Release of endogenous adenyl purines from rabbit ear artery.
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Biomedical subjects
Publications and source records attributed to R Ishii.
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Cerebrovascular disease is a lethal complication for patients with renal failure because of the hemostatic disturbance and equivocality about management of the central nervous system. Appropriate management of the renal failure in neurosurgical patients was considered on the basis of experience. Hemodialysis (HD), which is the most common dialysis method, has a serious disadvantage: the elevation of intracranial pressure during dialysis due to the "disequilibrium syndrome." It is important to stabilize the serum osmolarity during dialysis in order to prevent the disequilibrium syndrome. From this point of view, continuous ambulatory peritoneal dialysis (CAPD) has great advantages; serum osmolarity is not rapidly changed and no anticoagulants are required during dialysis. CAPD is recommended as the first method of choice in neurosurgical management of renal failure patients. However, if a patient has to be maintained with HD because of a history of laparotomy or peritonitis, it is essential to keep the serum osmolarity as stable as possible using the extracorporeal ultrafiltration method, hypernatremic HD, bicarbonate HD, and intravenous administration of glycerol.
A case is reported of aqueductal stenosis caused by an abnormal draining vein and demonstrated by computerized tomography and magnetic resonance imaging. Placement of a ventriculoperitoneal shunt relieved the patient's progressive headaches.
Around-the clock intraocular pressure (IOP) measurement were performed in 104 eyes of 52 low tension glaucoma (LTG) cases. Subjects were all hospitalized and IOP measurements were done every 2 hours from 6:00 AM to 12:00 PM and every 3 hours from 12:00 PM to 6:00 AM. All LTG patients met the following criteria, (1) glaucomatous optic nerve head change and corresponding visual field defect, (2) normal open angle, (3) IOP less than or equal to 21mmHg at any time of IOP measurement, (4) no obvious neurological or rhinological disorders that could affect the optic nerve, (5) no history of hemodynamic crisis or cardiovascular disorders except mild hypertension. Peak IOPs were most frequently observed at 10:00 AM, but about 55% of all observed peaks were in the time period from 6:00 PM to 8:00 AM. Most troughs were observed from 2:00 PM to 10:00 PM. The mean IOP, the diurnal variation and the difference between both eyes in the same person averaged 14.1, 4.9, and 0.6mmHg, respectively. Assuming that the period of rhythm is 24 hours, the results of IOP measurements fitted a cosine curve using the least square method. In 44% of all eyes, significant correlation coefficient (r greater than or equal to 0.6, p less than 0.05) between the measured and the predicted IOPs was noted, and an equation, IOP = 14.3 + 1.7cos 2 pi (t/24-0.4 radian), was obtained. Comparing the present results with former ones, we concluded that the IOP changes in LTG patients were similar to those in normal individuals.
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Ten patients with carotid cavernous fistula (CCF) were reviewed. Single photon emission computed tomography (SPECT) for regional cerebral blood flow (rCBF) study was performed in six patients with fast flow shunt. Five of these six patients with fast flow shunt angiographically demonstrated cortical venous drainage, and two of these patients suffered intracerebral hemorrhage. The rCBF decreased in the region demonstrating the cortical venous drainage in five patients, and in one patient the angiography demonstrated arterial steal and the rCBF decreased in a part of the ipsilateral cerebral hemisphere. SPECT proved to be useful in assessing the cerebral circulation in cases of CCF.
The influence of ventricular extrasystoles and postextrasystoles on cardiovascular dynamics were assessed in terms of maximum rate of rise of left ventricular pressure (max dP/dt), ascending aortic flow, left ventricular stroke volume, and left ventricular end-diastolic transverse dimension in anesthetized dogs. A single ventricular extrasystole, two and three consecutive ventricular extrasystoles (couplet and triplet) were induced by applying mechanical stimulation to the surface of the right ventricule. In any of these ventricular extrasystoles, max dP/dt, stroke volume and end-diastolic transverse dimension were decreased, compared with those in preceding sinus beats, i.e., pre-extrasystoles. Over the several postextrasystoles, max dP/dt was increased and gradually returned to its control level. This increase in max dP/dt, i.e., postextrasystolic potentiation paralleled an increase in ascending aortic peak flow but did not always bring about an increase in stroke volume, even when a left ventricular contraction was initiated by a significantly greater end-diastolic transverse dimension. The postextrasystolic potentiation seems to be associated with the Frank-Starling mechanism and does not compensate for the decreased in stroke volume elicited by the ventricular extrasystoles. In conclusion, not only ventricular extrasystoles per se but also postextrasystoles exert the adverse influence on cardiovascular dynamics consecutively.
