Biomedical subjects

N Hara

Publications and source records attributed to N Hara.

At least 199 records · Page 11Linked to original sources

PubMed1996

Roles of the lateral suprasylvian cortex in convergence eye movement in cats.

Ocular convergence and lens accomodation were evoked by microstimulation in the lateral suprasylvian area (LS cortex) in the parieto-occipital cortex in the cat. Electrolytic lesions in LS cortex reduced the amplitude and velocity of ocular convergence. Neurons in LS cortex discharged in relation to ocular convergence and/or lens accommodation. These results support the hypothesis that the LS cortex plays an important role in controlling ocular convergence The LS cortex receives visual inputs from cortical visual areas 17, 18 and 19, and in addition from the superior colliculus through the LP nucleus of the thalamus. Electrophysiological recordings have revealed that these visual inputs, which include cues about 3-dimensional target motion, are integrated in the LS cortex. The integrated output from LS cortex may provide the brainstem motor centers with the neural signals that facilitate eye movements, especially when the target is moving at high speeds. Outputs from the LS cortex travel directly to brainstem structures including the superior colliculus and pretectum. Evidence from monkey suggests that information may also travel to the mesencephalic reticular formation, where neurons have been recorded that are related to ocular convergence, lens accomodation or both. Although comparable data is lacking in the cat, it is suggested that the efferent circuit from the LS cortex to the motor nuclei in the brainstem included both the superior colliculus and the mesencephalic reticular formation. It is also suggested that this pathway is rather short, given that the mean latency of the early component of evoked disjunctive eye movements was approximately 60 ms.

Animals↗

PubMed1996

Thromboxane A2 mimetic (U-46619) induces hyperresponsiveness of smooth muscle in the canine bronchiole, but not in the trachea.

It has been reported that cholinergic agonists induce bronchoconstriction by directly stimulating M3 muscarinic receptors on the surfaces of smooth muscle cells. Although thromboxane A2 (TXA2) has been demonstrated to induce airway hyperresponsiveness to cholinergic agonists in vivo, it does not affect the contractile response of smooth muscle to cholinergic agonists in vitro. To investigate the causes for the discrepancy between the in vivo and in vitro data, we compared the effects exerted by a TXA2 mimetic, U-46619, on the smooth muscle of canine trachea and bronchiole. We measured the contractile response to exogenously applied acetylcholine (ACh) before and after the application of a subthreshold dose of U-46619. The subthreshold dose was determined as that dose which did not induce smooth muscle contraction, this being 10(-9) M in the present study. The contractile responses of tracheal strips to ACh were not affected by the subthreshold dose of U-46619. By contrast, the responses of bronchiolar rings were significantly enhanced by this subthreshold dose. The excitatory effect of U-46619 on the ACh-induced contraction was completely prevented by treatment with a TXA2 antagonist, BAY u3405. These results indicate that TXA2 directly increases the responsiveness of smooth muscle in the bronchiole, and suggest that increases in the responsiveness of small airways may play an important role in the development of the airway hyperresponsiveness induced by TXA2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1996

Thromboxane A2 antagonist inhibits leukotriene D4-induced smooth muscle contraction in guinea-pig lung parenchyma, but not in trachea.

Although the bronchoconstriction induced by leukotriene D4 (LTD4) has been reported to be partly mediated by thromboxane A2 (TXA2) in the guinea-pig airway, it is not known which part of the airway is susceptible to TXA2. In order to determine the role of TXA2 in the central and peripheral airways, we compared the effect of a TXA2 antagonist on tracheal strips to its effect on parenchymal strips of guinea-pigs. Tracheal and parenchymal strips were mounted in a 3.5 ml organ bath filled with Krebs-Henseleit solution aerated with 95% O2, 5% CO2 and kept at 37 degrees C. After equilibration for 60 min in Krebs solution, the strip was contracted by exposure to 10(-5) M of acetylcholine (ACh). Sixty minutes after ACh was eliminated, the concentration-response curve to LTD4 (10(-9) M-10(-7) M) was obtained, and the LTD4-induced contractions were expressed as the percent of the contraction evoked by 10(-5) M of ACh. We measured the contractile response to LTD4 in the presence or absence of the TXA2 antagonist, BAY u3405 (10(-8) M-10(-6) M). In the tracheal strips, BAY u3405 had no effect on the LTD4-induced contraction. However, in parenchymal strips, BAY u3405 significantly suppressed the contractile response to LTD4. These results suggest that in the central airway LTD4 contracts smooth muscle directly, but that in the peripheral airway LTD4 induces smooth muscle contraction both directly and indirectly, via TXA2.

