chloroquine/infarction

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[Disorder of the contractile function of the nonischemic portion of the heart in experimental infarct and its prevention by the phospholipase inhibitor chloroquine].

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Contractility of an isolated rat right auricle was studied one day after producing one day after producing experimental infarction in the left cardiac region, there was a pronounced decrease in elasticity, and contractility was depressed, which manifested in an approximately two-fold decline in the

Chloroquine treatment of interstitial lung disease in children.

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Seven children aged 3 months to 11 years with histologically confirmed interstitial lung disease (ILD) [6 with desquamative interstitial pneumonitis (DIP) and 1 with chronic interstitial pneumonitis] were treated with chloroquine, 10 mg/kg/day. One patient, diagnosed late in the course of the

[Cerebral infarction in pernicious malaria. Diagnostic value of computed tomography].

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Case report of a severe form of neuropaludism, contracted in a territory with Plasmodium falciparum completely insensitive to chloroquine. CAT Scan views displayed a small brain infarction. Complete recovery was obtained with a treatment including quinine, tracheal intubation and ventilatory

Activation of IK1 channel by zacopride attenuates left ventricular remodeling in rats with myocardial infarction.

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Activating IK1 channels is considered to be a promising antiarrhythmic strategy. Zacopride has been identified as a selective IK1 channel agonist and can suppress triggered arrhythmias. Whether this drug also exerts a beneficial effect on cardiac remodeling is unknown, and the present study sought

SNX17 produces anti-arrhythmic effects by preserving functional SERCA2a protein in myocardial infarction.

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BACKGROUND Sorting nexin 17 (SNX17) is a critical cytoplasmic adaptor protein that regulates endosomal trafficking of membrane proteins to determine their recycling and/or degradation. The potential role of SNX17 in cardiovascular pathophysiology has not been reported. RESULTS Cardiac arrhythmias

Effect of chloroquine in experimental myocardial ischaemia.

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The cardiac effects of the phospholipase A2 inhibiting agent chloroquine were studied in dogs, rats and cats. During left anterior descending coronary artery occlusion produced in anaesthetized mongrel dog, chloroquine pretreatment considerably reduced the epicardial ST-segment elevation in the

Stress damage to nonischemic divisions of the heart in experimental infarction and its prevention.

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Recently, it has been shown that nonischemic parts of the heart in myocardial infarction were separated from ischemic damaged ones by a sharp border zone. In this connection, the disturbance of contractile function of the myocardium of nonischemic parts is suggested to result from the

Opening of the inward rectifier potassium channel alleviates maladaptive tissue repair following myocardial infarction.

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Activation of the inward rectifier potassium current (IK1) channel has been reported to be associated with suppression of ventricular arrhythmias. In this study, we tested the hypothesis that opening of the IK1 channel with zacopride (ZAC) was involved in the modulation of tissue repair after

Serial follow-up of malaria-induced splenic infarction: A case report

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Malaria shows various clinical manifestations from mild fever to death depending on the Plasmodium species. Among the complications, reports of malaria-associated splenic infarctions are rare. Here we present a case in which a man suffered from malaria-induced splenic infarction with serial

Hyper-reactive malarial splenomegaly and splenic infarct in a caucasian toddler.

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A 4-year-old boy from the United States had been staying in Indonesia for five months when he presented with fever, severe lethargy, progressive weight loss, and abdominal distension. He was first diagnosed with Plasmodium vivax infection in Indonesia and received treatment with chloroquine.

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling.

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OBJECTIVE The alterations in myocyte autophagy after myocardial infarction (MI) and the underlying mechanisms have not been fully understood. In this study, we investigated the temporal changes of myocyte autophagy in the remote non-infarcted myocardium in rabbits after MI and the relationships

A case of symptomatic splenic infarction in vivax malaria.

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Splenic infarction is a rare complication in malaria cases, and is caused primarily by Plasmodium falciparum. Recently in South Korea, only P. vivax has prevailed since 1993. Although the probability that symptomatic splenic infarction may occur in vivax malaria cases is considered relatively high,

Inhibition of DPP-4 reduces acute mortality after myocardial infarction with restoration of autophagic response in type 2 diabetic rats.

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BACKGROUND Type 2 diabetes mellitus (T2DM) worsens the outcome after myocardial infarction (MI). Here, we hypothesized that inhibition of dipeptidyl peptidase-4 (DPP-4) improves survival after MI in T2DM by modifying autophagy in the non-infarcted region of the heart. RESULTS Under baseline

Exploration of Multiple Signaling Pathways Through Which Sodium Tanshinone IIA Sulfonate Attenuates Pathologic Remodeling Experimental Infarction.

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The level of maladaptive myocardial remodeling consistently contributes to the poor prognosis of patients following a myocardial infarction (MI). In this study, we investigated whether and how sodium tanshinone IIA sulfonate (STS) would attenuate the post-infarct cardiac remodeling in mice model of

Parkin Regulates Mitochondrial Autophagy After Myocardial Infarction in Rats.

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BACKGROUND To study the role of Parkin in the regulation of mitochondrial autophagy in the heart by assessing mitochondrial autophagy and changes in Parkin protein expression in rat myocardium after myocardial infarction (MI). MATERIAL AND METHODS Rats were randomly assigned to three groups:

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