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S Ono

Publications and source records attributed to S Ono.

At least 379 records · Page 21Linked to original sources

Adhesion molecule CD18 on polymorphonuclear cells correlates to the lung injury caused by continuous infusion of endotoxin in sheep.

We investigated the mechanisms of increase in the pulmonary vascular permeability, focusing on the changes in the peripheral white blood cell (WBC) counts and the surface expression of CD18 on polymorphonuclear cells (PMNs). Anesthetized sheep with chronic lung lymph fistulas were used in this study. We infused synthetic endotoxin (LPS) at a rate of 10 ng/kg/min (i.v.) continuously for 24 hr. We measured lung lymph flow, lymph-to-plasma protein concentration ratio and WBC counts in blood and lung lymph, and the PMNs' surface expression of CD18 before and at 2, 10 and 24 hr after the start of endotoxin infusion, respectively. CD18 was analyzed by flow cytometry using monoclonal anti-CD18 antibody. We found that the pulmonary vascular permeability increased during 2-4 hr after the start of endotoxin infusion, and returned to the baseline over 10 hr. At time 2 hr period, the number of WBCs in the lung lymph increased, the number of peripheral WBCs, mostly PMNs, decreased and the surface expression of CD18 on the peripheral PMNs was up-regulated. At time 10 and 24 hr, the number of WBCs in lung lymph decreased, the number of peripheral WBCs increased and CD18 expression was down-regulated. These data indicate that up-regulation of CD18 expression promotes the PMN adherence to the pulmonary endothelium, migration into the lung and increases the pulmonary vascular permeability. We conclude that the continuous endotoxin infusion up-regulates CD18, which contributes to the PMN migration into the lung.

Animals↗

[Effects of prostaglandin E1 (PGE1) on pulmonary hypertension and lung vascular remodeling in a rat monocrotaline model of human pulmonary hypertension].

Prostaglandin E1 (PGE1) has been shown to be a potent pulmonary vasodilator in humans and in many animals. The effects of PGE1 on the development of pulmonary hypertension and on pulmonary vascular remodeling were studied in a rat monocrotaline (MCT) model of human pulmonary hypertension. By 3 weeks after injection, MCT (80 mg/kg S.C.) had resulted in high values of mean pulmonary arterial pressure and of the ratio of right ventricular weight to left ventricle+septum weight (RV/LV+S). PGE1 inhibited the development of pulmonary hypertension (300 micrograms/kg) and right ventricular hypertrophy (300 and 100 micrograms/kg) induced by MCT. Three weeks after the injection, the media walls of pulmonary arteries in lungs from rats given MCT were significantly thicker than those from lungs of control rats. PGE1 (300, 100, and 30 micrograms/kg) resulted in significantly less of this morphologic change, in a dose-dependent manner. These results indicate that PGE1 inhibits the development of pulmonary hypertension associated with lung vascular thickening induced by MCT. PGE1 may be useful for the treatment of pulmonary hypertension in humans.

Alprostadil↗

[Effect of adhesiveness of white blood cells on pulmonary vascular permeability and resistance].

We studied pulmonary vascular injury evoked by mechanically activated white blood cells (WBCs). In isolated perfused rat lungs, changes in pulmonary vascular resistance were measured, and a gravimetric method was used to measure the pulmonary vascular filtration coefficient, which was taken as an index of pulmonary vascular injury. WBCs were activated by gentle agitation in a glass container for 10 sec. The filtration coefficient was measured under baseline conditions, and then inactive or activated WBCs were added to the perfusate. The perfusion was stopped for 90 minutes and then the lungs were reperfused. The expression of CD18 on the surface of WBCs was measured by flow cytometry. The filtration coefficient and the pulmonary vascular resistance in lungs exposed to activated WBCs were about 2.5 times and 3.3 times higher, respectively, than those in the lungs exposed to inactive WBCs. These results indicate increases in resistance and in pulmonary vascular permeability. The results of flow cytometry indicated that the mechanical agitation increased the expression of CD18 on the surface of WBCs. In conclusion, WBCs in which adhesiveness has been increased can induce pulmonary vascular injury and can increase pulmonary vascular resistance.

Animals↗

A small dose of human parathyroid hormone(1-34) increased bone mass in the lumbar vertebrae in patients with senile osteoporosis.

