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Biomedical subjects

K Aritake

Publications and source records attributed to K Aritake.

12 recordsLinked to original sources
PubMed1999

Post-stroke treatment with imidapril reduces learning deficits with less formation of brain oedema in a stroke-prone substrain of spontaneously hypertensive rats.

The present study was undertaken to examine the effects of the ACE (angiotensin converting enzyme) inhibitor imidapril, on the brain, when administered after the onset of stroke in a stroke-prone substrain of spontaneously hypertensive rats (SHRSP). Learning deficits and induced lesions in the brain as well as in the kidneys and heart were investigated in detail. SHRSP were divided into two groups with or without salt loading at the age of 4 weeks. The salt loading was performed for 7-9 weeks to increase the incidence of stroke. Within 24 h after the first observation of stroke, animals were subsequently treated with 5 mg/kg imidapril orally once a day or the vehicle for up to the age of 27 weeks. Imidapril attenuated progression of neurological abnormalities such as irritability, hyperkinesia and motor dysfunction, and increased survival rate. In three-panel runway testing, learning deficits did not develop significantly in the imidapril-treated group, and was comparable to that in the non-salt-loaded/non-stroke group. Imidapril reduced oedema formation in the cortex, hippocampus and striatum, and also suppressed lesion formation in the kidneys and heart. Imidapril thus suppressed progression of neurological deficits with loss of learning ability following onset of stroke, and also suppressed formation of oedema in the brain and decreased the number of lesions in other organs. Imidapril-induced reduction of cerebrovascular damage, which presumably occurs in the brain after stroke, may account for the inhibitory effects of imidapril on lesion formation and learning impairment.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Pharmacological studies on the novel antiallergic drug HQL-79: I. Antiallergic and antiasthmatic effects in various experimental models.

The effects of oral administration of 4-benzhydryloxy-1-[3-(1H-tetrazol-5-yl)-propyl]piperidine (HQL-79), a newly synthesized antiallergic drug, in various experimental allergic and asthmatic models were investigated. HQL-79 markedly inhibited immediate hypersensitivity reactions such as passive cutaneous anaphylaxis in rats, antigen-induced bronchoconstriction and nasal vascular permeability in actively sensitized guinea pigs, like epinastine and ketotifen did. Airway eosinophilia in repeatedly antigen-exposed guinea pigs was suppressed by chronic administration of HQL-79 for 2 weeks. In another experiment, the antigen-induced late asthmatic response (LAR) in metyrapone-treated guinea pigs was also ameliorated by chronic treatment with HQL-79. Moreover, HQL-79 partially inhibited the toluene diisocyanate-induced delayed-type hypersensitivity (DTH) reaction in mice when administered chronically during the immunization period. The corticosteroid dexamethasone inhibited the airway inflammatory responses in guinea pigs and the DTH in mice. These results indicate that HQL-79 has potent inhibitory effects on the immediate hypersensitivity reactions, and when administered chronically, it also inhibits airway eosinophilia, LAR and DTH, similarly to corticosteroids.

Animals↗
PubMed1998

Pharmacological studies on the novel antiallergic drug HQL-79: II. Elucidation of mechanisms for antiallergic and antiasthmatic effects.

The effects of 4-benzhydryloxy-1-[3-(1H-tetrazol-5-yl)-propyl]piperidine (HQL-79), a newly developed antiallergic drug, on various chemical mediators and on chemical mediator release were investigated. Orally administered HQL-79 strongly inhibited the histamine-induced skin reaction in rats, and histamine- and 5-hydroxytryptamine (5-HT)-induced bronchoconstriction in guinea pigs. HQL-79 inhibited antigen-induced release of leukotriene (LT) B4, LTC4, histamine and prostaglandin (PG) D2 from the chopped lung tissues of actively sensitized guinea pigs. On the other hand, release of PGE2, one of the bronchoprotective prostanoids, was significantly enhanced by HQL-79. In an in vivo experiment, chronic administration of HQL-79 clearly reduced PGD2 contents and enhanced PGE2 contents in the lungs of repeatedly antigen-exposed guinea pigs. In biochemical studies, HQL-79 inhibited mouse spleen PGD synthase in a concentration-dependent manner. None of the antiallergics such as epinastine, terfenadine, oxatomide and cetirizine inhibited the PGD synthase. HQL-79 did not affect PGE synthase in sheep vesicular gland microsomes. These results suggest that antiallergic and antiasthmatic effects of HQL-79 could be ascribed to antihistaminic- and anti-5-HT effects, chemical mediator release inhibition, PGE2-release enhancement and PGD synthase inhibition. It is considered, in particular, that the differential modulation of PGD2 and PGE2 production is a conspicuous pharmacological feature of HQL-79.