Animals↗

PubMed1996

Activation of Clostridium botulinum C3 exoenzyme-catalyzed ADP-ribosylation of RhoA by K+ in a Mg2+ -dependent manner.

The effect of KCl on ADP-ribosylation of the recombinant RhoA protein catalyzed by the Clostridium botulinum C3 enzyme was studied. When the recombinant glutathione S-transferase-RhoA fusion protein (GST-RhoA) was incubated with C3 and [adenylate-32P]NAD, incorporation of radioactivity into the recombinant RhoA increased in the presence of KCl. The increase in ADP-ribose incorporation into RhoA due to KCl appeared in the presence of MgCl2 and was abolished by EDTA. C3 was stabilized by KCl, but the stabilization was also seen with BSA. The KCl-induced increase in the ADP-ribosylation was observed even in the presence of BSA during the modification reaction, thus the effect of KCl was not due to the stabilization of C3. While the initial rate of the reaction was increased by KCl, maximum incorporation of ADP-ribose per GST-RhoA molecule did not increase in the presence of KCl. Kinetic analysis revealed that KCl increased Vmax but did not alter Km for either NAD or RhoA. The NAD glycohydrolase activity of C3 was also increased by KCl. These results indicate that KCl directly activates the C3 enzyme.

ADP Ribose Transferases↗

PubMed1996

Altered expression of human leukocyte antigen G (HLA-G) on extravillous trophoblasts in preeclampsia: immunohistological demonstration with anti-HLA-G specific antibody "87G" and anti-cytokeratin antibody "CAM5.2".

PROBLEM: Human leukocyte antigen-G (HLA-G) is suggested to be at play in the materno-fetal immune relationship during pregnancy. In the light of current concept that disruption of the materno-fetal immune relationship could account for several complications of pregnancy, including preeclampsia, we asked whether the expression of HLA-G protein on the trophoblasts is altered in preeclampsia. METHOD: The presence of HLA-G protein in the extravillous trophoblasts in placenta obtained from five preeclamptic patients and seven uncomplicated pregnant women was determined by means of an immunohistochemical technique. RESULTS: All of the extravillous trophoblasts, which were stained for cytokeratin, were stained for HLA-G protein in every woman with an uncomplicated pregnancy. In contrast, clusters of extravillous trophoblasts were insularly devoid of the staining for HLA-G in all the preeclamptic patients. CONCLUSION: The attenuated expression of HLA-G protein on the extravillous trophoblasts could be at play in the pathophysiology of preeclampsia.

Adult↗

PubMed1996

Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation.

We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. Exposure to cigarette smoke was carried out at tidal volume for 3 min. Airway responsiveness to histamine was determined before and after smoke exposure followed by bronchoalveolar lavage (BAL). Plasma extravasation was evaluated by measuring the extravasation of Evans blue dye in the airway. Cigarette smoke produced significant airway hyperresponsiveness and plasma extravasation, with an influx of neutrophils in BAL fluid. FK-224 (10 mg/kg i.v.), a tachykinin antagonist at NK1 and NK2 receptors, significantly inhibited these changes. The thromboxane (Tx) B2 concentration was increased in BAL fluid after smoke exposure and was significantly inhibited by FK-224. OKY-046 (10 mg/kg i.v.), a Tx synthase inhibitor, significantly inhibited airway hyperresponsiveness but had no effect on neutrophil influx or plasma extravasation. The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke.

Animals↗

PubMed1996

Cultured epithelial cells release cyclooxygenase-dependent and cyclooxygenase-independent factors that inhibit cholinergic contraction of canine airway smooth muscles.

