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Biomedical subjects

O Uyama

Publications and source records attributed to O Uyama.

36 records · Page 2Linked to original sources
PubMed1990

Protective effects of superoxide dismutase on acute reperfusion injury of gerbil brain.

It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and could cause brain edema and cell death. This study was undertaken in an attempt to examine the effect of recombinant human superoxide dismutase, a scavenger of superoxide radicals, on survival outcome and brain edema in gerbils undergoing 1-hour bilateral carotid occlusion and reperfusion. Superoxide dismutase was continuously infused over either 1 or 3 h of reperfusion. Neither low dose (100,000 U/kg bolus followed by 100,000 U/kg/h continuous infusion) nor high dose (100,000 U/kg bolus followed by 800,000 U/kg/h) recombinant human superoxide dismutase had an effect upon water and sodium content of whole brain at 1 h of reperfusion following 1 h of ischemia, but high-dose treatment effectively reduced brain water content at 3 h of reperfusion. All gerbils receiving high-dose treatment survived the 3 h of reperfusion, while 4 of the 7 gerbils in the control group died between 2 and 3 h of reperfusion (p less than 0.05). From this study, we conclude that prophylactic administration of superoxide dismutase can reduce the delayed vasogenic edema developing at 3 h of reperfusion and afford significant cerebroprotection in these models of transient global ischemia.

Animals↗
PubMed1990

Effects of hydrocortisone and aminophylline on plasma leukotriene C4 levels in patients during an asthmatic attack.

To study the role of leukotriene C4(LTC4) and the effect of hydrocortisone and aminophylline on plasma LTC4 levels in patients with asthmatic attacks, we measured LTC4 in plasma of 18 asthmatics during a wheezing attack and of 7 normal subjects. Blood samples were obtained before and after treatment with aminophylline and/or hydrocortisone injections. We extracted LTC4 using a Sep-Pak C18 cartridge for the measurement of LTC4 by radioimmunoassay. The plasma levels of immunoreactive LTC4 (i-LTC4) of the normal subjects were 142 +/- 25 pg/ml (n = 7), while those of nonatopic type asthmatic patients with wheezing attacks were 208 +/- 68 pg/ml (n = 15) (p less than 0.01). Before and after treatment with both hydrocortisone succinate (100 mg) and aminophylline (250 mg), 6 asthmatic patients with wheezing attacks had a mean plasma level of i-LTC4 181 +/- 24 and 132 +/- 18 pg/ml (p less than 0.01), respectively. On the other hand, the treatment with aminophylline 250 mg alone increased the i-LTC4 levels from 178 +/- 19 pg/mg to 213 +/- 16 pg/mg (n = 6)(p less than 0.05), while treatment with hydrocortisone succinate 100 mg decreased the i-LTC4 level 0.05 from 284 +/- 99 pg/ml to 249 +/- 85 pg/ml (n = 4)(p less than 0.05). In conclusion, the present study shows that the i-LTC4 level in venous blood of patients with asthmatic attacks is decreased significantly by treatment with hydrocortisone succinate.

Adult↗
PubMed1990

[Severe bronchial reaction induced by hydrocortisone sodium succinate in an aspirin-sensitive asthmatic patient].

This is a report of a female patient who had an anaphylaxis-like reactions to hydrocortisone sodium succinate (Saxizon). A 31-year-old female with intrinsic bronchial asthma and aspirin sensitivity was admitted to our hospital because of an episode of asthmatic attack. The patient had had episodes of dyspnea since 1976, and had been treated with oral bronchodilators and intermittent corticosteroids. After admission, she was given 100 mg of hydrocortisone sodium succinate intravenously. A few minutes later she developed severe bronchospasm and lost consciousness. An endotracheal tube was inserted and she was mechanically ventilated for 2 hours. The patient recovered after 1 hour. An inhalation challenge test with Sulpyrin was positive. When the provocation challenge test with 100 mg of hydrocortisone sodium succinate (Saxizon) injection was performed, she developed subjective and objective evidence of bronchospasm. Intradermal skin test revealed positive immediate reactions to Saxizon, Solu-cortef, Predonine. It is suggested that she had immediate hypersensitivity to hydrocortisone sodium succinate, but the mechanism of this anaphylaxis-like reaction to steroids is not certain.

