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T Shigeno

Publications and source records attributed to T Shigeno.

72 records · Page 4Linked to original sources
PubMed1983

[Hyperparathyroidism after radioactive iodine therapy for Graves' disease: a case report].

Herein we report a 36-year-old man with hyperparathyroidism and a past history of internal irradiation to the thyroid. Twelve years previously at age 24 years he had received 8 mCi of radioactive iodine for Graves' disease. An additional dose of 4 mCi was required 3 years later. A right lower parathyroid adenoma (28 X 23 X 20 mm, 5.7 g) was found at neck exploration. Although the association of external ionizing radiation to the head and neck and the subsequent development of hyperfunctioning parathyroid glands has been described in recent years, there are only 4 cases in the literature of parathyroid surgery for hyperparathyroidism secondary to earlier treatment with radioactive iodine for Graves' disease. In a long-term follow-up of 180 patients treated with radioactive iodine for Graves' disease, neither hypercalcemia nor hypophosphatemia was found. Whether internal radiation therapy can be a causative factor in the development of hyperparathyroidism should be elucidated in future. However, it seems reasonable to suggest that patients whose hyperthyroidism has been treated with radioactive iodine should have their serum calcium levels examined at 5-year intervals.

Adult↗
PubMed1982

Roles of subarachnoid blood clots and norepinephrine in cerebral vasospasm.

The content of norepinephrine (NE) in the ventricular, basal cisternal and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms. The cisternal CSF in patients with vasospasm contained a significantly higher level of NE (0.246 +/- 0.0490 ng/ml) compared with those without vasospasm (0.075 +/- 0.001 ng/ml) (p less than 0.001). However, this increase is not considered to be high enough to constrict cerebral arteries, unless there is an increased NE-sensitivity in subarachnoid haemorrhage. Vascular responses to NE in vivo were then studied after reversing blood-induced prolonged vasospasm of the rabbit's basilar artery through a transclival approach as well as a newly developed basal cisternal irrigation model. However, NE in molar concentrations between 1 x 10(-10) and 10(-2) failed to produce further contraction of the artery. In conclusion, the increase in NE with vasospasm might be only a secondary phenomenon, and not a causative factor of vasospasm. Early removal of subarachnoid blood clots seemed to prevent the development of vasospasm.

Animals↗
PubMed1982

Norepinephrine in cerebrospinal fluid of patients with cerebral vasospasm.

The content of norepinephrine (NE) in the ventricular, basal cisternal, and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms at different intervals according to the presence or absence of vasospasm. Twelve were operated on within 3 days after subarachnoid hemorrhage (SAH), prior to the occurrence of vasospasm. Postoperatively, CSF was continuously drained from a basal cistern or lateral ventricle. Norepinephrine was assayed by the highly sensitive automated fluorometric method. The concentration of NE increased in all sites of CSF sampling along with the appearance of vasospasm. Above all, the cisternal CSF of patients with vasospasm contained significantly higher NE (0.246 +/- 0.049 ng/ml, mean +/- SEM) compared to those without vasospasm (0.075 +/- 0.001 ng/ml) (p less than 0.001). However, since this increase cannot be considered to be high enough locally to constrict cerebral arteries, this might be only a secondary phenomenon due to release of NE into CSF from various sources in the brain.

Adult↗
PubMed1982

The determination of brain water content: microgravimetry versus drying-weighing method.

The microgravimetric technique and the drying-weighing method for the determination of brain water content are analyzed and compared. A new method has been devised for the automatic production of the gradient column. For gravimetry, tissue samples weighing more than 30 mg have proven adequate for measurement. Specific gravity (SG) should be determined as early as 1 minute after tissue is inserted into the gradient column. Calculations of cerebral blood volume (CBV) from changes in SG of both brain tissue and intravascular perfusate have shown that the SG of brain tissue is considerably influenced by changes in CBV. This is because the SG of blood is higher than that of brain tissue, and may lead to a decrease of SG of about 0.002 in anemic cortex and of 0.001 in anemic white matter, which will simulate a false increase in tissue volume as water of 4% and 2%, respectively. This methodological error may be relevant when the early stages of ischemic brain edema development are studied. Water content of brain tissue can also be determined with acceptable accuracy by vacuum freeze-drying samples of brain tissue weighing about 100 mg. In contrast to cortex, white matter shows a wide range of individual and regional differences in water content. Thus, conclusions on the presence of brain edema drawn from tissue water determinations should always be subjected to cautious analysis and criticism.

