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S Okawara

Publications and source records attributed to S Okawara.

At least 19 recordsLinked to original sources
PubMed2001

Phototoxic retinal degeneration and toxicokinetics of sitafloxacin, a quinolone antibacterial agent, in mice.

We examined drug concentrations and the incidence of retinal degeneration in the eyes of albino BALB/c mice after a single intravenous administration of sitafloxacin plus a 4 h period of UVA irradiation. Retinal degeneration was induced at 40 mg/kg or more plus UVA irradiation, and there was little decrease in ocular sitafloxacin concentration under UVA irradiation. We then examined the incidence of retinal degeneration with various periods of UVA irradiation in BALB/c mice given a single intravenous administration of 40 mg/kg sitafloxacin. Retinal degeneration occurred in all the groups receiving UVA irradiation immediately after sitafloxacin administration, whereas no retinal degeneration occurred in the groups receiving UVA irradiation starting 30 min or later after administration. In addition, we examined both the retinal degeneration and auricular inflammation in BALB/c mice given a 7-day repeated administration of sitafloxacin at 1, 3.3 and 10 mg/kg per day, which never induce retinal or auricular change by a single administration. Retinal degeneration was not induced at any dose level, although auricular skin inflammation was augmented by repeated administration. These results suggest that the occurrence of retinal degeneration depends on maximum ocular sitafloxacin concentration during UVA irradiation, whereas the severity of auricular inflammation is directly proportional to the total decrease in area under the drug concentration curve for auricular sitafloxacin under UVA irradiation. This difference between retinal degeneration and auricular inflammation may derive from their respective mechanisms of pathogenesis.

Animals↗
PubMed2000

Possible relationship between phototoxicity and photodegradation of sitafloxacin, a quinolone antibacterial agent, in the auricular skin of albino mice.

We compared the phototoxic potential of the quinolone antibacterial agent sitafloxacin with those of lomefloxacin and sparfloxacin. Female BALB/c mice were given a single intravenous administration of sitafloxacin, lomefloxacin, or sparfloxacin at 10 or 40 mg/kg, followed by ultraviolet-A (UVA) irradiation for 4 h (21.6 J/cm(2)). At 10 mg/kg, all quinolones induced either none or minimum inflammation in the auricle. At 40 mg/kg, sitafloxacin induced mild phototoxic inflammation in the dermal skin, while lomefloxacin and sparfloxacin induced very severe inflammation. In particular, 2/5 animals of the lomefloxacin group showed partial necrosis in the dermis and epidermis. We then determined the time course change of sitafloxacin concentrations in serum and auricular tissue by high performance liquid chromatography. Sitafloxacin concentrations in the auricle were markedly decreased under UVA irradiation, whereas those in sera were not affected. Furthermore, we examined the severity of sitafloxacin-induced phototoxicity under varied duration of UVA irradiation. The severity of phototoxicity increased with increasing duration of UVA irradiation, and statistical analysis showed a close correlation between the severity and the decreased area under the drug concentration curve under UVA irradiation (DeltaAUC(auricle)). The severity was decreased with delay in commencement of UVA irradiation, indicating the importance of commencement time of irradiation in the experimental condition of the phototoxicity study. It might be attributed to the decrease in DeltaAUC(auricle) after administration. These results suggest that sitafloxacin possesses milder phototoxic potential than lomefloxacin or sparfloxacin and is degraded in the auricular skin under UVA irradiation, and that the severity of phototoxicity is directly proportional to the DeltaAUC(auricle).

Animals↗
PubMed1996

[Peptidoleukotriene receptor antagonists in asthma therapy].

Peptidoleukotrienes reproduce some of the functional and histological features of clinical asthma, such as potent bronchoconstriction, airway microvascular leakage, mucus hypersecretion, eosinophilic airway infiltration, in addition to inducing bronchial hypersensitivity. An important role for peptidoleukotrienes has been demonstrated in experimental challenge studies in asthmatic patients and in acute asthma attacks. Antagonists of peptidoleukotrienes can inhibit bronchoconstriction in response to inhaled allergen, exercise or inhaled cold air, and oral or inhaled aspirin. These compounds demonstrate beneficial effects in clinical studies with improvement in symptoms and lung function. Peptidoleukotriene antagonists may provide a new therapeutic approach for the treatment of asthma.

Asthma↗
PubMed1995

[Therapeutic effect of a mineralocorticoid in patients with hyponatremia of central origin].

