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S W Chang

Publications and source records attributed to S W Chang.

At least 91 records · Page 5Linked to original sources
PubMed1989

Dibutyryl-cAMP blocks endotoxin-induced lung injury in rats.

We investigated the effect of dibutyryl-cAMP pretreatment on endotoxin-induced hemodynamic changes and lung vascular injury in rats. In catheter-implanted, unanesthetized rats, intraperitoneal injection of Salmonella enteritidis endotoxin (2 mg/kg) decreased cardiac output and systemic blood pressure while increasing total pulmonary vascular resistance. Db-cAMP (1 mg given intraperitoneally every 30 min), although not significantly affecting cardiac output and systemic blood pressure, blocked the increase in total pulmonary resistance caused by endotoxin. Ninety minutes after intraperitoneal endotoxin injection, perfused lungs from endotoxin-treated rats exhibited increased pulmonary vascular permeability, as assessed by increased extravascular accumulation of 125I-albumin and water. Db-cAMP treatment in vivo markedly attenuated the increases in lung albumin leak index and wet-to-dry weight ratio caused by endotoxin without affecting lung microvascular pressures. This protective action of db-cAMP is not due to its effect on prostaglandin or leukotriene synthesis since endotoxin-stimulated increases in lung tissue 6-keto-prostaglandin F1 alpha, thromboxane B2 and leukotriene C4 were not inhibited. We conclude that db-cAMP blocks endotoxin-induced lung injury in the rat by a mechanism independent of eicosanoid products and speculate that agents that increase intracellular cAMP may be therapeutically useful in acute lung vascular injury.

Albumins↗
PubMed1989

Lung eicosanoid metabolism.

Eicosanoids are metabolites of the essential fatty acid, arachidonic acid, which is an integral part of all cell membranes. Membrane damage (as in lung injury) and stretching of tissues are recognized stimuli for lung prostaglandin release, indicating a spectrum of possible roles of eicosanoids in the function of the normal and diseased lung. This article reviews the most pertinent issues regarding the roles of arachidonic acid metabolites in the lung.

Animals↗
PubMed1989

Diagnosis of pulmonary hamartoma by bronchoscopic transbronchial biopsy.

Intraparenchymal pulmonary hamartomas are benign lesions that cannot reliably be distinguished from malignant solitary pulmonary nodules by routine chest x-ray or computerized tomography. Thoracotomy or transthoracic needle aspiration or biopsy is usually required to establish the histologic diagnosis of hamartoma. We report a patient in whom a solitary pulmonary nodule was diagnosed as a pulmonary hamartoma by bronchoscopic transbronchial biopsy, obviating the need for a more invasive procedure. Fiberoptic bronchoscopy with transbronchial biopsies should be considered initially in the evaluation of a solitary pulmonary nodule. Special stains for cartilage and fat may aid in the diagnosis of pulmonary hamartomas.

Aged↗
PubMed1988

Endotoxin causes neutrophil-independent oxidative stress in rats.

Endotoxin-induced oxidative stress is investigated in rats by measuring changes in plasma and lung tissue levels of glutathione disulfide (GSSG) using a modified enzymatic assay that allows simultaneous measurement of up to 80 samples. Salmonella enteritidis endotoxin (2 and 20 mg/kg) acutely increased both plasma reduced glutathione and GSSG with a rise in the ratio of GSSG to total glutathione. This increase in GSSG was enhanced by pretreatment with 1,3-bis(2-chloroethyl)1-nitrosourea (BCNU), an inhibitor of the glutathione reductase enzyme. However, there was no significant arteriovenous difference in plasma GSSG across the lung, and lung tissue GSSG did not increase after endotoxin treatment. The increase in plasma GSSG was not blocked by vinblastine-induced neutropenia and could not be reproduced by incubating rat blood in vitro with endotoxin. Receptor antagonists of platelet-activating factor (PAF), at a dose that previously inhibited endotoxin-induced lung injury, attenuated the endotoxin-induced increase in plasma GSSG. We conclude that endotoxin causes neutrophil-independent oxidative stress in rats, which may be enhanced by the action of platelet-activating factor.

Animals↗
PubMed1988

Platelet-activating factor antagonists increase vascular reactivity in perfused rat lungs.

Platelet-activating factor (PAF) administered to the pulmonary circulation in low dose (nanogram) has vasodilatory properties. Therefore, we investigated whether endogenous PAF plays a role in the control of tone in the pulmonary circulation. The PAF receptor antagonists, SRI 63-441 (2.6 X 10(-4) M) and L659,989 (1 X 10(-5) M), were the major investigative tools. In isolated perfused rat lungs, both agents caused a persistent increase in base-line perfusion pressure (Ppa), potentiated angiotensin II (ANG II) vasoconstriction, and potentiated hypoxic vasoconstriction (HPV). This potentiation of ANG II and HPV was found to be independent of circulating blood elements. Vasodilation in the presence of PAF blockade was also impaired. The combination of cyclooxygenase inhibition and PAF receptor blockade had an additive effect on ANG II vasoconstriction but did not cause more potentiation of HPV than achieved with PAF antagonism alone. In vivo, SRI 63-441 (10 mg/kg) caused only a transient increase in base-line Ppa without altering ANG II and hypoxic vasoconstriction. These findings support a vasodilatory role for endogenous PAF in the pulmonary circulation.