Animals↗
PubMed1982

[Cerebral edema following experimental subarachnoid hemorrhage (author's transl)].

Despite the fact that cerebral edema appears to be a common complication of subarachnoid hemorrhage (SAH) due to a ruptured cerebral aneurysm, measurements of brain tissue water content have not been carried out in this entity. For this reason, the development of cerebral edema has been analized in a newly developed experimental SAH model. SAH was induced in cats under controlled ventilation by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Intracranial pressure (ICP), blood pressure, cortical EEG and somatosensory evoked potentials (SEP) to sciatic nerve stimulation were monitored for 3 to 24 hours. Using labelled microspheres of 15 mu diameter, four serial determinations of regional cerebral blood flow (rCBF) were performed in one group of five animals before and immediately after SAH as well as 10 to 20 min, and 3 to 6 h post SAH. RCBF were obtained in 60 areas of the brain from tissue samples weighing about 150 mg. Brain tissue water content was determined by the vacuum freeze-drying weighing procedure in the same brain samples. In another group of five, brain tissue specific gravity (SG) was measured by microgravimetry in samples of brain tissue weighing 30 to 50 mg. Regional differences in SG as well as in water content were calculated from 21 untreated control animals.+2

Animals↗
PubMed1981

[Fundamental problems and improved methods in the measurement of specific gravity of cerebral tissues. (author's transl)].

Gravimetric determination of brain tissue water content through the measurement of specific gravity (SG) still poses some basic problems. We have studied some of them with the aid of a new gradient column. Using a specially designed conical cylinder to distribute the solution in a graded manner, and a floating apparatus, a gradient column was automatically prepared with a high linearity (r greater than 0.99990). Analysis of equilibration time-course curves of cat brain tissue fragments with various sizes showed that it was more accurate to use volumes as large as 50 mg, and to measure as early as one minute after tissue insertion. In normal brain, SG of grey matter was usually higher than that of white matter. In contrast, in a brain with oligemia or with low hemoglobin contents of blood, this relationship was reversed. Thus, SG can be influenced not only by water content, but also by other factors. As SG of blood is higher than that of brain tissue, cerebral blood volume (CBV) is of particular interest. Assuming the total brain volume as equal to 1, CBV and volume of brain proper excluding intravascular blood can be expressed as x and 1-x respectively. In a given brain tissue, SG of blood or perfusate a, and SG of whole brain tissue A can be measured. If SG of brain proper is expressed as y, the following equation can be introduced: ax + y(1-x)=A. If a and A are obtained from two different brains under the condition of constant CBV, x, 1-x and y can be calculated. For this purpose, values from normal brain and those from perfused brain with isotonic saline were applied. The calculated CBV was 7% in the grey and 3% in the white. SG of brain proper was as low as 0.002 in the grey and 0.001 in the white as compared to that of whole brain tissue. When these values are applied to the equation of percent change in tissue volume as water = (SG of control tissue-1)-(SG of experimental tissue-1)/(SG of experimental tissue-1) x 100%, the false positive increase of water in a completely ischemic brain without edema is approximately 4% in the grey and 2% in the white. Then, care should be taken in the assessment of water increase from SG, particularly in the early stage of ischemic edema.

Animals↗
PubMed1979

Vasospasm assessed by angiography and computerized tomography.

