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Biomedical subjects

K Shigemori

Publications and source records attributed to K Shigemori.

34 records · Page 2Linked to original sources
PubMed1995

Leukotoxin, 9,10-epoxy-12-octadecenoate causes edematous lung injury via activation of vascular nitric oxide synthase.

We examined the mechanism of leukotoxin, 9,10-epoxy-12-octadecenoate (Lx)-induced lung injury in blood-free, physiological salt solution-perfused rat lungs under constant flow conditions. Mean pulmonary arterial (Ppa) and pulmonary capillary pressure (Pcap, estimated by the double-occlusion method), wet lung weight (WLW), pulmonary capillary filtration coefficient (Kfc), lung perfusate lactate dehydrogenase (LDH) activity, and nitrite levels were assessed. Bolus injection of Lx (200 microM) caused insidious and significant lung weight gain, which was not associated with remarkable elevation of Ppa or Pcap but was associated with an increase of perfusate LDH activity and nitrite levels. Lx (20 microM) elevated Kfc, indicating that Lx had affected pulmonary vascular permeability. Because Lx causes endothelium dependent pulmonary vasodilation, we studied the effect of NG-monomethyl-L-arginine (L-NMMA), NG-monomethyl-D-arginine (D-NMMA), superoxide dismutase (SOD), human oxyhemoglobin (oxyHb), and methylene blue (MB) on Lx-induced lung injury. L-NMMA, SOD, and oxyHb, but not MB or D-NMMA, protected the lungs against Lx (200 microM)-induced injury. Lx increased pulmonary vascular permeability and caused lung injury. Because both nitric oxide synthase inhibitors and SOD inhibited the Lx-induced lung injury, it is possible that peroxynitrite is involved in the mechanism whereby Lx causes lung injury.

Amino Acid Oxidoreductases↗
PubMed1995

Endothelin-1 potentiates leukotoxin-induced edematous lung injury.

We tested the hypothesis that leukotoxin (Lx), a cytochrome P-450-dependent linoleate product of leukocytes, can stimulate the release of endothelin-1 (ET-1) from the lung and further that exogenous ET-1 synergizes with Lx to produce edematous lung injury. In isolated rat lungs perfused with Earle's balanced salt solution, Lx (10 mumol) alone caused lung edema and increased the perfusate and lung tissue ET-1 levels. The combination of ET-1 (5 nM) and Lx (5 mumol), at concentrations that by themselves did not increase wet lung weight, significantly increased wet lung weight, wet-to-dry lung weight ratio, as well as the lung effluent lactate dehydrogenase activity. Pretreatment with BQ-123 (5 x 10(-6) M), an endothelin A receptor antagonist that significantly attenuated the ET-1 (5 nM)-induced increase in pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Ppc), suppressed the edematous lung injury generated by the combination of ET-1 and Lx, suggesting that the edema-enhancing effect of ET-1 in Lx-treated lungs occurred through endothelin A receptor-dependent elevation of Ppa and Ppc. Elevation of the pulmonary venous pressure in Lx-treated lungs (13.5 cmH2O) mimicked the effect of ET-1 on Ppa and Ppc and produced a degree of lung edema that was comparable to that after combined ET-1 + Lx treatment but without increase in the perfusate lactate dehydrogenase. These data support the idea that ET-1 and Lx promote lung edema in a synergistic fashion.

Animals↗
PubMed1995

[Lung injury and pulmonary vascular endothelial cell injury].

Pulmonary vascular endothelial cells are an important barrier that helps keep lung tissue intact. These cells are exposed to potentially injurious cells and to harmful mediators that are produced in or released into the blood. The endothelial cells may then be stimulated and injured. Stimulated and injured pulmonary vascular endothelial cells can themselves produce and release injury-promoting mediators. Using isolated perfused rat lungs and cultured human pulmonary endothelial cells, we assessed the effect of neutrophil-derived injurious mediators, leukotoxin, and neutrophil elastase on the pulmonary endothelium. Both mediators caused high-permeability pulmonary edema in the isolated lungs and caused dose-dependent and time-dependent damage in the cell cultures. Injury due to leukotoxin was suppressed in the presence of LNMMA or superoxide dismutase and injury due to neutrophil elastase was suppressed by neutrophil elastase inhibitors. These data indicate that these mediators cause lung injury via different mechanisms and that they may synergistically evoke clinical lung injury.

Acute Disease↗
PubMed1993

[Adult case of bronchial asthma induced by chironomid midges].

