chloroquine/opuch

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[The inhibitory effects of chloroquine and dexamethasone on the formation of pulmonary edema in the early stage of smoke inhalation injury in rats].

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OBJECTIVE To explore the inhibitory effects of chloroquine and dexamethasone on the formation of pulmonary edema in the early stage of smoke inhalation injury in rats. METHODS Wistar rats were used and randomly divided into 10 groups, i.e. normal control, 1 PBH (postburn hour), 3 PBH, 6 PBH, 12 PBH

[Effect of chloroquine on edema induced by ovalbumin and dextran and on Ambrose and Eds test in rat].

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[Bilateral edema of optic nerve (toxic edema) during therapy with chloroquine because of p.c.P. ].

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Anthrax toxin protective antigen: inhibition of channel function by chloroquine and related compounds and study of binding kinetics using the current noise analysis.

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Protective antigen (PA) of the tripartite anthrax toxin binds to a cell surface receptor and mediates the transport of two enzymatic components, edema factor and lethal factor, into the cytosol of host cells. Here recombinant PA(63) from Bacillus anthracis was reconstituted into artificial lipid

Chloroquine retinopathy and secondary trauma.

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This report describes a patient who initially presented with established chloroquine retinopathy resulting in reduced distance visual acuity, color vision anomalies and maculopathy in each eye. Subsequent trauma to the left side of the head produced a further decline in vision, accompanied by iritis

The effect of chloroquine upon the developing eye of the chick embryo.

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The effect of chloroquine on the eyes of 8 (8DE) and 15 (15DE) day old chick embryos has been studied. Microphthalmus was observed in 30% of the 8DE and 80% of the 15DE. The most conspicuous changes were seen in the retina. In the 8DE, chloroquine mostly prevented the development of photo-receptors

Falciparum malaria in an overseas traveler complicated by disseminated intravascular coagulation and pulmonary edema.

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A 24-year-old woman was infected with falciparum malaria during travel to Kenya, complicated by intravascular coagulation and pulmonary edema. She was successfully treated with anti-malarial drugs including chloroquine, quinine sulfate and pyrimethamine, with a combined regimen of heparin,

Effect of antirheumatics and inhibitors of cyclooxygenase, lipoxygenases and thromboxane synthetase on cobra venom factor rat paw edema.

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The cobra venom factor (CVF) rat paw edema was inhibited by cyclooxygenase (indomethacin, piroxicam, aspirin), lipoxygenase (BW 755c) and thromboxane synthetase (imidazole) inhibitors as well as by dexamethasone and, at high doses, by paracetamol and phenacetin. No definite results were obtained

Chloroquine exerts neuroprotection following traumatic brain injury via suppression of inflammation and neuronal autophagic death.

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The antimalarial drug, chloroquine (CQ), has been reported as an autophagy inhibitor in a variety of disorders, including Alzheimer's disease and brain ischemia. To the best of our knowledge, no studies to date have examined the potential for CQ to provide neuroprotection in animal models of

The effect of chloroquine administration on two experimental models of acute pancreatitis.

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BACKGROUND Recent experimental findings have suggested that activation of trypsinogen by cathepsin B within acidic pancreatic acinar cell cytoplasmic vacuoles may be a critical early event in both secretagogue and diet-induced pancreatitis. The weak base chloroquine accumulates within acidic

Full recovery after a chloroquine suicide attempt.

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The nonfatal case of a 20 year-old woman who ingested 6 grams of chloroquine in a suicide attempt is reported. After initial ventricular fibrillation, she rapidly developed a pulmonary edema with cardiogenic shock. She was successfully treated with diazepam, epinephrine, dobutamine and mechanical

Protection from anthrax toxin-mediated killing of macrophages by the combined effects of furin inhibitors and chloroquine.

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Cell surface proteolytic processing of anthrax protective antigen by furin or other furin-related proteases is required for its oligomerization, endocytosis, and function as a translocon for anthrax lethal and edema factors. Countering toxin lethality is essential to developing effective

Quinolines attenuate PAF-induced pulmonary pressor responses and edema formation.

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In the present study we have investigated the mechanisms of pulmonary edema caused by platelet-activating factor (PAF) in isolated rat lungs as well as in mice in vivo. In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 +/- 0.18 g. The cyclooxygenase inhibitor aspirin

Integrin αDβ2 influences cerebral edema, leukocyte accumulation and neurologic outcomes in experimental severe malaria.

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Malaria is an infectious disease of major worldwide clinical importance that causes a variety of severe, or complicated, syndromes including cerebral malaria, which is often fatal. Leukocyte integrins are essential for host defense but also mediate physiologic responses of the innate and adaptive

[Therapy for malaria and amoebiasis].

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Treatment of malaria depends on the infecting Plasmodium species. In Plasmodium falciparum malaria the treatment also depends on whether chloroquine resistances occur and whether the course is uncomplicated or complicated. Uncomplicated cases are cared for with chloroquine and with mefloquine or

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