Intermittent treatment with human parathyroid hormone (hPTH) has been shown to increase cancellous bone mineral density (BMD) in osteoporosis, but its effects on cortical bone remain controversial. In this study, the effects of hPTH(1-34) administered at a dose of 6 micrograms (20 units) per day subcutaneously for 26 weeks were investigated in 16 patients with senile osteoporosis. The changes in BMD in lumbar vertebrae were measured using dual energy x-ray absorptiometry. BMD in the second metacarpal bone was simultaneously measured with radiogrammetry to find changes in BMD in cortical bone. Serum and urinary biochemical parameters were also evaluated. The lumbar BMD increased significantly at the end of the treatment without decrease in the cortical bone mass. Biochemical markers of bone formation were also elevated, while markers of bone resorption did not show striking changes during the treatment. In conclusion, daily administration of low doses of hPTH(1-34) stimulated bone formation and increased bone mass in patients with senile osteoporosis without combination with another therapeutic agent.

Aged↗

[A hemodialysis patient with HTLV-1-associated myelopathy (HAM)].

We report here a case of maintenance hemodialysis with HTLV-1 associated myelopathy (HAM). A 53-year-old female hemodialysis patient was admitted to Teikyo University Ichihara hospital because of paralytic ileus. She had a history of blood transfusion and had been under dialysis treatment for 8 years. She had experienced gait disturbance and sensory disturbance in her lower extremities for 8 years. Neurological examination revealed myelopathy and neuropathy. Laboratory data revealed that serum anti-HTLV-1-antibody was over 1260 x (PA) and liquor HTLV-1-antibody was over 160 x (PA). Her liquor revealed a cell count of 4/3 cmm, protein 22 mg/dl, glucose 45 mg/dl, chloride 125 mEq/l and no atypical cells. To the best of our knowledge this is a rare case in Japan. Our findings suggest that HAM should be taken into consideration when we diagnose a maintenance hemodialysis patient showing neuropathy and myelopathy.

Female↗

Modulation of B-cell abnormalities in lupus-prone (NZB x NZW)F1 mice by normal bone marrow-derived B-lineage cells.

(NZB x NZW)F1(NZB/WF1) mice spontaneously develop an autoimmune disease characterized by abnormality of haemopoietic stem cells. The present study examined a possible regulatory cell interaction between NZB/WF1 and normal bone marrow cells using radiation-induced chimeras. We demonstrated that the ability of NZB/WF1 bone marrow cells to transfer the typical disease with hypergammaglobulinemia including autoantibodies into lethally irradiated normal recipients was prevented by cotransfer of bone marrow from normal CBA/J mice but not from xid CBA/N mice carrying a selective defect in B-cell function. Flow cytometric analysis revealed that the generation of NZB/WF1 cells was reduced in the mixed chimeras given CBA/J but not CBA/N bone marrow cells. Interestingly, radiation chimeras reconstituted with a mixture of NZB/WF1 bone marrow and CBA/J splenic B cells did not show elevation of serum immunoglobulin levels, although most of the spleen cells were dominated by NZB/WF1 cells. On the other hand, NZB/WF1 B cells maturated in vivo in the presence of CBA/J bone marrow or splenic B cells lost the hyper-responsiveness to lipopolysaccharide (LPS) in the autoantibody production in vitro. These results suggest that radiosensitive normal B-lineage cells have the regulatory activity to ameliorate the hypergammaglobulinemia of NZB/WF1 mice by reducing the generation of NZB/WF1 B cells and/or by correcting their hyper-responsiveness, and that NZB/WF1 mice may have a defect(s) in the regulatory cell function. In addition, CBA/J splenic B cells were shown to modulate the B-cell abnormality even when injected into non-irradiated NZB/WF1 mice manifesting autoimmunity.

Animals↗

[General pharmacology of T-3761, a new oral quinolone antibacterial agent (1). Effect on the central nervous system].

