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H Kohrogi

Publications and source records attributed to H Kohrogi.

52 records · Page 3Linked to original sources
PubMed1992

[A case of intractable hemoptysis due to malignant hemangioendothelioma].

A 65-year-old man who died of respiratory failure due to malignant hemangioendothelioma is reported. He was admitted to our hospital because of intractable hemoptysis. Chest roentgenogram revealed multiple patchy shadows in both lungs, but we could not make a diagnosis by usual clinical examinations including transbronchial lung biopsy. Since the patient's condition became critical, oxygen therapy, anticoagulants and antibiotics were started. In addition, corticosteroid therapy and double filtration plasmapheresis were performed since immunological disorder was suspected because of positive immunological examinations such as antinuclear antibodies and an increase in circulatory immune complexes. There was little response to the treatments and the patient finally died of respiratory failure. At autopsy, multiple tumor nodules were found throughout the lungs and the liver. Metastasis to mediastinal lymph nodes was also discovered. These findings made it impossible to confirm the primary lesion. Microscopy showed proliferation of anastomosing capillaries encasing tumor cells of unknown origin. Silver staining demonstrated capillaries encompassing the atypical cells, suggesting a vascular origin of the tumor. Furthermore, factor VIII related-antigen in the tumor cells was confirmed by the peroxidase-antiperoxidase (PAP) method. The final diagnosis of malignant hemangioendothelioma was made from these histological findings. Malignant hemangioendothelioma is rare, but is an important cause of intractable hemoptysis.

Aged↗
PubMed1991

Enkephalinase inhibitor potentiates substance P- and capsaicin-induced bronchial smooth muscle contractions in humans.

To determine the roles of endogenously released tachykinins (substance P, neurokinins A and B) in human bronchial tissues, and to determine the roles of enkephalinase (neutral endopeptidase, E.C. 3.4.24.11) in regulating the effects of the tachykinins, we studied the effects of substance P and capsaicin, which releases tachykinins, on human bronchial smooth muscle contraction in the presence or absence of enkephalinase inhibitor phosphoramidon in vitro. Substance P alone caused human bronchial smooth muscle contraction at 10(-6) M or more. Phosphoramidon (10(-7) to 10(-5) M) potentiated the substance P-induced contraction in a dose-dependent fashion, and phosphoramidon shifted the dose-response curve to lower concentrations. Capsaicin (10(-5) or 10(-4) M) alone caused bronchial smooth muscle contraction in four tissues from nine patients. After the contraction by capsaicin reached a plateau, phosphoramidon (10(-5) M) increased and prolonged the contraction significantly. Furthermore, pretreatment of bronchial tissues with phosphoramidon (10(-5) M) potentiated capsaicin-induced contraction in all tissues from five patients. Phosphoramidon (10(-5) M) shifted the dose-response curve to capsaicin to lower concentrations more than 1 log unit. Captopril did not alter the contractile response to substance P, suggesting that angiotensin-converting enzyme does not regulate the contractile response to substance P in human bronchial smooth muscle in vitro. These results suggest that enkephalinase regulates the contractile effects of exogenous substance P and endogenous substances, probably tachykinins, released by capsaicin in the human bronchus.

Adult↗
PubMed1991

Inhibition of neutral endopeptidase potentiates bronchial contraction induced by immune response in guinea pigs in vitro.