Angiotensin II↗
PubMed1988

Role of oxidants, eicosanoids, and neutrophils in amphotericin B lung injury in rats.

Administration of the antifungal antibiotic amphotericin B (AmB, 1 mg/kg) to intact rats produced acute lung injury as indicated by the extravascular leakage of protein and water and histological examination. The injury was neutrophil independent because it occurred in neutropenic rats. AmB produced vasoconstriction and injury in isolated lungs perfused with a cell- and plasma-free physiological solution, and this injury was independent of pulmonary perfusion pressure. In vivo administration of AmB produced an increase in lung tissue and plasma-oxidized glutathione disulfide (GSSG) indicative of oxidant stress. In the isolated lung, the radical scavengers p-hydroxybenzoate (methylparaben) and catalase attenuated AmB lung injury as did 1-phenyl-3-pyrazolidone (Phenidone), a combined radical scavenger and lipoxygenase/cyclooxygenase inhibitor, and the leukotriene antagonist CGP 35949B. Methylparaben and CGP 35949B prevented the elevation in lung tissue leukotriene C4 and B4 levels noted after AmB. We conclude that AmB in the rat produces neutrophil-independent lung injury, which is associated with oxidant stress and eicosanoid production.

Albumins↗
PubMed1987

Pulmonary vascular injury by polycations in perfused rat lungs.

Polycations, such as protamine sulfate and polylysine, have been implicated in the cause of pulmonary edema, but the mechanism is unknown. We studied the vascular effect of protamine in isolated rat lungs perfused with a cell- and plasma-free solution. Protamine (50-1,000 micrograms/ml) increased lung perfusion pressure and caused edema. Blocking the pulmonary vasoconstriction with papaverine (10(-4) M) did not prevent lung edema. In addition, lungs treated with protamine and papaverine showed increased extravascular leakage of 125I-albumin, indicating increased vascular permeability. Histological examination of these lungs showed marked endothelial injury. Functional endothelial damage was further demonstrated by the impairment of the acetylcholine-induced vascular relaxation in protamine-treated vascular rings. Antihistamines and indomethacin failed to block the pulmonary vasoconstriction and increased vascular permeability caused by protamine. In addition, we found that anionic substances, heparin and albumin, blocked the lung injury induced by protamine, whereas other polycations, polylysine and hexadimethrine bromide, caused pulmonary vasoconstriction and increased vascular permeability similar to protamine. We conclude that protamine causes pulmonary endothelial injury and lung edema and suggest that the injury may be charge mediated.

Animals↗
PubMed1987

Platelet-activating factor mediates hemodynamic changes and lung injury in endotoxin-treated rats.

Within 20 min after intraperitoneal injection of Salmonella enteritidis endotoxin in rats, blood platelet-activating factor (PAF) increased from 4.3 +/- 1.3 to 13.7 +/- 2.0 ng/ml (P less than 0.01) and lung PAF from 32.3 +/- 4.9 to 312.3 +/- 19.6 ng (P less than 0.01), but not lung lavage PAF. We tested the effect of PAF receptor antagonists, CV 3988 and SRI 63-441, on endotoxin-induced hemodynamic changes and lung vascular injury. Pretreatment with CV 3988 attenuated systemic hypotension, preserved hypoxic pulmonary vasoconstriction, and prolonged survival of awake catheter-implanted endotoxin-treated (20 mg/kg) rats. Pretreatment with SRI 63-441 prevented the depressed hypoxic pulmonary vasoconstriction after low dose (2 mg/kg) endotoxin. Both CV 3988 and SRI 63-441 blocked the increased extravascular accumulation of 125I-albumin and water in perfused lungs isolated from endotoxin-treated rats. We conclude that PAF is produced in the lung during endotoxemia and may be an important mediator of the systemic and pulmonary hemodynamic changes as well as the acute lung vascular injury after endotoxemia.

Animals↗
PubMed1987

[A comparative clinical trial with tegafur plus lentinan treatment at two different doses in advanced cancer].