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the therapeutic effect assessed. The subjects of this study were 14 patients (5 with subarachnoid hemorrhage, 2 with hypertensive intracerebral hemorrhage and 7 with head injury) who developed hyponatremia as a complication during their hospital stay for treatment of their intracranial lesions between March 1993 and April 1994. Hyponatremia of central origin was defined as serum Na+ levels below 135 mEq/l for at least two consecutive days with no other discernible etiology. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. The mean interval until the onset of hyponatremia was 7.5 days, and the mean minimum serum sodium level was 125.7 mEq/l. The dose of fludrocortisone was 0.3 congruent to 0.6 mg/day, the mean period of administration 5.8 days, and route was via a stomach tube in 3 cases and by mouth in 11 cases. The therapeutic effect was good (improvement within 5 days) in 11 cases and fair (improvement in 5 to 8 days) in 3 cases. None of the patients manifested side effects. All of the patients had lower urinary sodium excretion than before administration, with the mean rate of decrease of 66.9%. Mineralocorticoids, which suppress natriuresis, are safe and effective in the treatment of hyponatremia of central origin. It appears that mineralocorticoid therapy may be aggressively tried in severe cases in which NaCl loading is ineffective.

Adult↗
PubMed1995

[Subacute subdural hematoma: findings in CT, MRI and operations and review of onset mechanism].

Subacute subdural hematoma was investigated in terms of findings in CT, MRI and operations and of onset mechanism. The subjects were 7 cases of subacute subdural hematoma in which CT and MRI were performed during the past 5 year period. Subacute subdural hematoma here was defined as a nonoperated case with acute subdural hematoma, accompanied by subacute exacerbation 1-3 weeks after head trauma. The time from the injury to the onset averaged 13.7 days. CT revealed mixed density in 4 cases, low density in 3 cases and cerebral atrophy in all cases, with increasing mass sign due to the enlarged low density area. MRI revealed mixed intensity in 5 cases and high intensity in 2 cases, with increasing mass sign due to the enlarged high intensity area. Operation disclosed the outer membrane of the hematoma only in 1 case, but the inner membrane could not be identified in any case. Analysis of the hematoma contents showed a low hemoglobin concentrations and a high level of methemoglobin. Lack of outer membrane in cases with subacute subdural hematoma suggests that this is a different disease entity from chronic subdural hematoma. It is surmised that subacute subdural hematoma is the result of subdural effusion in the subacute stage, because, judging from the findings of CT and MRI each performed over time, cerebrospinal fluid is considered accountable for the increase in the mass sign.

Aged↗
PubMed1994

[Therapeutic effect of mineralocorticoid in patients with hyponatremia of central origin].

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the pathogenetic mechanism of the hyponatremia was assessed based on the therapeutic effect obtained. The subjects were 14 patients (6 with subarachnoid hemorrhage, 3 with hypertensive intracerebral hemorrhage, 2 with cerebral infarct and 3 with head injury) who developed hyponatremia, as a complication during their hospital stay for their intracranial lesions from April to December 1992. Patients with serum Na levels below 135 mEq/l for more than 2 days with no other discernible etiology were defined as having hyponatremia of central origin. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. When improvements occurred within 3 days, in 3 to 7 days, or 8 days or more efficacy was rated "excellent", "good" or "poor", respectively. The mean interval until the onset of hyponatremia was 10.4 days, its mean duration was 5.7 days, and the mean minimum serum sodium level was 129.5 mEq/l. The dose of fludrocortisone administration was 0.1 mg/day except for one patient who was treated with 0.3 mg/day. The mean period of administration was 3.7 days (range: 3 to 6 days), and the route was via a stomach tube in 5 cases and oral in 9 cases. The therapeutic effect was excellent in 9 cases, good in 3 cases and poor in 2 cases, the efficacy rate being 86%. None of the patients manifested side effects. Plasma atrial natriuretic peptide levels were above 100 pg/ml in 2 patients and 50-100 pg/ml in 8 patients and neither of the former 2 patients exhibited "excellent" efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Subacute subdural hematoma--reexamination of mechanism by CT and MRI findings].