To study the role of tachykinins and neutral endopeptidase (NEP), an enzyme that degrades tachykinins, in the immune response in the airways of guinea pigs sensitized to ovalbumin (OVA), we examined the bronchial contractile response to OVA by inhibiting NEP in vitro. After incubating bronchial tissues with the NEP inhibitors phosphoramidon and thiorphan, we added 10(-5)% (10 micrograms/ml) OVA. Phosphoramidon and thiorphan (10(-5) M) significantly maintained the contraction that followed the peak contraction. In the next stages of the experiment, when the contraction induced by 10(-5)% OVA reached a plateau and began to relax, we added 10(-5) M phosphoramidon. Phosphoramidon inhibited the relaxation and significantly potentiated the contraction. In tissues treated with 10(-5) M capsaicin to deplete tachykinins, phosphoramidon did not potentiate the OVA-induced contraction, but substance P (10(-6) M) caused contraction. These results suggest that the immune response causes the release of tachykinin-like substances from capsaicin-sensitive nerves to induce bronchial contraction in part. To confirm the mediators that cause the release of the tachykinin-like substances from the bronchus, we also examined whether phosphoramidon potentiates the effect of leukotriene C4 (LTC4), serotonin, histamine, and platelet-activating factor on bronchial contraction. When the contractions induced by these agonists reached a plateau and began to relax, we added phosphoramidon. Phosphoramidon inhibited the relaxation and significantly potentiated the contractile response to 10(-5) M LTC4, and it significantly reduced the relaxing rate of the 10(-6) M serotonin-induced contraction. However, it did not change the effect of histamine and platelet-activating factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Preventive effect of a novel leukotrienes antagonist ONO-1078 on leukotriene C4- and D4-induced human bronchial smooth muscle contraction].

To study whether a novel leukotrienes antagonist ONO-1078 (4-oxo-8-[4-phenylbutyloxy) benzoylamino]-2-(tetrazol-5-yl)-4H-1-benzopyran hemihydrate) prevents leukotrienes C4- and D4-(LTC4, LTD4) induced human bronchial smooth muscle contraction, we examined the bronchial contractile response to LTC4 and LTD4 in the presence or in the absence of ONO-1078 in human bronchial strips. We prepared 4 strips from each of 5 patients undergoing lobectomy of the lung because of lung cancer. We mounted the strips in organ baths and measured the contractile response to LTC4 and LTD4 from 10(-11) M to 10(-7) M after incubation with ONO-1078 (10(-8) M, 10(-7) M and 10(-6) M) and without ONO-1078. ONO-1078 shifted the dose response curve to LTC4 to higher concentration in dose dependent fashion, and it significantly inhibited the contractile response to LTC4 and LTD4. In the presence of L-serine borate complex (45 mM), an inhibitor of gamma-glutamyl transpeptidase, ONO-1078 significantly inhibited the LTC4-induced contraction. On the other hand, ONO-1078 had no effect on the contractile response to acetylcholine. These results suggest that ONO-1078 is a specific antagonist of LTC4 and LTD4 receptors in human bronchial smooth muscle. Because the effect of LTC4 and LTD4 is thought to be an important part of the pathogenesis of bronchial asthma, our results also suggest that ONO-1078 may be a useful prophylactic drug for bronchial asthma.

Bronchi↗
PubMed1989

Recombinant human enkephalinase (neutral endopeptidase) prevents cough induced by tachykinins in awake guinea pigs.

To determine whether recombinant enkephalinase (neutral endopeptidase, EC 3.4.24.11) prevents cough induced by exogenously applied and endogenously released neuropeptides, we measured cough responses to aerosolized solutions of substance P or of capsaicin for 2 min in random-source guinea pigs before or after exposing them to aerosolized recombinant human enkephalinase. Substance P (10(-16) M) increased coughing compared with its vehicle. Enkephalinase (120 micrograms) inhibited cough induced by subsequent exposure to substance P compared with the response to substance P alone, but after further exposure to the enkephalinase inhibitor leucine-thiorphan (10(-5) M), substance P increased cough significantly. Similar results were obtained for capsaicin-induced cough. In pathogen-free guinea pigs, after they inhaled inactive recombinant enkephalinase (33 micrograms), capsaicin (10(-13) M) increased cough significantly. In contrast, after they inhaled active recombinant enkephalinase (33 micrograms), capsaicin increased cough only slightly. These results suggest that aerosolized enkephalinase reaches the sites of release or actions of endogenous neuropeptides and, by degrading them, prevents cough induced by their release. Furthermore, these studies suggest that recombinant enkephalinase might be useful in the treatment of cough and other symptoms of diseases involving peptides cleaved by this enzyme.