In 44 consecutive cases of ruptured cerebral aneurysm, vasospasm was demonstrated pre- or postoperatively. These cases were examined by bilateral carotid angiography and computerized tomography (CT), and the relationship between the angiographically visualized distribution of vasospasm, the neurological symptoms, and infarction seen on CT was evaluated. Vasospasm occurred in only some intracranial portions of the cerbral arteries that were immersed in blood-stained cerebrospinal fluid. Angiographically, diffuse vasospasm extensively involving bilateral carotid systems indicated the gravest prognosis for patients. Vasospasm affecting one carotid system and the anterior cerebral arteries on the opposite side often produced permanent neurological deficits. On the contrary, when vasospasm was restricted to one carotid system or to bilateral anterior cerebral arteries, it was usually associated with temporary neurological symptoms; however, it always produced residual neurological symptoms if it extended to the ascending branches (M3) of the middle cerebral arteries. Computerized tomography definitely demonstrated a low-density area or infarction in the territory of the spastic arteries in 25 (71%) of 35 cases with vasospasm. A low-density area was always detected when vasospasm occurred in M3 segments.

Adult↗
PubMedDate not supplied

Cerebral edema following experimental subarachnoid hemorrhage.

The development of cerebral edema after experimental subarachnoid hemorrhage (SAH) was studied in cats by determining regional brain tissue water content with the microgravimetric technique as well as the drying-weighing method. SAH was induced by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Serial determinations of regional cerebral blood flow (rCBF) by labelled microspheres, and monitorings of vital signs such as intracranial pressure (ICP), blood pressure and EEG were carried out up to 24 h after SAH. Animals could be classified into three grades according to the severity of SAH. In grade I, the increase of ICP was transient and minor. In grade II, ICP increased up to 200 mm Hg with a marked reduction of rCBF below 20% of control in cerebral hemispheres. Following subsequent reduction of ICP, rCBF increased over control, indicating reactive hyperemia. Thereafter, a great reduction of rCBF was again observed. In grade III, rCBF was sustained at essentially zero flow with the presence of continuously increased ICP above 100 mm Hg. Cerebral edema was observed particularly in the parasagittal water-shed areas of all grade II animals. It is concluded that cerebral edema complicating SAH is caused by the combination of an initially induced global cerebral ischemia and the subsequent recovery of cerebral circulation. Post SAH hypertension is another factor to exacerbate the development of cerebral edema.

Animals↗
PubMedDate not supplied

Effects of indomethacin on rCBF during and after focal cerebral ischemia in the cat.

The effect of indomethacin on rCBF was studied in cats anesthetized with Nembutal either under resting conditions or with temporary middle cerebral artery (MCA) occlusion. RCBF was measured by the microsphere method. In control animals (n = 3), indomethacin (4 mg/kg, i.v.) significantly reduced rCBF by about 25% in both cortex (from 44 +/- 6 to 32 +/- 3 ml/100 g/min, p less than 0.001) and white matter (from 36 +/- 4 to 26 +/- 2 ml/100 g/min, p less than 0.001). After MCA occlusion rCBF was markedly decreased in the sylvian region ipsilateral to occlusion (ischemic core) (from 38 +/- 4 to 14 +/- 2 ml/100 g/min in cortex, 4 animals). Although pretreatment with indomethacin (4 mg/kg) (4 animals) 30 min prior to occlusion did not alter rCBF during ischemia, a marked enhancement of reactive hyperemia was observed in the ischemic core immediately upon reperfusion following 2 h occlusion (54 +/- 11 untreated vs 95 +/- 13 treated, p less than 0.05). In the delayed postischemic period, namely 2 h after recirculation, rCBF still remained to be higher in the animals treated with indomethacin (40 +/- 6 untreated vs 96 +/- 9 treated, p less than 0.001). Such an effect of indomethacin for ameliorating postischemic blood flow in both the immediate and delayed period was less prominent in the adjacent area (penumbra) ipsilateral to occlusion. In the contralateral hemisphere, indomethacin caused slight reduction in rCBF during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

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