We have already reported about the importance of establishing the concept of subacute subdural hematoma. But the mechanism by which this disease develops has not as yet been elucidated fully. In one case of subacute subdural hematoma, we were able to perform CT and MRI over time and obtained findings which were of use in studying the mechanism of development. The case was a 56-year-old male. He developed with seizure. CT on admission revealed acute subdural hematoma and subarachnoid hemorrhage. But neurological deficits were absent. So he was treated conservatively. On the 16th hospital day there appeared seizure, anisocoria and an increase in the mass sign due to subdural hematoma was noted on CT, so a diagnosis of subacute subdural hematoma was made. Cerebrospinal fluid was considered accountable for the increase in the mass sign judging from the findings of CT and MRI each performed over time. It was surmised that subdural effusion developed concurrently in the subacute stage. Three conditions, namely, presence of (1) arachnoid tear, (2) clots, (3) no intracranial hypertension are considered important as the mechanism by which subacute subdural hematoma develops.

Acute Disease↗
PubMed1993

[A study of plasma atrial natriuretic peptide, antidiuretic hormone and cerebral vasospasms in patients with aneurysmal subarachnoid hemorrhage].

The relationship between plasma atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) both of which show high values after subarachnoid hemorrhage and cerebral vasospasm was studied. The subjects were 23 patients who were admitted because of aneurysmal subarachnoid hemorrhage during three years from March, 1989 to March, 1992 and in whom plasma ANP and ADH levels could be determined over time. Cerebral vasospasm was evaluated by the finding of cerebral angiography, clinical symptoms, and presence or not of low density areas on CT. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less for two days or more. Angiographical vasospasm was found in 17 patients (85%), symptomatic vasospasm in 15 patients (65.2%), low density areas on CT in 9 patients (40.9%) and hyponatremia in 8 patients (34.8%). Symptomatic vasospasm was noted in 7 of the 8 patients (87.5%) with hyponatremia, low density areas on CT in 4 patients (50%), the detection rate being high. The plasma ANP and ADH levels were 76.7 +/- 32.1 pg/ml and 2.2 +/- 0.7 pg/ml respectively in the patients with symptomatic vasospasm against 38.3 +/- 21.3 pg/ml and 2.4 +/- 0.6 pg/ml respectively without symptomatic vasospasm, the plasma ANP level being significantly high in the patients with symptomatic vasospasm (p < 0.01). The plasma ANP and ADH were 71.2 +/- 33.8 pg/ml and 2.0 +/- 1.1 pg/ml respectively in the patients with low density areas on CT against 51.2 +/- 31.3 pg/ml and 1.8 +/- 0.5 pg/ml respectively without low density areas on CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1992

Subtemporal transpetrosal approach to ruptured midbasilar trunk aneurysm.

Aneurysms arising from the midbasilar trunk are not common, and surgical management of these aneurysms remains a difficult challenge to neurosurgeons because of its anatomic characteristics. The authors report on a patient with a ruptured aneurysm arising from the basilar artery at the origin of the anterior inferior cerebellar artery and projecting to the right and upward. The aneurysm was successfully treated by a subtemporal transpetrosal approach in an acute stage.

Journal Article↗
PubMed1992

[Hyponatremia and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage].

We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. It was mild (126 to 130 mEq/l) in 15 patients, moderate (121 to 125 mEq/l) in 3 patients, and severe (116 to 120 mEq/l) in 1 patient. Cerebral vasospasm was evaluated by angiography, symptoms and CT finding. Angiographical vasospasm was found in 57 patients, symptomatic vasospasm in 38 patients and low density area on CT in 20 patients. Angiographical vasospasm developed in 15 of the 19 patients (78.9%) with hyponatremia, symptomatic vasospasm in 16 patients (84.2%), low density area on CT in 8 patients (42.1%), the difference being significantly high. (respectively, p < 0.01, p < 0.001 and p < 0.01 by chi-square test) Polyuria of 2500 ml or more immediately before the onset of hyponatremia developed in 14 patients (87.5%). When symptomatic vasospasm and hyponatremia coincided, there were only 4 patients in which symptomatic vasospasm was preceded by hyponatremia. So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.

Dehydration↗
PubMed1992

[A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia].

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.

Adult↗
PubMed1991

[CT and 123I-IMP SPECT findings of head injuries with hyponatremia].

CT and SPECT findings were examined and the relationship between development of hyponatremia and lesions was studied in cases who developed hyponatremia following head injury. Six cases of hyponatremia after head injury in the last two years were used as the subjects. SPECT was performed by the 123I-IMP intravenous injection method using Tomomatic 64. Slice 2 of 4 to 6 cm on the OM line in the early image was used as the subject site. The data of development of hyponatremia was 5.8 patients days, duration 9.2 days, minimum serum Na level 117.2 mEq/l and minimum plasma osmotic pressure 247.6 mOsm/lH2O. CT findings in the hyponatremic stage showed frontal subdural effusion in all the cases. SPECT findings revealed a decrease of CBF in the frontal region on both sides and in the central region. CBF in the central region also tended to improve at a time when hyponatremia improved. In hyponatremia after head injury, lesions are often found in the frontal region on CT, and CBF in the central region is also decreased bilaterally on SPECT, which is presumed to be concerned with the development of hyponatremia.