Aerosols↗
PubMed1988

Neutral endopeptidase inhibitors potentiate substance P- and capsaicin-induced cough in awake guinea pigs.

To study the roles of substance P and endogenous neutral endopeptidase in mediating cough, we measured cough responses in awake guinea pigs in response to exogenous substance P and capsaicin aerosols in the presence and absence of the neutral endopeptidase inhibitors leucine-thiorphan and phosphoramidon. Substance P stimulated cough in very low concentrations (10(-17)-10(-16) M). In a second study where the investigator did not know whether substance P or diluent alone was aerosolized, substance P (10(-16) M) caused cough. Leucine-thiorphan (10(-5) M) and phosphoramidon (10(-5) M) potentiated substance P-induced cough; NEP inhibitors also potentiated capsaicin-induced cough significantly. These findings suggest that substance P is a potent stimulator of cough responses, that capsaicin-induced cough is mediated by substance P or another similar neuropeptide, and that cough responses are modulated by endogenous neutral endopeptidase.

Animals↗
PubMed1985

Nifedipine inhibits human bronchial smooth muscle contractions induced by leukotrienes C4 and D4, prostaglandin F2 alpha, and potassium.

The effects of nifedipine, a calcium channel blocker, on human bronchial smooth muscle contractions induced by leukotrienes C4 and D4 (LTC4, LTD4), prostaglandin F2 alpha (PGF2 alpha), and potassium were studied in vitro. The LTC4, LTD4, PGF2 alpha, and potassium caused bronchial smooth muscle contractions. After incubation with nifedipine at 2.9 X 10(-6)M, the contractions caused by LTC4, LTD4, PGF2 alpha, and potassium were significantly decreased. Nifedipine also significantly reversed human bronchial smooth muscle contractions previously initiated by these agonists. The effect of nifedipine on potassium contraction was significantly greater than that on LTC4, LTD4, and PGF2 alpha-induced contractions. The pharmacologic feature of nifedipine is that it inhibits the calcium influx associated with membrane depolarization. Therefore, these results suggest that there are two mechanisms of calcium movements in human bronchial smooth muscle contractions induced by LTC4, LTD4, and PGF2 alpha: membrane-depolarization-dependent and -independent mechanisms.

Aged↗
PubMed1984

Surface morphology and function of human pulmonary alveolar macrophages from smokers and non-smokers.

Pulmonary alveolar macrophages were obtained by saline lavage from 23 healthy male volunteers--10 non-smokers and 13 cigarette smokers. Lavage produced three times as many alveolar macrophages in smokers than in non-smokers. When macrophages from smokers and from non-smokers were incubated in vitro, more cells from smokers adhered to glass, spread out, and showed enhanced nitroblue tetrazolium (NBT) reduction. The surface morphology of alveolar macrophages from smokers showed more with a plate like appearance and ridge like membrane surface, while the macrophages from non-smokers were predominantly spherical with ruffles. The proportions of cells which stained highly for beta galactosidase were 55% in smokers and 11% in non-smokers. Thus, in a resting state in vitro, alveolar macrophages from smokers were more active than those from non-smokers. When, however, macrophages from smokers and non-smokers were incubated with immunobeads and with opsonised or non-opsonised BCG, the phagocytic activity and stimulated NBT reduction of alveolar macrophages from smokers were similar to or somewhat less than those of non-smokers.

Adult↗
PubMed1984

Preventive and reverse effects of nifedipine on human bronchoconstriction "in vitro".