General pharmacological effects of T-3761, a new oral quinolone antibacterial agent, on the central nervous system were investigated in laboratory animals. The results obtained are summarized as follows. 1. T-3761 exerted no significant effects on spontaneous motor activity, motor coordination, pentobarbital-induced hypnosis, electroshock-, pentetrazole- or strychnine-induced convulsion, acetic acid-induced writhing responses, reserpine-induced hypothermia and ptosis in mice at oral doses of 100, 300 and 1,000 mg/kg. The same oral doses of T-3761 exerted no significant effects on body temperature and passive avoidance response in rats. 2. T-3761 had no effects on EEG in cats and spinal reflex in rats at intravenous doses of 10, 30 and 100 mg/kg. 3. Convulsions were not observed in mice after any oral combinations of T-3761 at a dose of 200 or 1,000 mg/kg with 14 different nonsteroidal anti-inflammatory drugs (NSAIDs) including fenbufen. 4. An oral combination of T-3761 even at a higher doses of 3,000 mg/kg with 4-biphenylacetic acid (BPAA) which is a principally active metabolite of fenbufen also did not induce convulsions in mice. 5. T-3761 did not inhibit GABA receptor binding in rat brain synaptic membranes at 10(-4) M in either the absence or presence of BPAA. These results suggest that T-3761 is an antibacterial agent which would be unlikely to produce any side effects on the central nervous system and to produce convulsion when combined with NSAIDs in clinical use.

Animals↗

[General pharmacology of T-3761, a new oral quinolone antibacterial agent (2). Effect on the respiratory and cardiovascular systems, autonomic nervous system and other functions].

General pharmacological effects of T-3761, a new oral quinolone antibacterial agent, on the respiratory and cardiovascular systems, autonomic nervous system and other functions were investigated in laboratory animals. The results obtained are summarized as follows. 1. Respiratory and cardiovascular systems: Oral administration of T-3761 at doses of 100-1,000 mg/kg did not affect in conscious rats. But intravenous administration of T-3761 at doses of 10-100 mg/kg caused an increase in respiratory rate, induced hypotension, caused increase or decrease in heart rate and altered ECG patterns (elevation of T waves and reduction of voltage of QRS complexes, etc.) in anesthetized dogs. Intravenous administration of T-3761 at doses of 10-100 mg/kg showed respiratory rate increase or decrease, hypertension, heart rate decrease and ECG patterns changes (T waves elevation and extrasystole) in anesthetized rabbits. 2. Autonomic nervous system and smooth muscle organs: T-3761 increased the epinephrine-induced contraction of the isolated guinea pig vas deferens at concentration of 10(-5)-10(-4) g/ml. T-3761 decreased the acetylcholine-induced contraction of the isolated guinea pig ileum and epinephrine-induced relaxation of the isolated guinea pig trachea-chain at concentration of 10(-4) g/ml. T-3761 increased the norepinephrine-induced contraction of the isolated rabbit thoracic aorta at concentration of 10(-4) g/ml. Oral administration of T-3761 at a dose of 1,000 mg/kg exerted slight mydriasis in mice. 3. Digestive system: T-3761 decreased the spontaneous motilities of isolated ileum and colon at concentration of 10(-4) g/ml. Oral administration of T-3761 at a dose of 1,000 mg/kg inhibited gastric output and intestinal transit time in rats or mice. 4. Renal functions: Oral administration of T-3761 at a dose of 300 mg/kg increased Na+ excretion but did not affect PSP excretion in rats. 5. Hematological examinations: T-3761 showed no effects on resistance to hemolysis, blood coagulation and platelet aggregation in rabbits at concentration of 10(-6)-10(-4) g/ml. Oral administration of T-3761 at dose of 100-1,000 mg/kg did not affect bleeding time or blood glucose level in rats. 6. Miscellaneous effects: Intravenous administration of T-3761 at a dose of 100 mg/kg slightly inhibited the twitch tension of gastrocnemius in anesthetized rats. Oral administration of T-3761 at doses of 300-1,000 mg/kg exerted slight augmentation of carrageenin-induced hind paw edema in rats. From these results, it can be assumed that T-3761 had a wide safety margin as an oral antibacterial agent.

Animals↗

[Serial 123I-IMP SPECT in a case of cryptococcal meningoencephalitis].

We performed serial brain perfusion SPECT studies using 123I-IMP in the course of cryptococcal meningoencephalitis. Increased perfusion was detected in the cerebellum coinciding with the appearance of the abnormality on MRI. The perfusion in the lesion was then decreased as the abnormality on MRI disappeared. Cryptococcal meningoencephalitis should be also taken in the differential diagnosis when the inflammatory brain lesion shows increased perfusion.

Aged↗

[A new 3-dimensional head fixation device for brain imaging].