Adult↗
PubMed1988

Quantitative evaluation of vascular permeability in the gerbil brain after transient ischemia using Evans blue fluorescence.

Mongolian gerbils were used to evaluate brain edema during restoration of flow following bilateral carotid occlusion for 1 h. We have modified the method for fluorometric measurement of Evans blue to monitor vascular protein leakage (vasogenic edema). The extraction of extravasated Evans blue was performed by homogenizing the whole brain in 50% trichloroacetic acid. The supernatant was diluted fourfold with ethanol and the Evans blue fluorescence was measured. The tissue blank was negligible. Evans blue content of the plasma was similarly determined and the ratio of tissue to plasma Evans blue content was calculated. Furthermore, Evans blue fluorescence was used for microscopic investigation. It is suggested that Evans blue fluorescence can be applied for quantification of protein leakage with much more sensitivity and accuracy than the colorimetric absorbance method, as well as for tissue localization of protein leakage.

Animals↗
PubMed1985

The effect of isosorbide dinitrate and isosorbide-5-mononitrate on prostacyclin (PGI2) and thromboxane A2 (TXA2) generation in rat and human arteries.

The mechanism by which nitrates produce relaxation of the vascular smooth muscle and anti-aggregatory effect on platelets has not been understood. Several reports have suggested that vasoactive prostaglandin generation may account for part of the pharmacological action of nitroglycerin. However, few studies have been reported that isosorbide dinitrate or its main metabolite, isosorbide-5-mononitrate, directly stimulates prostacyclin (PGI2) generation in blood vessels. We examined the effect of ISDN and 5-ISMN on PGI2 and thromboxane A2 (TXA2) generation in rat thoracic aorta and human thoracic aorta and coronary artery. The stimulation of PGI2 generation was dependent on the concentration of ISDN and the maximum PGI2 generation was effected by ISDN 5.0 ng/ml in both rat and human vessels. The ratio of peak to basal PGI2 generation was about 1.6 with rat thoracic aorta and about 1.6 with human thoracic aorta and about 1.3 with human coronary artery. On the other hand, TXA2 generation showed a smaller increase than that of PGI2 with ISDN used in the therapeutic dose range and 5-ISMN did not significantly affect PGI2 or TXA2 generation. Previous studies of the effect of cyclooxygenase inhibitor, for example indomethacin, on the vasodilating response to nitrates have given conflicting results. It is believed, however, that ISDN is partially, not wholly, associated with the hemodynamic and platelet antiaggregation effects due to vascular PGI2 generation, which may play a beneficial role in inhibiting coronary vasospasm during anginal attacks.

Aged↗
PubMed1984

Platelet accumulation in carotid atherosclerotic lesions: semiquantitative analysis with indium-111 platelets and technetium-99m human serum albumin.

To evaluate platelet accumulation in carotid atherosclerotic lesions semiquantitatively, a dual-tracer technique was applied, using In-111 platelets and Tc-99m human serum albumin. With this approach, we investigated the ratio of radioactivity in In-111 platelets deposited on the vascular wall to those circulating in the blood pool, platelet accumulation index ( PAI ). This study included 12 normal subjects and 25 patients with ischemic cerebrovascular disease (CVD). Angiographic abnormalities were observed at 34 of 50 carotid bifurcations in the CVD patients. The mean PAI value was significantly higher at the carotid bifurcations with angiographic abnormality than at the normal ones (p less than 0.001). Furthermore, elevations of mean PAI were prominent at the lesions with severe stenosis or ulceration. The degree of platelet accumulation was well demonstrated by this technique, which can also yield information on thrombogenicity and efficiency of antiplatelet therapy in carotid atherosclerotic disease.

Adult↗
PubMed1984

[A case of normal pressure hydrocephalus associated with cerebrovascular disorders].