Animals↗
PubMed1991

Correlation between bromodeoxyuridine-labeling indices and patient prognosis in cerebral astrocytic tumors of adults.

Bromodeoxyuridine (BUdR), a nonradioactive thymidine analogue, is taken up by cells in S-phase, and the ratio of BUdR-positive nuclei to the total number of cells counted is defined as the labeling index (LI). In this study, BUdR LI and the clinical course of 50 cerebral astrocytic tumors in adults were analyzed. The obtained LI distributed continuously in a broad range from 0% to 19%. The mean LI of 28 glioblastomas, 12 anaplastic astrocytomas, and ten astrocytomas were 8.5%, 4.2%, and 1.2%, respectively, and these differences were statistically significant (P = 0.05). In the analysis of LI and the recurrence-free period (RFP), regardless of the histologic findings, 23 patients with LI more than 5% had a median RFP of 9.0 months; the median RFP of nine patients with LI of 3% to 5% was 14.7 months. Nine of 13 patients with LI less than 3% have not yet recurred after a median follow-up of 36 months. These differences were also statistically significant by the generalized Wilcoxon test (P = 0.05). The proliferative potential reflected by the BUdR LI is a good clinical indicator for predicting the rate of tumor growth in cerebral astrocytic tumors. In combination with histologic diagnosis, BUdR LI could help in determining a patient's prognosis more precisely.

Adult↗
PubMed1990

[A case of surgical excision of intracerebral cavernous angioma in a patient with thrombasthenia].

A case of thrombasthenia (Glanzmann) associated with an intracerebral cavernous angioma in a 32-year-old woman is reported. Since her childhood, the patient had experienced a tendency to develop purpura following minor trauma. But she had not had major bleeding even during pregnancy and delivery. On April 4, 1987, she presented generalized convulsion. A high density mass in the right temporal lobe was demonstrated with CT scan. Carotid angiogram was normal except that the right anterior choroidal artery was stretched. Inhomogeneous signal intensities in T1- and T2-weighted MRI images were seen in the tumor locus. The clinical diagnosis was cavernous angioma which was complicated with intracerebral hemorrhage. The patient had a disorder of platelet function without thrombocytopenia. Her bleeding time was markedly prolonged. Because of this, we did not try surgical excision at first. During the 13-month observation period, however, intracerebral bleeding occurred 5 times. We decided to operate on the patient using fresh blood and platelet transfusion. The postoperative course was uneventful and pathological diagnosis confirmed cavernous angioma. We would like to emphasize possible pitfalls in treating cases of intracerebral angioma with thrombasthenia.

Adult↗
PubMed1989

[A case of acute spinal epidural hematoma in a patient with antiplatelet therapy].

The authors report a case of acute spinal epidural hematoma occurring in a patient receiving antiplatelet drugs. A 76-year-old man with a history of cerebral infarction had been taking antiplatelet agents for one year. He suddenly developed severe back pain which woke him from sleep, and numbness of his lower extremities was then noted. He was hospitalized 15 hours later. Neurological examination revealed flaccid paralysis of both lower extremities with negative Babinski's reflex, and sensory disturbance below the level of L1. The bleeding time and prothrombin time were prolonged. Computed tomographic (CT) scan revealed a biconvex, relatively hyperdense mass in the posterior spinal canal at the level of T12. Metrizamide myelography disclosed an incomplete blockage caused by an epidural mass at the level of T11. Post-myelographic CT scan demonstrated a sharply demarcated extradural filling defect at the level of T11. Seventeen hours after the onset of symptoms, an emergency laminectomy was performed extending from T12 to L3, and the epidural clot was totally evacuated. Histological examination of the capsule of the hematoma revealed no vascular anomalies. The patient made a good postoperative recovery. To the authors' knowledge, this is the first reported case of spontaneous intraspinal hemorrhage in a patient taking antiplatelet drugs. Acute onset of persistent pain anywhere along the spinal axis and the development of spinal neurological deficits in a patient on antiplatelet therapy should raise the suspicion of a spinal epidural hematoma. It should be stressed that prompt neuroradiological diagnosis and rapid surgical decompression are essential to allow good recovery. The present case illustrates that neurological emergencies can occur in patients receiving antiplatelet therapy.

Acute Disease↗
PubMed1986

[Cerebral hemodynamics in chronic hypoxic hypoxia].

