vasospasm or of cerebral ischemia with relatively slight angiographical vasospasm were not rarely encountered. Those results lead us to a hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobical changes of subarachnoid clots may be factor upsetting the balance of the synthesis of TXA2 and PGI2 from PG endoperoxides on the inner surface of cerebral arteries, in favor of TXA2--which plays a role in arterial contraction and in thrombosing with platelet aggregation. On this basis we have been testing the administrations of trapidil, an antagonist and selective synthesis inhibitor of TXA2, in 20 consecutive suitable cases so far, for the prevention of cerebral vasospasm after aneurysmal rupture. Angiographical vasospasm was seen in 9 of the 20 cases, but no signs of cerebral ischemia were detected in 7 of the 9 cases, either clinically or in CT scan. The importance of thrombus formation by platelet aggregation in symptomatic vasospasm are thus suggested.
The authors made neuropsychological studies by the tachistoscope and the dichotic listening test on a subject who had undergone the transection of the posterior part of the corpus callosum. As to the tachistoscopic recognition, stimulus material was composed with the various Japanese letters (Katakana, Hiragana, Kanji), various faces (variations of the eyebrow form and the mouth form) and various slopes of line. Table 1 shows results of the cases (the subject was the present case, subjects 1 and subject 2 were past cases). It was seen that the performance of the subject on Japanese letters tasks showed greater right visual field superiority than the one of subject 1 and subject 2. As to the auditory recognition, the tasks used for the dichotic listening test were the following (Table 2, 3, 4). Different digits (three pairs) of the subject showed greater right ear superiority (right ear: 61.1, left ear 5.9) than the ones of subject 1 and subject 2.
Neck clipping has been widely believed to be one of the most reliable and typical treatment of the cerebral aneurysm. Recently we experienced two cases of recurrence of cerebral aneurysm several years after surgery, in spite of confirmation of perfect neck clipping not only by intraoperative inspection but postoperative angiographical studies. The histological findings demonstrated that the arterial wall at the clip edge changed into thinning, interruption, and atrophy both of the muscle layer and internal elastic lamina. Therefore, local fragility of the arterial wall adjacent to clip edge seemed to cause formation of a new aneurysm. In addition, we discussed the usefulness of riskless CT in postoperative follow-up study of the cerebral aneurysm.
Explore the source record for details and available documents.
In our in vitro study of subarachnoid haemorrhage, the anaerobic incubation of CSF-blood mixture led to marked fall in the pH value thereof, which suggested to us that intracranial focal acidosis may play some role in the pathogenesis of cerebral vasospasm or disturbance of consciousness after the haemorrhage. To test this hypothesis, we treated 16 clinical cases of such disorders with carotid injection of 7% sodium bicarbonate solution. The treatment resulted in considerable improvement of the disturbance of consciousness by dilating the cerebral peripheral arteries; this we could observe angiographically 15 minutes after carotid injection. We found no morphological changes, however, in the spastic vessel itself up to 30 minutes after the injection. Given the result both of this study and of our previous experiments, we offer the hypothesis that the synthesizing process of thromboxane A2 and intracranial focal acidosis might play an important role in the pathogenesis of cerebral vasospasm.
Explore the source record for details and available documents.
We used the isotope dilution technique to monitor circulating blood volume (CBV) in three patients with ruptured cerebral aneurysms who developed pre- or postoperative ischemic symptoms that responded well to intravascular volume expansion therapy with blood transfusion and plasma expanders. In the first and second cases, predeterioration CBVs were obtained. Both of these patients showed hypovolemia and a decreased red blood cell volume at the time of neurological deterioration. A predeterioration CBV was not available for the third patient for comparison, but his red cell volume was also markedly decreased. Postrecovery CBVs were obtained in the second and third cases. Our data suggested that a depleted red blood cell volume was more responsible for neurological deterioration than was a lowered plasma volume. To prevent the occurrence of hypovolemia and anemia in aneurysm patients, we should monitor CBV not only at the time of neurological deterioration, but also at the time of admission and during the immediate postoperative period.
Explore the source record for details and available documents.
The results of our previous experimental and clinical studies led us to the hypothesis that, in the pathogenesis of cerebral vasospasm, subarachnoid focal acidosis resulting from anaerobic changes of subarachnoid clots may be a factor upsetting the balanced synthesis of both thromboxane A2 and prostaglandin I2 from prostaglandin endoperoxides on the inner surface of cerebral arteries. Thus, there is a higher concentration of thromboxane A2, a prostanoid that causes arterial contraction and platelet aggregation. We tested the administration of trapidil, an antagonist and selective synthesis inhibitor of thromboxane A2, in a series of 20 cases for the prevention of cerebral vasospasm and cerebral ischemia after aneurysmal rupture. Vasospasm was demonstrated by angiography in 9 of these cases, but only 2 of the 9 showed mild signs of cerebral ischemia. Of the 20 patients, 15 were discharged from the hospital as cured and 3 had a neurological deficit at discharge. Our findings suggest the significance in symptomatic vasospasm of thrombus formation by platelet aggregation and the effectiveness of trapidil as a preventive.
Explore the source record for details and available documents.
In consecutive 13 cases of the carotid occlusive lesions the carotid thromboendarterectomy was performed with some of our devices as follows: 1) Superior cervical ganglionectomy was added to this operation, bringing efficacy to increase cerebral blood flow. 2) Removal of atheroma plaque en block, as far as possible, shortened the operation time and diminished the arterial wall damage. 3) We could approach to the carotid artery without dissection of the common facial vein by antero-medial retraction of the internal jugular vein. 4) The operation without internal shunt made the technique simple and shortened the operation time. 5) Interlacing vascular suture with microsurgical technique prevented narrowing or shortening of the carotid artery. 6) We used a pair of small needle holders with teeth for anterior wall suture. We could pick up the adventitia easily and exactly, and did not need change of the needle holding with these instruments. 7) Others: The clamping time ranged 15-45 minutes without any neurological deficits.
Explore the source record for details and available documents.
The effect of antifibrinolytic therapy on posthaemorrhagic subarachnoid fibrosis was observed experimentally in dogs with the scanning electron microscope (SEM). The subchronic subjects, given intravenous injections of tranexamic acid (1 mg/day) for 12 days and sacrificed 3 weeks after cisternal blood injection, showed residual clot with thick fibrosis, especially around the haemorrhage. The chronic subjects, to which the same procedure was applied and which were sacrificed three months after cisternal blood injection, showed significant increases in the subarachnoid fibrosis, most remarkably in the parasagittal region. Tranexamic acid is widely used for preventing the recurrence of subarachnoid haemorrhage. However, it was revealed in this study that antifibrinolytic therapy might increase chronic posthaemorrhagic subarachnoid fibrosis, which is considered to be responsible for communicating hydrocephalus by disturbing epicortical CSF flow.
The author used the polarization microscope and topo-optical reactions such as phenol reaction, collagen-specific sulphation, and picrosirius red F 3 BA staining to investigate the nature of subarachnoid fibrosis after experimental subarachnoid haemorrhage. It is strongly suggested that the subarachnoid fibrotic deposits--which here analysed in a previous study by scanning electronmicroscopy--contain a high amount of collagen as a main component both three weeks and three months after the SAH.
Explore the source record for details and available documents.