We observed the effects of supernatants from cultured epithelial cells on the contraction of tracheal smooth muscle evoked by acetylcholine (ACh) or by electrical field stimulation (EFS). Cultured canine tracheal epithelial cells were incubated in Krebs solution with or without indomethacin (10(-5)M) for 30 and 120 min. The amplitude of the tracheal smooth muscle contractions evoked by EFS or exogenously applied ACh were measured before and after the application of each supernatant in the combined presence of both indomethacin (10(-5)M) and propranolol (10(-6)M). The control supernatant incubated without indomethacin markedly suppressed the amplitude of the contraction evoked by EFS, but not by ACh. The supernatant incubated with indomethacin for 30 min did not show any effects on the contractile responses evoked by EFS or ACh. However, the supernatants from the cultured epithelial cells incubated for a longer period (120 min) in the presence of indomethacin significantly suppressed the contraction evoked by EFS, but not by ACh. The prostaglandin E2 (PGE2) concentration was markedly higher in the supernatants incubated without indomethacin (1.39 +/- 0.51 ng/ml, 30 min incubation) than in those with indomethacin (0.02 +/- 0.01 ng/ml, 30 min incubation, and 0.06 +/- 0.01 ng/ml, 120 min incubation). To determine whether PGE2 is responsible for the inhibitory effect of the supernatants, we evaluated the effects of PGE2 on the resting tone, and EFS- or ACh-evoked contraction. 10(-12) to 10(-6) M of PGE2 showed no significant effect on the resting tone. 10(-9) M of PGE2, corresponding to the concentration of the supernatants incubated without indomethacin, and 10(-11) M of PGE2, to that of the supernatants incubated with indomethacin, showed a similar extent of inhibitory effects to the corresponding supernatants on the EFS-evoked contraction, and no effect on the ACh-evoked contraction. These results suggest that cultured airway epithelial cells release at least two factors spontaneously even without stimulation. One of these factors may be prostanoid (PGE2), which acts prejunctionally to inhibit the contractile response. The other factor is distinct from prostanoid and inhibits smooth muscle contraction, presumably by suppressing ACh release from vagus nerve termini.

Acetylcholine↗

PubMed1996

P21Waf1/Cip1/Sdi1 and p53 expression in association with DNA strand breaks in idiopathic pulmonary fibrosis.

The tumor suppressor p53 protein is a transcription factor that plays a central role in the cellular response to DNA damage, and it can cause either G1 arrest or apoptosis. Recently, it was shown to induce the tumor suppressor p21Waf1/Cip1/Sdi1 (p21), which inhibits cyclin-CDK complex kinase activity. Although the etiology of idiopathic pulmonary fibrosis (IPF) is still uncertain, it is postulated that IPF begins with an initial inflammatory lesion localized to the alveolus and progresses on to chronic inflammation with alveolitis. We examined whether p53 and p21 are upregulated in association with chronic DNA damage in the bronchial and alveolar epithelial cells in patients with IPF in an attempt to repair the injury. We performed in situ detection of DNA strand breaks or apoptosis (TUNEL) in the tissues as well as immunohistochemistry (IHC) for p53 and p21. Positive signals by TUNEL were detected mainly in the bronchiolar and alveolar epithelial cells in 10 of 14 lung specimens from patients with IPF. On the other hand, no positive signal by TUNEL was detected in normal lung parenchyma or in specimens of pulmonary emphysema. The IHC demonstrated that p53 and p21 were expressed especially in hyperplastic bronchial and alveolar epithelial cells of lung tissues from all patients with IPF, except five specimens for p21. These results are consistent with those obtained by TUNEL. In normal lung parenchyma and specimens of pulmonary emphysema, p53 and p21 were not detected except in scattered alveolar macrophages and in the epithelial cells within localized fibrotic regions. These results suggest that p53 and p21 are upregulated in association with chronic DNA damage, resulting in either G1 arrest or apoptosis so that the DNA damage can be repaired in IPF. We speculate that chronic DNA damage and repair may lead to mutation of the p53 gene and tumorigenesis in IPF.

Aged↗

PubMed1996

Lung cancer cell lines inhibit leukotriene B4 production by human polymorphonuclear leukocytes at the level of phospholipase A2.