There has been much argument in recent years about the diagnostic and pathogenetic differences between normal pressure hydrocephalus (NPH) and vascular dementia (Multi-infarct dementia) or Binswanger's disease. We experienced an interesting patient, a 54-year-old male, who had left hemiparesis due to two past attacks of cerebral infarction and possible hydrocephalus had been pointed out by CT findings in 1981. He was seen on May 22, 1982, with the chief complaints of dementia, gait disturbance and urinary incontinence. He had the clinical and pathogenetic features, common to NPH and MID or Binswanger's disease. The followings were observed. These symptoms (dementia, gait disturbance, urinary incontinence) and computed tomographic findings (bilateral ventricular dilatation, periventricular lucency), as is often the case in NPH, are at times similar to those of MID or Binswanger's disease and it is difficult to distinguish NPH from MID or Binswanger's disease. We consider that there are probably many patients who are on the borderline of these three diseases. For treatment, the V-P shunt was very effective in combination with the preceding bilateral STA-MCA shunt but it is not clear whether the preceding STA-MCA shunt was required before the V-P shunt. We believe that the clinical symptoms will not appear until the ventricle is dilated to a critical degree. There was a correlation between the degree of dementia and Huckman number, one of the assessment methods for ventricular dilatation.

Brain↗
PubMed1983

Role of prostacyclin in the response of cerebral blood flow to CO2.

The prostacyclin (PGI2) formation in cerebral vessels, as reflected by the difference in concentration of internal carotid arterial and internal jugular venous radioimmunoassayed 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), was determined under normocapnic and hypercapnic conditions in 5 patients with mild cerebral thrombotic infarction. There was no evidence that endogenous PGI formation in cerebral vessels was stimulated at mild hypercapnia, while an increase of cerebral blood flow (CBF) induced by hypercapnia was observed. These results suggest that endogenous PGI2 may not be a mediator for the response of CBF to CO2.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Platelet hyperaggregability in ischemic cerebrovascular disease and effects of aspirin.

Platelet aggregation was studied in 24 patients in the chronic stage of ischemic cerebrovascular disease (CVD), with cerebral affluent and effluent blood, i.e., carotid arterial and internal jugular venous blood, and also with peripheral venous blood. Aggregation tests were performed at various final concentrations of sodium arachidonate (A.A.) and ADP. In 17 patients, not taking aspirin, platelet aggregability in jugular venous blood was significantly accentuated compared with that in arterial and peripheral venous blood. This tendency was more marked in the patients with cerebral artery stenosis and/or occlusion than in those with normal cerebral angiogram. In 7 patients taking 500 mg or more oral aspirin, aggregation differences across the brain were not observed and A.A. aggregation and the second phase of ADP aggregation were completely suppressed. These results suggest that a prophylactic administration of aspirin may be beneficial for patients in chronic stage of CVD.

Arteries↗
PubMed1982

Regional blood flows measured in Mongolian gerbil by a modified microsphere method.

Regional blood flow to major organs and regional cerebral blood flow were determined in seven anesthetized male gerbils by a modified microsphere method. Carbonized microspheres, 15 micrometers in diameter and labeled with 85Sr or 141Ce, were injected into the left ventricle by cardiac puncture through the closed thorax, and reference samples of known volume were withdrawn from tail-artery cannula. No significant hemodynamic alterations were observed during microsphere administration, and extraction of 15-micrometers microspheres by the pulmonary or systemic capillary beds was nearly 100%. The adequacy of mixing of microspheres in the left ventricle was also validated. The absolute regional blood flow to various organs and regional cerebral blood flow were expressed in terms of milliliters per minute per gram tissue weight, and the values mostly agreed with those reported previously in rats. The results indicate that the reference sample method can be applied to the gerbil. This method should allow the gerbil, which is an animal widely used in stroke research, to be conveniently used for hemodynamic studies when organ blood flow and regional cerebral blood flow are necessary.

Adrenal Glands↗
PubMed1981

Platelet aggregation induced by arachidonic acid and thromboxane generation in patients with hypertension or cerebrovascular disease.