A 48-year-old woman who was diagnosed to have bronchial asthma induced by chironomid midges is reported. In spring of 1985, massive growth of chironomid midges occurred in the river beside her house. Since then, moderate growth has occurred in every spring or summer. She had wheezing attacks every May or June since June 1986. On May 2, 1991, she was hospitalized because of exacerbation of wheezing and dyspnea. Wheezing attacks were improved by appropriate medical treatment during hospitalization. Examination was performed during the state of stable clinical symptoms. RAST scores to Chironomus thummi thummi (CTT) and Chironomus plumosus (CP) were 4 and 3, respectively. Allergic skin reaction showed the threshold dilution of CP of 10(-6). CP skin test concomitantly provoked a mild acute asthma attack. The midges found swarming around her house were identified as Chironomus nippodorsalis. According to her clinical history and allergic skin reactions followed by acute asthmatic attack, this patient was diagnosed to have bronchial asthma induced by chironomid midges. Chironomid midge can be one of the inhalant allergens in adults.

Adult↗
PubMed1993

[Effects of cilostazol, a cyclic AMP phosphodiesterase inhibitor, on pulmonary vascular tone].

We examined the effect of Cilostazol, a cyclic AMP phosphodiesterase inhibitor, rat isolated pulmonary arterial ring tone. Cilostazol dilated pulmonary arterial rings pre-contracted with 10(-6) M phenylephrine in a dose-dependent manner (ED50 3.00 x 10(-6) M). This vasodilatory effect of Cilostazol was not affected by pretreatment with meclofenamate (10(-5) M), mechanical endothelium denudation, methylene blue (10(-5) M) or nitro-L-arginine (2 x 10(-4) M). The vasodilatory effect of Cilostazol on rat thoracic aortic rings was stronger than that on rat pulmonary arterial ring (ED50 1.89 x 10(-6) M). Cilostazol (10(-6) M-10(-4) M) inhibited hypoxic contraction of rat pulmonary rings in a dose-dependent manner. Our experimental data indicated that Cilostazol caused vasodilation regardless of vascular endothelium function and inhibited hypoxic contraction due to inhibition of cyclic AMP phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

The relationship between low Km aldehyde dehydrogenase phenotype and drinking behavior in Japanese.

The relationship between the low Km aldehyde dehydrogenase (ALDH2) phenotype determined by the isoelectric focusing of hair root lysates, facial flushing and alcohol drinking patterns in Japanese (N = 282) was examined. Men who had inactive ALDH2 drank significantly less alcohol than those with active ALDH2. Although the effect was less noticeable, a similar relationship was detected in women. Two types of flushing responses were determined: one due to the inactive ALDH2, the other unrelated to this variant form of the isozyme. A striking difference between these flushing types, in terms of the inhibitory influence over drinking patterns, was noted. Nearly 86% of the subjects who reported always flushing in the face were shown to have inactive ALDH2, whereas infrequent flushing and absence of flushing were associated with active ALDH2. Thus, facial flushing may be used as an indicator of ALDH2 phenotype.

Adolescent↗
PubMed1991

[Problem drinkers among high school students in Japan].

In Japan, an increase in the consumption of alcohol by young people has been noted. This survey on drinking problems was performed on 1062 students of second year high school in 1990 using the Adolescent Alcohol Involvement Scale (AAIS). The results revealed that among all of the survey subjects of both sexes, 21.4% were abstainers, 4.2% normal adolescents, 60.9% non-problem drinkers, 12.6% alcohol misusers and 0.9% alcoholic-like drinkers. A high alcohol consumption rate and high percentages of those with drinking problems were observed among high school students. Students who used other addictive substances (i.e., smoking or thinner inhalation) reported significantly higher AAIS scores than those who didn't. Similarly high mean AAIS scores were found among students with family problems such as drinking parents or broken homes than those without this problem. Alcohol misusers and alcoholic-like drinkers accounted for 14.2% of males and 12.7% of females. In a survey performed 10 years previously on high school students, no alcoholic-like drinkers were found and only 1% were alcohol misusers. These results indicated that problem drinkers have dramatically increased among Japanese high school students in the last 10 years.

Adolescent↗
PubMed1989

Ethanol patch test--a simple and sensitive method for identifying ALDH phenotype.

The ethanol patch test, which is considered to be a cutaneous model of flushing, was performed on 311 healthy Japanese (237 adults and 74 children). By comparing the results with aldehyde dehydrogenase (ALDH) phenotype determined by isoelectric focusing from hair roots samples, it was demonstrated that the ethanol patch test is a good indicator of the ALDH phenotype. The usefulness of this test in future studies was discussed.

Adult↗