We studied cellular interactions between human polymorphonuclear leukocytes (PMN) and lung cancer cell lines by investigating the influence of cancer cells on the production of leukotriene B4 (LTB4) and superoxide anion (O2-) by stimulated PMN. Of the nine cancer cell lines established from human lung cancers that we examined, H23 cells showed the highest LTA4 hydrolase activity. When PMN were stimulated by the calcium ionophore A23187 in the presence of H23 cells, the production of LTB4, 5(S)-hydroxyeicosatetraenoic acid (5-HETE), and 12(S)-hydroxyeicosatetraenoic acid (12-HETE) decreased in a dose-dependent manner. On the contrary, H23 did not inhibit O2- production by PMN. Two other cell lines (N417 and Q9) caused similar inhibition of LTB4 production by PMN. These three cancer cell lines alone did not generate any metabolites of the arachidonic acid (AA) lipoxygenase pathway or any O2- upon stimulation with A23187 alone. The addition of AA dose-dependently reversed the H23-induced inhibition of LTB4, 5-HETE, and 12-HETE production by PMN, suggesting inhibition at the phospholipase A2 (PLA2) level. Furthermore, addition of the cancer cell line Q9 inhibited 14C release from [14C]AA prelabeled PMN in a cell number-dependent manner in the buffer, with and without albumin. The supernatant of H23 cells also inhibited the production of LTB4 by PMN stimulated by A23187, as did the addition of H23 lysate or its 10(4) x g centrifugation supernatant. While neither the 10(5) x g supernatant (cytosol) nor the pellet (microsome) exhibited inhibitory activity, the combination of the separated cytosol and microsomal fractions restored the inhibitory activity. Furthermore, addition of the 10(4) x g supernatant of Q9 lysate to partially purified human cytosolic PLA2 inhibited PLA2 activity in a dose-dependent manner. Our results indicate that the lung cancer cell lines used in our study inhibit LTB4 production by human PMN through inhibition of phospholipase A2 activity, which may contribute to a predisposition to pulmonary infections in patients with lung cancer.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1996

Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs.

Acute exposure to cigarette smoke provokes bronchoconstriction and increases the concentration of thromboxane (Tx) A2 in bronchoalveolar lavage (BAL) fluid. The purpose of this study was to investigate the role of TxA2 and cholinergic mechanisms in the airway response induced by exposure to cigarette smoke in guinea-pigs. Anaesthetized animals were exposed to 200 puffs of smoke for 10 min. The amount of Evans blue dye extravasated into the bronchial tissue was then measured BAL was performed to determine cell counts and the concentration of TxB2, a stable metabolite of TxA2. The effects of pretreatment with a Tx synthase inhibitor, OKY-046 (10 mg.kg-1), and/or atropine (1 mg.kg-1) were evaluated. Exposure to cigarette smoke caused significant bronchoconstriction (284 +/- 33% of baseline pulmonary resistance (RL)) and plasma extravasation (30.0 +/- 3.8 vs 16.8 +/- 2.6 ng.mg-1 of sham control; main bronchi). OKY-046 or atropine significantly inhibited the bronchoconstriction to a similar extent, without affecting the plasma extravasation. Combined use of these compounds had no additive effect. The cigarette smoke caused significant increase in TxB2 (48 +/- 10 vs 14 +/- 1 pg.mL-1 of sham control) in BAL fluid, which was abolished by OKY-046 but not by atropine. The cellularity in BAL fluid was not different among groups. These results suggest that the bronchoconstriction induced by cigarette smoke is partially mediated by thromboxane A2, which is dependent on a cholinergic pathway.

Animals↗

PubMed1996

Lysophosphatidylserine enhances exogenous type II phospholipase A2-induced activation of rat serosal mast cells.

We have previously shown that exogenous type II phospholipase A2 (PLA2) alone elicits degranulation of mast cells, including rat serosal mast cells (SMC) and mouse bone marrow-derived mast cells (BMMC). Here we report that lysophosphatidylserine (lysoPS), a co-factor for activation of rodent SMC in response to some tyrosine kinase-coupled agonists, enhanced type II PLA2-elicited histamine release from rat SMC. In contrast, mouse BMMC was insensitive to lysoPS. Our findings demonstrate a novel route for activation of SMC in that type II PLA2 can act as a direct activator of SMC with enhancement by lysoPS, which is generated from membrane phosphatidylserine possibly by the action of the same enzyme.

Animals↗

PubMed1996

BAY u3405, a thromboxane A2 antagonist, reduces bronchial hyperresponsiveness in asthmatics.