The effects of chronic-hypoxic hypoxia on cerebral blood flow and its regulating mechanisms were investigated by means of intracardiac injection of radioactively labelled microspheres. In a gas chamber designed and constructed for the purpose, adult cats were exposed to stepwise decreasing inspiratory oxygen concentrations (for 4.5 months with a final O2 concentration of 8 vol%). Using animals adapted to hypoxic hypoxia, responsiveness of cerebral blood flow either to alterations in systemic arterial pressure (SAP) or to alterations in arterial blood oxygen tension (PaO2) were assessed. Flow measurement was done under three different conditions: normoxic normotension (PaO2 greater than 100 mmHg; SAP greater than 100 mmHg), hypoxic normotension (PaO2 = 30 mmHg; SAP greater than 100 mmHg), or normoxic hypotension (PaO2 greater than 100 mmHg; SAP = 60 mmHg). Hematocrit values continuously increased to 56% during the process of adaptation to hypoxia. There was also a remarkable increase in cardiac output of hypoxia-adapted animals subjected to hypoxia and to normoxia. Chronic-hypoxic hypoxia led to increased cerebral blood flow, which persisted even when animals were returned to normoxia. Under hemorrhagic hypotension, cerebral blood flow fell significantly in animals adapted to chronic-hypoxic hypoxia but did not fall short of the absolute values in controls. The relative reduction in cerebral blood flow might be attributable to the decrease in cardiac output and to altered blood viscosity. This implied that, even in animals subjected to long-standing graded hypoxic hypoxia, autoregulatory capacity might be partly preserved.

Adaptation, Physiological↗
PubMed1983

[Peroxidation of arachidonic acid and brain edema].

Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the intracerebral injection of AA is associated with the injury of the surrounding brain tissues such as brain edema. Rats received the intracerebral injection of 10 microliters of test solution (160 microgram of AA emulsified in 1% bovine serum albumin, BSA) or the same volume of BSA as the control. The measurement of specific gravity (SG) (74 rats) and the local CBF by H2 clearance technique (21 rats), and electron microscopical studies with tracers (Evans blue and horseradish peroxidase, HRP) (24 rats) were carried out. The effect of pretreatment with indomethacin (PI, 10 mg/kg) was evaluated in separate groups. AA transiently produced a significant decrease in SG and in 1CBF adjacent to the injection sites (p less than 0.01). The increased pinocytotic transportation, an accumulation of edema fluid containing HRP in extracellular space and endothelial injuries were observed only after AA injection. The above-mentioned falls in SG and in 1CBF, and the extravasation of HRP were inhibited by PI. The fact that PI prevented the edema formation, 1CBF change and the disturbance of blood-brain barrier induced by AA, indicates that peoxidation of AA through the arachidonate cascade is involved in the mechanism of brain edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Selective destruction of the outer leaflet of the capillary endothelial membrane after intracerebral injection of arachidonic acid in the rat.

A peculiar ultrastructural change of the cytoplasmic membrane is described. It concerns selective destruction of the outer leaflet of the luminal side of the capillary endothelium in the white matter of the rat brain, 30 min and 3 h after intracerebral injection of arachidonic acid (AA). The cristae of the mitochondria disappeared in the endothelium of many capillaries. These changes were observed mainly in the central part of brain edema, where the extracellular space was markedly widened. The possible mechanism whereby these changes developed is discussed.

Animals↗
PubMed1982

[Computed tomographic measurement of regional cerebral blood flow by xenon enhancement (author's transl)].

The present study was conducted to overcome some of disadvantages of cerebral blood flow study by radionuclide, such as poor regionality of flow values and errors involved in pathological brains. Serial CT scanning was carried out during and after inhalation of 50 to 70% non-radioactive xenon in humans. Diffusible gas with high atomic number enhanced gray matter first 19 +/- 4 HU (mean +/- SD) on an average in Hounsfield unit (HU) and later white matter 24 +/- 4 HU. In seven normal subjects, blood flow in gray matter was 82 +/- 11 and that in white matter 24 +/- 5 ml/100 gm/min. Partition coefficient which is not readily obtainable by radionuclide study was 0.9 +/- 0.1 in normal gray matter and 1.4 +/- 0.2 in normal white matter. Two cases were presented to show k-map (clearance rate), lambda-map (partition coefficient) and CBF map, which displayed images of values calculated automatically, in black and white or color on CRT. The first case was a patient with metastatic brain tumor from lung in the left parietal region. The blood flow of the tumor was close to that of gray matter, whereas blood flow of edematous white matter surrounding the tumor was decreased to below 10 ml/100 g/min with partition coefficient ranged from 0 to 0.9. The second case was presented to demonstrate the resolution of the blood flow map obtained by this method. Multiple lacunar infarcts of the basal ganglia and white matter in the size of 1 to 3 mm, which were hardly identified on regular CT picture, were well visualized on CBF map. This method appeared to have several advantages over conventional isotope method and to provide useful clinical and research informations.

Aged↗
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↗