The aggregability of platelets to arachidonic acid (AA) was investigated in 26 control subjects, 40 patients with essential hypertension, 20 patients with ischemic cerebrovascular diseases (CVD) not taking aspirin and 11 patients with CVD taking aspirin. The aggregability of platelets was evaluated on the basis of threshold concentrations of AA to induce irreversible platelet aggregation. The enhanced sensitivity of platelets to AA was observed more frequently in hypertensives and/or CVD patients not taking aspirin than in the controls. The relationship between platelet aggregation induced by AA and thromboxane B2 (TXB2) formation from AA or prostaglandin H2 (PGH2) in platelets was also studied in the subjects taking or not taking aspirin. It was proposed that the assessment of platelet aggregability with AA could provide a tool for identifying a subgroup of patients who might substantially benefit from the secondary preventive treatment with aspirin or other anti-platelet drugs. The clinical usefulness of this aggregation test for the management of the patients taking aspirin was also discussed.

Adolescent↗
PubMed1981

Diurnal variations in monoamine contents in discrete brain regions of the mongolian gerbil (Meriones unguiculatus).

Under controlled conditions of environmental light and darkness of 12:12 h, the concentrations of noradrenaline, dopamine, and serotonin in six brain regions (i.e., cortex, hippocampus, striatum, midbrain including hypothalamus, pons-medulla oblongata, and cerebellum) of the male Mongolian gerbil, an animal widely used in stroke research, were measured fluorometrically at different times of the day. The significant daily fluctuations in these monoamine concentrations were observed in cortex, striatum, hippocampus, midbrain including hypothalamus, and pons-medulla oblongata. Thus, diurnal variations have to be taken into account when studying the effects of ischemia on the change of monoamine concentrations in these brain areas of the gerbil.

Animals↗
PubMed1980

Thromboxane generation in patients with essential hypertension or cerebrovascular disease and effect of oral aspirin.

The ability of platelets to synthesize thromboxane B2 (TxB2) from arachidonic acid (AA) or prostaglandin H2 (PGH2) was studied in 26 control subjects, 40 patients with essential hypertension, 20 patients with cerebrovascular disease (CVD) not taking aspirin and 11 patients with CVD taking aspirin. The activity of platelets to form TxB2 from AA or PGH2 was measured using 1-14C arachidonic acid or 1-14C PGH2 as a substrate. There was no significant difference in TxB2 generation from AA or PGH2 among the platelets collected from the control subjects, hypertensive patients and CVD patients not taking aspirin. In CVD patients taking aspirin, marked suppression was observed in TxB2 synthesis from AA, but no suppression in TxB2 synthesis from PGH2. At least 750 mg aspirin per day were required for nearly complete suppression of TxB2 generation from AA.

Adolescent↗
PubMedDate not supplied

Plasma concentrations of 6-keto-prostaglandin F1 alpha in patients with hypertension, cerebrovascular disease or Takayasu's arteritis.

The peripheral venous plasma levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined by radioimmunoassay in 23 control subjects, 14 patients with essential hypertension, 19 patients with cerebrovascular disease (CVD) not taking aspirin, 12 patients with DVD taking aspirin, and 12 patients with Takayasu's arteritis. There was no significant difference in 6-keto-PGF1 alpha levels between the control subjects and hypertensive patients. In CVD patients and patients with Takayasu's arteritis, the plasma 6-keto-PGF1 alpha levels were significantly lower than those in control subjects. The internal jugular venous and femoral arterial plasma levels of 6-keto-PGF1 alpha and thromboxane B2 (TxB2) were measured in 10 CVD patients not taking aspirin. The patients with occlusive lesions of major arteries exhibited higher TxB2/6-keto-PGF1 alpha ratios in the internal jugular venous plasma.

Adolescent↗
PubMedDate not supplied

The effect of a thromboxane synthetase inhibitor, OKY-046, on urinary excretion of immunoreactive thromboxane B2 and 6-keto-prostaglandin F1 alpha in patients with ischemic cerebrovascular disease.