OBJECTIVE: Thromboxane A2 (TXA2) is reported to induce bronchial hyperresponsiveness along with the well-documented bronchoconstrictor action on smooth muscles. We examined the effect of the TXA2 antagonist, BAY u3405, on bronchial hyperresponsiveness to methacholine (MCh) in asthmatics. PATIENTS: Twelve adult asthmatics were studied in a randomized, double-blind, placebo-controlled, crossover fashion. DESIGN: Following a 2-week run-in period, the subjects were administered 75 mg of BAY u3405 or placebo orally, twice a day for 2 weeks each in a crossover design, interposing a 2-week washout period. Bronchial hyperresponsiveness was measured by the astograph method. Briefly, the respiratory resistance (Rrs) was measured by the forced oscillation method during continuous inhalation of MCh in stepwise incremental concentrations, until Rrs reached twice the baseline value. Bronchial hyperresponsiveness was evaluated as the minimum cumulative dose (Dmin) of MCh that induced an increase in Rrs. Dmin was calculated so that 1 U of Dmin equals to 1 min of inhalation of aerosol solution at 1.0 mg/mL during quiet breathing. RESULTS: Three subjects were withdrawn from the evaluation because they had asthmatic attacks or wheezing during the study. The Dmin value of 0.533 U (GSEM 1.675) after the BAY u3405 treatment was significantly greater than that of 0.135 U (GSEM 1.969) after the placebo treatment (p = 0.0139). There were no safety concerns in either treatment group. CONCLUSION: We conclude that BAY u3405 may be a useful drug for attenuating bronchial hyperresponsiveness in bronchial asthma.

Adult↗

PubMed1996

Empyema following the percutaneous instillation of antifungal agents in patients with aspergillosis.

We report two cases of empyema as a complication of the percutaneous instillation of antifungal drugs for pulmonary and pleural aspergillosis. Case 1 underwent percutaneous administration of amphotericin B and fluconazole for 2 months. Six months later, the patient was found to have an Aspergillus empyema with a bronchopleural fistula. Case 2 with pulmonary and pleural aspergillosis underwent percutaneous administration of amphotericin B for one month. Four months later, the patient underwent pleural drainage due to empyema. Pleural biopsy revealed pleural aspergillosis. In both cases, it was suggested that the preceding Aspergillus infection and percutaneous instillation of antifungals resulted in the development of empyema.

Aged↗

PubMed1996

[Small cell lung cancer associated with ectopic ACTH syndrome].

A 70-year-old woman was referred to our hospital for diagnosis and treatment of a pulmonary mass detected on a chest X-ray film. Small cell lung cancer was diagnosed from pathological examination of a specimen of the tumor obtained by transbronchial biopsy. Paraneoplastic Cushing's syndrome was diagnosed on the basis of an elevated serum ACTH level (2000 pg/ml), the serum cortisol level (171.9 micrograms/dl), elevated excretion of urinary 17-OHCS (67 mg/day), persistent hypokalemia, metabolic alkalosis, hyperglycemia, central obesity, hypertension, systemic pigmentation, and the lack of a history of diabetes mellitus. Immunohistochemical staining with a polyclonal anti-ACTH antibody of a biopsy specimen from a lymph node with metastasis showed that tumor cells were weakly positive. The patient responded well to intensive chemotherapy with VP-16 (100 mg/m2 day 103), CBDCA (100 mg/m2 day 1-3), and CDDP (80 mg/m2 day 1). Complete response was obtained after 6 courses of chemotherapy. The serum ACTH level decreased rapidly as the tumor shrank. The primary tumor, however, relapsed after 3 months and the patient died of progressive disease, 11 months after diagnosis.

ACTH Syndrome, Ectopic↗

PubMed1996

[Early phase II study of BMS-181339 (paclitaxel) in patients with non-small cell lung cancer. BMS-181339 Non-Small Cell Lung Cancer Study Group].