In order to evaluate the clinical efficacy of combined tegafur plus lentinan treatment, a comparative trial was performed on patients with advanced cancer using two different doses, a conventional-dose group and a high-dose group. Thirty-four patients were evaluable in this trial. The doses of medication were 600 mg of tegafur p.o. daily and 1-2 mg of lentinan i.v. weekly in the conventional-dose group, and 1,200-800 mg of tegafur p.o. daily and 4 mg of lentinan i.v. weekly in the high-dose group. The response was evaluated using the criteria of Koyama. The response rates were 14.3% for the conventional-dose group and 25.0% for the high-dose group, although no statistical difference was observed. Acute toxicities such as oppression in the anterior chest and dryness of the throat, which were considered to be probably due to lentinan, were noted in patients given rapid administration with 20 ml of solution. However, these effects disappeared with slow-drip infusion using 100-200 ml of solution. These results suggest that the combined tegafur plus lentinan treatment would be better administered at a dose higher than the conventional one for the treatment for advanced cancers.

Adult↗
PubMed1986

PAF antagonists: different effects on platelets, neutrophils, guinea pig ileum and PAF-induced vasodilation in isolated rat lung.

The effects of structurally different PAF receptor blockers were investigated in platelets, neutrophils, guinea pig ileum, rat isolated lung and rat isolated pulmonary artery. PAF caused serotonin release from platelets and a characteristic shape change and adhesion of neutrophils. The antagonists (CV 3988, alprazolam, 48740 RP and Merck-Sharp and Dohme L-652, 731) inhibited platelet serotonin release but not neutrophil shape change adhesion or lysosomal enzyme release. The antagonists in high concentrations (10(-5)-10(-4)M) inhibited nonspecifically the PAF-induced (10(-8)M) guinea pig ileum contraction, but were ineffective at concentrations which inhibited platelet responses. In the rat lung the compounds, in high concentrations, partially inhibited the low dose PAF-induced pulmonary vasodilation and the high dose PAF induced pulmonary vasoconstriction and edema. Our data indicate that some platelet PAF antagonists may be ineffective in blocking the action of PAF on neutrophils and smooth muscle preparations and suggest either PAF-receptor independent actions of PAF or different classes of PAF receptors.

Alprazolam↗
PubMed1986

Actions of opiate agonists, naloxone, and paraben preservatives in the rat lung circulation.

Previous studies have documented direct vascular effects of opiate substances in the systemic circulation. Because opiate receptors have been identified in the lung, we wondered whether opiate substances might affect vasoreactivity in the lung circulation. We studied the pulmonary vascular effects of three opiate agonists: morphine, leucine-enkephalin, and dynorphin, as well as the opiate receptor antagonist naloxone, in isolated rat lungs perfused with a cell- and plasma-free salt solution. Because of previous reports of the smooth muscle effects of the methyl- and propylparaben preservatives in the naloxone preparation, we also studied the pulmonary vascular effects of these preservatives in the rat lung circulation. We found that morphine, a mu-receptor agonist, leucine-enkephalin, a delta-receptor agonist, and dynorphin, a kappa-receptor agonist, caused no immediate vascular effect when injected into the pulmonary artery. In addition, morphine did not affect the pulmonary vasoconstrictions induced by hypoxia, angiotensin II, or potassium chloride. The commercial preparation of naloxone, Narcan, caused a marked vasodilation during hypoxic pulmonary vasoconstriction. However, this effect was entirely attributable to the preservatives methyl- and propylparaben, as pure naloxone had no effect on either the baseline pulmonary vascular tone or the vasoconstrictive response to hypoxia. We conclude that opiate receptor agonists and antagonists do not affect vasoreactivity in the rat lung circulation and that the methyl- and propylparaben preservatives in Narcan are pulmonary vasodilators.

Angiotensin II↗
PubMed1986

Aspergillus terreus causing invasive pulmonary aspergillosis with air-crescent sign.

Aspergillus terreus is an uncommon cause of human disease. A patient with acute myelomonocytic leukemia is described who developed an invasive pulmonary infection with A terreus characterized by an air-crescent sign on chest roentgenogram. Previous reports of A terreus infections and the pathogenesis and significance of an air-crescent sign in invasive pulmonary aspergillosis are reviewed.

Aspergillosis↗
PubMed1984

[A case of hepatocellular carcinoma (acute abdominal type) misdiagnosed as acute appendicitis and satisfactorily treated by a two-stage operation].

A 66-year-old man was admitted because of right lower abdominal pain and was operated on for acute appendicitis on March 12, 1983. It was found that his appendix was not inflamed, but a bleeding tumor was encountered in the posterior segment of the liver. Bleeding was controlled by suturing the liver above the tumor. Postoperative celiac angiography revealed many daughter tumors scattered in, but restricted to, the right lobe of the liver. The patient was treated by transcatheter arterial embolization combined with transcatheter arterial infusion of lipiodol and Adriamycin on April 25. Subsequently, a curative operation (right hemihepatectomy) was performed on May 24. The patient is still alive without recurrence 6 months after the resection. In case of ruptured hepatocellular carcinoma, it appears to be better to perform a two-stage operation with careful estimation of functional reserve of the liver, and to conduct transcatheter arterial embolization between operations to prevent the growth of the tumor during that period.

Abdomen, Acute↗