The effects of nifedipine, a calcium channel blocking agent, on human bronchoconstriction induced by acetylcholine and histamine were studied in vitro. Bronchial preparations were obtained from 13 patients undergoing surgery for bronchial carcinoma. Bronchial strips were mounted for continuous isometric tension recording. Acetylcholine and histamine caused bronchoconstrictions, but the constrictive effects were inhibited by 2.9 X 10(-6) M nifedipine. At a concentration of 2.9 X 10(-6) M nifedipine increased by 22-fold the concentration of acetylcholine required to produce a 50% of maximal contraction of bronchial strips, and by 160-fold the concentration of histamine required. Nifedipine also reversed already established bronchoconstrictions by acetylcholine and histamine. The percentage of contraction at 20 min after 2.9 X 10(-6) M nifedipine was 7 +/- 11.1% (mean +/- SEM) and - 21 +/- 20.0% of the control maximal response by 10(-3) M acetylcholine and 10(-3) M histamine, respectively. Thus, nifedipine clearly prevented and reversed pharmacologically-induced bronchoconstriction in humans. These results suggest that it is valuable to administer nifedipine to prevent and treat asthma attack.

Acetylcholine↗
PubMed1983

A proposal for smoldering adult T-cell leukemia: a clinicopathologic study of five cases.

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly, but flared up after several years. Skin lesions appeared in the form of erythema, papules, or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was 0%-2%. The serum lactate dehydrogenase (LDH) value was within normal range and was not associated with hypercalcemia; lymphadenopathy, hepatosplenomegaly, and bone marrow infiltration were very slight. In most cases, hypergammaglobulinemia was seen, and in one case, monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their anti-ATLA antibodies were positive; none had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness and died of cryptococcus meningitis. Based on clinical and pathologic differences, we believe that these cases should be distinguished from typical ATL cases for the purposes of prognosis and treatment.

Antibodies↗
PubMed1983

A proposal for smoldering adult T-cell leukemia--diversity in clinical pictures of adult T-cell leukemia--.

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly but flared up after several years. Skin lesions appeared in the form of erythema, papules or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was from 0% to 2%. The serum lactic dehydrogenase value was within normal range, and was not associated with hypercalcemia, lymphadenopathy, or hepatosplenomegaly, and bone marrow infiltration was very slight. In most cases, hypergammaglobulinemia was seen, and in one case monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their sera were positive for anti-ATL-associated antigen antibodies. None of them had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness, and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness, and died or cryptococcus meningitis. These cases were clinically and pathologically different from typical ATL cases already reported, and we feel it necessary to make distinctions from the viewpoints of prognosis and treatment. In discussing these cases, we compared smoldering ATL with typical ATL, and deliberated upon the causes of both.

Antibodies, Viral↗
PubMedDate not supplied

Bronchoalveolar lavage studies in uveitis patients without radiological intrathoracic involvement of sarcoidosis.

In the present study, we investigated thirty uveitis patients who had a possible diagnosis of ocular sarcoidosis, no respiratory symptoms, and normal chest X-rays, in order to determine whether bronchoalveolar lavage was useful for establishing a diagnosis of subclinical pulmonary involvement of sarcoidosis. Sixteen of 30 uveitis patients showed bronchoalveolar lymphocytosis (39 +/- 11%) as compared to normal controls (14 +/- 3%). Ten of these 16 patients were associated with significantly increased proportions of CD3+ cells with elevated CD4+/CD8+ ratios (P less than 0.01). These data were consistent with those of patients with active pulmonary sarcoidosis (stage 1 and 2) except for total cell count in lavage fluid, but different from those of patients with hypersensitivity pneumonitis. Transbronchial lung biopsy showed noncaseating epithelioid cell granuloma in 4 of 10 uveitis patients with bronchoalveolar T-lymphocytosis and increased CD4+/CD8+ ratios. Immunohistochemical studies of biopsied lung tissues showed many CD3+ cells and CD4+ cells with very few CD8+ cells in the granuloma. These results suggest that T-lymphocytosis with elevated CD4+/CD8+ ratios in bronchoalveolar lavage fluid could be a good marker in predicting the pulmonary involvement of sarcoidosis in patients with suspected ocular sarcoidosis and normal chest X-rays.

Adolescent↗