We conducted a multi-institutional (11 facilities), early phase II study of BMS-181339 (paclitaxel), a novel anti-cancer drug, for non-small cell lung cancer (NSCLC). The 150 mg/m2 dose of paclitaxel was given by intravenous infusion over 24 hours every three weeks. When fifteen patients were accumulated, the interim review revealed that three of 15 eligible patients had a partial response for a response rate of 20%. The most common toxic effects were grade 3 or 4 leukopenia seen in 73.3% (11/15), and grade 4 neutropenia in 93.3% (14/15). One patient with neutropenia had suspected septic shock, which could be managed by G-CSF and antibiotics. No serious hypersensitivity reaction was seen with premedication of anti-allergic drugs, although mild allergic reactions such as skin rash and flush, were observed in 20.0% (3/15). Other adverse reactions, including alopecia, fever, arthralgia, myalgia and peripheral neuropathy, were mild in most cases. We conclude that it is relevant to proceed to a late phase II study for NSCLC.

Adult↗

PubMed1996

[DNA strand breaks in epithelial cells from mice with bleomycin induced pulmonary fibrosis].

Bleomycin-induced cytotoxicity is believed to be caused by single- and double-strand DNA breaks. To examine the effect of bleomycin on DNA strand breaks and the role of these breaks in bleomycin induced pulmonary fibrosis in mice, we analyzed DNA strand breaks in situ by TdT-mediated dUTP-biotin nick end labeling (TUNEL), previously described by Gavrieli et al. The nuclei of bronchiolar epithelial cells were strongly stained 1 hr to 12 hr after bleomycin administration, and after that period DNA damage was repaired. Nuclei of alveolar epithelial cells showed positive signals correlated with progression of fibrosis. Although corticosteroids did not block the early DNA damage in bronchiolar epithelial cells, they did inhibit later damage to alveolar epithelial cells and fibrosis. We speculate that the DNA damage in alveolar epithelial cells and the progression of fibrosis in later stages are associated with inflammatory cytokines. These findings show the location and the time course of the DNA damage in bleomycin-induced pneumonitis in mice, and they indicate that the prolongation of DNA damage in alveolar epithelial cells is closely related to fibrinogenesis.

Animals↗

PubMed1996

[Effects on visual functions following several hours' usage of a head mounted display].

We investigated the effects of viewing video movies with a head-mounted display (HMD) for 4 to 6 hours on visual functions such as refraction, visual acuity, and accommodation-vergence system. Two or three video movies were watched without any breaks by 13 normal volunteers (age: 22 approximately 40). Measurements were made of (1) objective and subjective refraction, (2) corrected visual acuity, (3) tonic level and step response of accommodation with a computer-assisted infrared optometer, and (4) near and far phorias and AC/A ratio. Significant transient myopia was found following 4 hours' viewing, but not following 6 hours' viewing. Scrutinizing individual data, myopia was consistently found in some subjects, and hyperopia in others. We presumed that many subjects might have been influenced by initial instrumental myopia when they adjusted the focus by using the mechanism built in the HMD. No significant change was observed in any other examination. However, there was a tendency for the AC/A ratio to change after a short time, and then to recover to its original value. Based on the results in this study, it appears that some changes in accommodation and vergence systems are caused by viewing video movies with the HMD. Although the amount of changes was within normal physiological variation in this study, the possibility still remains that usage for a longer time may lead to other changes in visual function. Care is also necessary when using the HMD in subjects with subclinical problems.

Accommodation, Ocular↗

PubMed1996

[Pulmonary arterio-venous fistula treated by embolization with steel coils].

A 63-year-old man was referred to our hospital for evaluation and treatment of severe dyspnea on exertion which had persisted for a few years. He presented with cyanosis and markedly clubbed fingers, and laboratory data disclosed hypoxemia, polycythemia, and liver dysfunction. A chest X-ray film showed increased vascular markings in both lower lung fields. Arterial blood gas analysis showed severe hypoxemia, with a PaO2 of 46 Torr and a PaCO2 of 31 Torr while the patient was breathing room air. The PaO2 increased only slightly with inhalation of 100% oxygen, which suggested the presence of a large R-L shunt. The hepatopulmonary syndrome was diagnosed. Angiography of the pulmonary artery revealed a large pulmonary arterio-venous fistula with markedly dilated arteries in both lower lobes. Transarterial embolization was done three times with a total of 62 metal coils. There were no complications. Embolization reduced the shunt from 56% to 31%, increased the PaO2, and relieved the dyspnea. Pulmonary artery embolization can be useful in treating pulmonary arterio-venous fistulas associated with the hepatopulmonary syndrome.

Arteriovenous Fistula↗