We have developed a new head fixation device for studies of brain function. This device was designed to immobilize subject's heads during image scanning and to precisely reproduce the head position for two different imaging modalities such as MRI and PET. The device consists of a plastic frame, a pillow filled with beads of styrene foam, and a face mask of thermoplastic resin which was originally intended for application in radiotherapy. A bridge for biting was incorporated into the mask for stable fixation. The device enables immobilization of subject's heads with good reproducibility of position at the practical level. Our results indicate that this head fixation system is useful for fixation of head during activation studies using PET.

Brain↗

[Study on tumor accumulation property of 99mTc-HM-PAO and 99mTc-MIBI in rabbits bearing VX-2 cancer].

Each of blood flow imaging agents has a potential usefulness as an agent for tumor scintigraphy. The usefulness for tumor scintigraphy of two agents, i.e. cerebral blood flow scintigraphy agent 99mTc-HM-PAO and myocardial blood flow scintigraphy agent 99mTc-MIBI, was comparatively studied using rabbits bearing VX-2 cancer. From then to twenty days after the implantation of VX-2 cancer into the femoral region of five rabbits, tumor to soft tissue accumulation ratio (T/S ratio) of each agent was calculated in early images (5 min after injection) and in late images (50 min after injection). Compared with 99mTc-MIBI, the T/S ratio of 99mTc-HM-PAO was higher and, moreover, the washout was delayed. These results suggest that there is a difference in tumor accumulation property between these two agents.

Animals↗

[Hydraulic conductivity of the visceral pleura with hemodynamic lung edema in dogs].

Hydraulic conductivity of the visceral pleura was measured in situ in anesthetized dogs. There were two groups: control (n = 7), and edema (n = 5). The 7th intercostal space of the left thorax was opened. In each group, a hemispherical capsule, filled with physiological salt solution, was attached to the visceral pleura of left lobe by negative pressure made with a vacuum pump. In the edema group, pulmonary venous pressure was increased by ligation of the pulmonary vein. The transpleural fluid flow (V) was measured at different intracapsular pressures (delta P). The hydraulic conductivity was calculated from the relation between the fluid flow rate (v) and the intracapsular pressure, i.e., the slope of the linear regression line. The hydraulic conductivities in the control and edema groups were 1.49 +/- 0.68 and 3.19 +/- 1.13 nL.min-1.cmH2O-1.cm-2, respectively. We conclude that the pleural tissue may play an important role in hydraulic conductivity of the visceral pleura when pulmonary venous pressure is high.

Animals↗

[Vasoactive intestinal peptide (VIP)-induced pulmonary vasodilation mediated by EDRF/NO in isolated perfused rat lungs].

We studied the effects of Vasoactive Intestinal Peptide (VIP) on the pulmonary circulation in isolated perfused rat lungs. VIP caused pulmonary vasodilation in a dose-dependent manner. This effect was inhibited by pretreatment with L-N omega-nitro-arginine (L-NNA), a competitive inhibitor of endothelium-derived relaxing factor (EDRF/NO), but not by meclofenamate, a cyclooxygenase inhibitor. Addition of L-arginine, a substrate of EDRF/NO, after treatment with L-NNA reversed VIP-induced pulmonary vasodilation. These results indicate that VIP causes pulmonary vasodilation, and they suggest a role for EDRF/NO in VIP-induced pulmonary vasodilation in isolated rat lungs.

Animals↗

[Surgical treatment of lung cancer over 80 years of age: investigation from post operative complications].

Seventeen patients with lung cancer over 80 years were treated surgically from 1983 through 1993 in our department. Thirteen patients were male and four were female. The histology of the tumor was adenocarcinomas, squamous, large and small cell carcinomas, in 9, 6, 1 and 1 cases, respectively. More than single lobectomy was performed in each patient. Unilateral pulmonary occlusion test was applied in patients whose expected contralateral FEV1.0/BSA was less than 800 ml.m2, or expected residual FEV1.0/BSA was less than 850 ml.m-2. Postoperative cardiovascular complications, such as PAT, PAC, PVC or Af, were seen in 9 patients, respiratory problems, namely, sputa retention, retained secretions or atelectasis, in 7 patients. Blood chemistry and hematology were performed for about three weeks after operations, and found increases in serum transaminases, and leukocytosis. However, there were no operative death. We conclude that some patients over 80 years of age are candidates for surgery after careful cardiopulmonary preoperative evaluation.

Adenocarcinoma↗

Cerebral blood flow measurement with iodine-123-IMP SPECT, calibrated standard input function and venous blood sampling.