Adult↗
PubMed1991

[Serum ANP and ADH after subarachnoid hemorrhage and hyponatremia].

We determined serum atrial natriuretic peptide (ANP) and anti-diuretic hormone (ADH) on a time course basis in cases of subarachnoid hemorrhage and studied their influence on the development of hyponatremia. Twenty six cases of subarachnoid hemorrhage were admitted to our hospital in the past 1 year, and by the site of ruptured aneurysms, there were Acom 6 cases, ICA 6 cases, MCA 5 cases and VA BA 4 cases. Serum ANP and ADH levels were determined in the acute phase on Day 1-4, in the hyponatremia phase on Day 5-14 and in the chronic phase on Day 15 downward. Levels of not more than 130 mEq/l were regarded as hyponatremia. Cases showing other evident causes such as heart failure and renal insufficiency were excluded. In the normal control group (n = 20) which was admitted to this hospital for a close check-up, serum ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of more than 50 pg/ml were regarded as being abnormally high. 1) Hyponatremia was observed in 7 cases (26-9%); the day of onset was 11.9 hospital day. The duration was 5.0 days and the minimum serum Na level was 126.4 mEq/l. 2) The serum ADH level was high regardless of whether or not there was the development of hyponatremia in the acute phase but tended to decrease gradually and became normal in the hyponatremia phase. 3) The serum ANP level in the cases of hyponatremia was 40.7 +/- 9.1 pg/ml in the acute phase, 69.0 +/- 25.7 pg/ml in the hyponatremia phase and 40.2 +/- 21.5 pg/ml in the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1991

[Internal carotid artery stenosis and external carotid artery occlusion with unusual extracranial collateral pathway: case report].

A patient with stenosis of the internal carotid artery and occlusion of the external carotid artery associated with an unusual extracranial collateral pathway is presented. A 63-year-old man was hospitalized for sudden onset of black-out after urination. He was alert, and no neurological deficit was found. MRI showed multiple lacunae in the bilateral putamens. Cerebral angiogram demonstrated severe stenosis of the left internal carotid artery at its cervical segment and complete occlusion of the left external carotid artery at its origin. The ascending pharyngeal artery originated from the left internal carotid artery above its stenotic lesion and the superior thyroid artery originated from the left common carotid artery. The sternocleidomastoid branch from the left superior thyroid artery and the muscular branch from the left vertebral artery anastomosed with the muscular branch of the ascending pharyngeal artery. The ascending pharyngeal artery maintained patency of the internal carotid artery. It is important to perform vertebral angiography when there is proximal occlusion and severe stenosis of the internal carotid artery, and when the ascending pharyngeal artery has not been clearly identified as a branch from the ipsilateral external carotid artery on the common carotid angiogram.

Arterial Occlusive Diseases↗
PubMed1990

[An interesting case of pituitary apoplexy showing abnormality in water-electrolyte before and after surgery].

Cases which present abnormality in water-electrolyte before and after operation of pituitary adenoma are occasionally reported. The authors have encountered a case in which neurological symptoms became aggravated abruptly with pituitary apoplexy after admission, hyponatremia was noted before operation and polyuria, not hypotonic urine was observed after operation. As a result of an endocrinological examination which may have an influence on water-electrolyte (ADH, aldosterone, ANP, etc.) the ADH level in hyponatremia before operation was high at 6.8 pg/ml; so, it was taken as SIADH. According to a study at the time of polyuria after operation, the ADH level was normal at 2.4 pg/ml, the ANP level was abnormally high at 140 pg/ml and the specific gravity of the urine was kept at 1.010 or more. So, polyuria was considered due to abnormally increased content of serum ANP. In polyuria due to abnormally increased content of serum ANP, the osmotic pressure of the urine is maintained relatively well, which is a clinical feature evidently different from diabetes insipidus. After operation for pituitary adenoma, water-electrolyte should be controlled with polyuria due to abnormally increased content of serum ANP in addition to diabetes insipidus taken into consideration.

Atrial Natriuretic Factor↗