The hemodynamics of the anterior cerebral arteries (ACAs) were studied in 28 children with moyamoya disease. In 39% of 56 cerebral hemispheres, antegrade filling of the ACAs was not verified by preoperative angiography. On the other hand, adequate collateral pathways to the ACA territory were generally not achieved by encephalomyosynangiosis (EMS) or superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis. The authors have devised new surgical methods for the revascularization of the ACA territory, which they term "encephaloarteriosynangiosis" (EAS) and "encephalogaleosynangiosis" (EGS). In these procedures, one or several burr holes are made in the frontal skull, the dura mater is incised, and either the frontal branch of the STA or the pedicled galea aponeurotica stump is placed on the surface of the frontal cortex. In addition to EMS or STA-MCA anastomosis, these methods were applied to 23 cerebral hemispheres in 14 pediatric patients. In 14 cerebral hemispheres (61%) of 10 patients, postoperative external carotid angiograms showed some cortical branches in the ACA territory, and clinical improvement was achieved in patients with transient ischemic attacks affecting the lower extremities. The results of this study demonstrate that EAS and EGS are simple and useful techniques for revascularization of the ACA territory. In addition, EGS can be applied to the territory of the posterior cerebral artery.
A case of subarachnoid hemorrhage caused by the rupture of a dissecting aneurysm of the vertebral artery is reported. The initial angiogram was normal, and repeat angiography carried out 12 days later revealed a dissecting aneurysm of the right vertebral artery. This angiographic change seems to be due to the progression of minimal dissection that was not found at the time of first angiogram.
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As brain capillaries do various works necessary for maintaining the homeostasis of neurons, their disruptions may play an important role in the establishment of ischemic brain damage. It is also said that brain capillaries response to ischemia more functionally than structurally and their microstructural features remain unchanged for a long time of ischemia. Therefore, a new method is expected to be introduced that can evaluate the ischemic changes of endothelial cells on a histological level more sensitively than conventional histological methods. In the present study we investigated immunohistochemical reactivity of factor VIII related antigen (F VIII RAg), a specific and representative marker of vascular endothelial cells, in normal and ischemic brains. In the experiment, cerebral ischemia was induced by occlusion of the unilateral common carotid artery in adult mongolian gerbils. The periods of occlusion were 1, 2, 3, 6, 12, and 24 hours, in five animals respectively. After occlusion each brain was obtained by decapitation and quickly frozen at -80 degrees C and 5-6 micron sections were cut in a cryostat at -20 degrees C and dried at 37 degrees C. The staining for F VIII RAg was done by the peroxidase-antiperoxidase method using specific antiserum to human F VIII RAg. In normal gerbil's brains, the positive staining for F VIII RAg was observed in endothelial cells of arteries, veins and capillaries. In major vessels the staining was intense, but neurons and glia were not stained.(ABSTRACT TRUNCATED AT 250 WORDS)
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In multiparameter fluorescence-activated cell sorter studies presented here, we use the highly fluorescent protein phycoerythrin (PE) as an immunizing antigen and as a fluorescent probe to reveal and isolate antigen-binding memory B cells. We demonstrate directly that memory B cells in spleens from PE-primed mice stain brightly with PE and produce strong IgG1 anti-PE responses when sorted and cultured with L3T4+ helper T cells. That is, as few as 500 sorted PE-binding cells per culture well are sufficient to produce high-level anti-PE responses, presenting antigen in a form that induces helper T cells. Three-color immunofluorescence studies reveal that cells staining brightly with PE reside primarily in a population of B220+(IgM,IgD)- cells and comprise 0.02-0.05% of the spleen cells. Complementary studies with 2,4-dinitrophenyl memory B cells show that whereas this B220+-(IgM,IgD)- population (which comprises only 1-2% of the spleen cells) gives high-affinity anti-dinitrophenyl responses, the predominant B220+(IgM,IgD)+ population yields only low-affinity antibody. Finally, we find that although both populations have similar Ia levels, cells in the high-affinity fraction have greatly reduced levels of surface immunoglobulin.
We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30-120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.
We report the long term results of the treatment of 23 intracranial ruptured aneurysms by coating. Twenty-three patients treated by coating were followed for a mean period of 11.2 years. The mean interval between the last hemorrhage and the operation was 22.4 days. Ten aneurysms underwent total coating, 9 with Biobond and 1 with Aron Alpha. Thirteen aneurysms underwent partial coating, 11 with Biobond and 2 with Aron Alpha. Six aneurysms were reinforced partially by other materials, but no aneurysm was wrapped totally with these materials. Rebleeding occurred in 6 patients, of whom 5 died. The mean interval between coating and rebleeding was 4 years. All patients suffering rebleeding had been treated with Biobond, and 3 patients had undergone total coating of aneurysms. The risk of recurrent hemorrhage after total coating with Biobond was 33%. One rebleeding patient underwent a second operation 10.5 years after total coating of the aneurysm. Biobond was found only at the tip of the aneurysmal sac. From these results, reinforcement of ruptured aneurysms with Biobond seems to be of little value, and a more reliable method must be developed for aneurysms that cannot be clipped.
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