Thromboxane synthetase activity is selectively inhibited by (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate (OKY-046). A single dose of 100 mg OKY-046 was orally administered to patients with ischemic cerebrovascular disease and healthy volunteers. Platelet aggregation and thromboxane B2 (TXB2) generation of intact and homogenised platelets induced by 1.0 mM sodium arachidonate were measured before and at 1, 4, 6 and 8 h after dosing. OKY-046 inhibited arachidonate-induced aggregation in platelet rich plasma from some, but not all, individuals, whereas platelet TXB2 generation was almost completely inhibited by a single dose of 100 mg OKY-046, in all of the patients and healthy volunteers. Endogenous TXA2 and prostacyclin (PGI2) biosynthesis were assessed by measurement of urinary immunoreactive TXB2 (i-TXB2) and 6-keto-PGF1 alpha (i-6-keto-PGF1 alpha) before and at 0-3, 3-6, 6-9 h after dosing. OKY-046 increased the urinary i-6-keto-PGF1 alpha coincidently with a decrease of urinary i-TXB2, both in patients and healthy volunteers. These effects of a selective thromboxane synthetase inhibitor will improve a disturbed balance between TXA2 and PGI2, associated with the development of ischemic cerebrovascular disease.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

A new approach to antithrombotic therapy--evaluation of combined therapy of thromboxane synthetase inhibitor and very low dose of aspirin.

The effect of a selective thromboxane (TX) synthetase inhibitor (OKY-046), alone and in combination with a very low dose of aspirin, on the platelet function was studied in healthy and diseased subjects. A single dose of 100 mg OKY-046 was orally administered to patients with ischemic cerebrovascular disease (CVD) and healthy volunteers. TXB2 generation and platelet aggregation were measured before and at 1, 4, 6 and 8hr after dosing. In addition, after the administration of a very low dose of aspirin (0.1-0.25 mg/kg/day) for at least one month, a single dose of OKY-046 was given to CVD patients. TXB2 generation and platelet aggregation were measured in the same manner as OKY-046 alone. The effect of OKY-046 on platelet aggregation induced by arachidonic acid (AA) was different in each subject whereas platelet TXB2 generation was almost completely inhibited in all of the patients and healthy volunteers. OKY-046 had a slight inhibitory effect on collagen induced aggregation. A combination of OKY-046 with a very low dose of aspirin, on the other hand, produced additional inhibition of the platelet aggregation induced by both AA and collagen. The present results suggest that the accumulation and metabolism of cyclooxygenase products that accumulate when TX synthetase is blocked, differ in each subject, additional inhibition is caused by the combined use of TX synthetase inhibitor and a very low dose of aspirin because the very low dose of aspirin partially reduces the proaggregatory cyclooxygenase products that accumulate when TX synthetase is blocked.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylates↗
PubMedDate not supplied

Effect of aspirin and ticlopidine on platelet deposition in carotid atherosclerosis: assessment by indium-111 platelet scintigraphy.

The antiplatelet effects of aspirin and ticlopidine were studied by a dual-tracer method, using indium-111 labeled platelets and technetium-99m human serum albumin, in a group of 12 patients with suspected ischemic cerebrovascular disease. The magnitude of platelet accumulation at the carotid bifurcation was expressed as the ratio of radioactivity of indium-111 platelets deposited on the vascular wall to those circulating in the blood-pool (PAI, platelet accumulation index), 48 hr after injection of labeled platelets. PAI values were measured before (baseline studies) and after the antithrombotic therapies (aspirin studies: 325 mg bid for 22.3 +/- 1.3 days, ticlopidine studies: 100 mg tid for 21.8 +/- 2.1 days). At the baseline, the mean PAI value at 24 carotid bifurcations in the patient group was 15.7 +/- 15.3% (mean +/- S.D.) compared to -4.3 +/- 9.1 at 24 carotid bifurcations in 12 normal subjects (p less than 0.01). We defined the upper limit for a normal PAI (%) value to be +13.9, namely the mean PAI plus 2 SD for the carotid bifurcation in normal subjects and used this value for semiquantitative analysis. At the baseline, significant elevation of PAI (more than 13.9%; positive scintigram) was observed at 12 of 24 vessels, while 12 other regions were negative (less than 13.9%). In the lesions with positive scintigraphic results at the baseline, the mean PAI (%) value from the baseline, aspirin and ticlopidine studies was 29.5 +/- 7.0, 11.2 +/- 8.5 (p less than 0.01 versus baseline) and 21.4 +/- 21.3 (not significant from baseline), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