UNLABELLED: We previously reported simple methods for measuring cerebral blood flow (CBF) with 123l-labeled N-isopropyl-p-iodoamphetamine (IMP) and SPECT: table look-up method and autoradiography. With these methods, the arterial input function is obtained by calibrating the standard input function using one-point arterial blood sampling 10 min after IMP infusion. In this study, we sought to determine if these approaches can be as successful when used with venous blood sampling. METHODS: After IMP infusion, simultaneous arterial and venous blood samples were drawn from 30 subjects without heart or lung disease. RESULTS: The activity ratios of venous whole blood from the cubital vein to arterial blood were 0.75 +/- 0.09, 0.77 +/- 0.10, 0.78 +/- 0.03 and 0.83 +/- 0.11, respectively, at 10, 20, 30 and 50 min after IMP infusion. Venous blood activities were always 20% lower than the artery values over 50 min. When blood was sampled from the dorsal hand vein, however, the respective ratios were 0.92 +/- 0.03, 0.93 +/- 0.05, 0.97 +/- 0.04 and 0.98 +/- 0.08 after 10, 20, 30 and 50 min. Furthermore, when the palm was exposed to heat during the sampling period, blood activity levels increased to 0.92 +/- 0.04, 0.96 +/- 0.04, 0.99 +/- 0.05 and 0.98 +/- 0.03. Thus, venous blood activities were consistent with arterial activity, presumably because of the numerous arteriovenous anastomoses in the palm. Optimal times for venous blood sampling, with and without palm heating, were determined by error analysis to be 15 and 20 min, respectively, after IMP infusion. CONCLUSION: Venous blood sampling from the dorsal hand can be substituted for arterial blood sampling in IMP-CBF studies.

Amphetamines↗

[Normal cerebral perfusion of 99mTc-HMPAO brain SPECT--evaluation by ananatomical standardization technique].

Single photon labeled tracer 99mTc-hexamethylpropylene amine oxime (HMPAO) has been used for rCBF studies by SPECT. However, normal perfusion pattern of this agent still remains unclear. The purpose of this study was to investigate normal 99mTc-HMPAO SPECT image voxel by voxel. Eighteen male subjects without any prior or present history of medical illness participated in this study. All SPECT images were globally normalized to 100 count/voxel. Each subject had an X-ray CT scan at the same day of SPECT measurement. All subjects had normal X-ray CT scans. The standard anatomical structures of the computerized brain atlas of Roland et al. were fitted to X-ray CT images of a subject by linear and non-linear parameters. These parameters were subsequently used to transform SPECT images of the subject. After the anatomical standardization, mean and SD images of eight standardized images were calculated voxel-by-voxel basis. In the mean image, following structures showed relatively higher radioactivity; the putamen, the cerebellum, and the frontal lobe. In addition, the occipital lobe, parietal lobe, frontal lobe, and the putamen showed large degree of SD. Anatomical standardization of SPECT images may be useful as a reference to diagnose and evaluate various brain disorders.

Adult↗

[Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells].

To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These date indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

Animals↗

[Contribution of oxidative stress to pulmonary hypertension induced by chronic hypoxia].

Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with media wall thickening of pulmonary arteries in rats. Platelet-activating factor plays an important role in the pulmonary vascular remodeling induced by chronic hypoxia, and reactive oxygen species are involved in tissue injury induced by platelet activating factor. We therefore hypothesized that reactive oxygen species contribute to the pulmonary hypertension induced by chronic hypoxia, and examined the effect of N-acetyl-L-cysteine (NAC), a free radical scavenger and the precursor of glutathione sulfhydryl (GSH), on hypoxia-induced pulmonary hypertension. We used a chemiluminescence-HPLC assay to measure the levels of phosphatidylcholine hydroperoxide (PCOOH) in the rat lungs exposed to hypoxia. Three weeks of normobaric hypoxia (FiO2 = 0.1) with NAC significantly reduced pulmonary hypertension, right ventricular hypertrophy, and media wall thickening of the pulmonary arteries. NAC had no effect on the hematocrit of normoxic or chronically normobaric hypoxic rats. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. These results indicate that hypoxia induces oxidative stress in the lung tissue, and that oxidative stress may have a role in the development of pulmonary hypertension induced by chronic hypoxia in rats.

Acetylcysteine↗