nicotinamide/infarction

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Ukurasa 1 kutoka 249 matokeo

Delayed treatment with nicotinamide (vitamin B3) reduces the infarct volume following focal cerebral ischemia in spontaneously hypertensive rats, diabetic and non-diabetic Fischer 344 rats.

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Ingia / Ingia

Since hypertension and/or hyperglycemia are risk factors for stroke, we examined whether the putative neuroprotectant, nicotinamide (NAm), could protect spontaneously hypertensive rats (SHR) or diabetic Fischer 344 rats against focal cerebral ischemia using a model of permanent middle cerebral

Post-treatment with nicotinamide (vitamin B(3)) reduces the infarct volume following permanent focal cerebral ischemia in female Sprague-Dawley and Wistar rats.

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Ingia / Ingia

Delayed treatment with nicotinamide (NAm) protects male rats against cerebral ischemia. Since the preponderant use of male animals in stroke research may produce results not applicable to female stroke patients due to gender-related differences, we examined whether delayed NAm treatment could

Delayed multidose treatment with nicotinamide extends the degree and duration of neuroprotection by reducing infarction and improving behavioral scores up to two weeks following transient focal cerebral ischemia in Wistar rats.

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Ingia / Ingia

A single, delayed dose of nicotinamide (NAm) was shown to be protective against focal cerebral ischemia in rats, but the protection was limited to three to seven days following stroke. The investigation reported here was conducted to examine if the use of multiple doses of NAm, administered after

Nicotinamide and ketamine reduce infarct volume and DNA fragmentation in rats after brain ischemia and reperfusion.

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Ingia / Ingia

The possible ability of nicotinamide and ketamine to decrease infarction volume and DNA fragmentation was investigated in a middle cerebral artery occlusion rat model. DNA fragmentation was measured with an enzyme linked immunoassay. Control infarct volume was 223.8 +/- 10.6 mm(3). Ketamine alone

Mechanisms of transformation of nicotinamide mononucleotides to cerebral infarction hemorrhage based on MCAO model.

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Ingia / Ingia

The study aims at discussing the effect of nicotinamide mononucleotides on protecting hemorrhagic transformation of cerebral infarction in the middle cerebral artery occlusion (MCAO) model.Male mice aged 4-5 weeks and weighing about 22-35 g in Shanghai

Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in Wistar rats.

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Ingia / Ingia

Ischemia depletes ATP and initiates cascades leading to irreversible tissue injury. Nicotinamide is a precursor of nicotinamide adenine dinucleotide (NAD+) which increases neuronal ATP concentration and protects against malonate-induced neurotoxicity, trauma and nitric oxide toxicity. We therefore

Delayed treatment with nicotinamide (Vitamin B(3)) improves neurological outcome and reduces infarct volume after transient focal cerebral ischemia in Wistar rats.

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Ingia / Ingia

OBJECTIVE We have previously shown that nicotinamide (NAm) acutely reduces brain infarction induced by permanent middle cerebral artery occlusion (MCAo) in rats. In this study, we investigate whether NAm may protect against ischemia/reperfusion injury by improving sensory and motor behavior as well

Delayed treatment with nicotinamide inhibits brain energy depletion, improves cerebral microperfusion, reduces brain infarct volume, but does not alter neurobehavioral outcome following permanent focal cerebral ischemia in Sprague Dawley rats.

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Ingia / Ingia

Delayed treatment with nicotinamide (NAm) reduces infarction induced by middle cerebral artery occlusion (MCAO) in rats. This study explored some potential mechanisms by which delayed NAm treatment may confer protection in the brain of Sprague-Dawley rats following permanent MCAO (pMCAO). NAm (500

Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction by activating nicotinamide adenine dinucleotide phosphate oxidase during reperfusion.

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Ingia / Ingia

OBJECTIVE Acute hyperglycemia is independently associated with larger myocardial infarct size in both diabetic and nondiabetic patients. We hypothesized that the oxidative stress imposed by acute hyperglycemia contributes to the exacerbation of infarct size during reperfusion. METHODS C57BL/6 mice

Inhibition of nicotinamide phosphoribosyltransferase reduces neutrophil-mediated injury in myocardial infarction.

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Ingia / Ingia

OBJECTIVE Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and recent evidence indicates its role in inflammatory processes. Here, we investigated the potential effects of pharmacological Nampt inhibition with FK866 in a

Puerarin improves cardiac function through regulation of energy metabolism in Streptozotocin-Nicotinamide induced diabetic mice after myocardial infarction.

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Ingia / Ingia

It is well recognized that the incidence of heart failure and the risk of death is high in diabetic patients after myocardial infarction (MI). Accumulating evidence showed that puerarin (PUE) has protecting function on both cardiovascular disease and diabetes. The aim of this study is to explore

Nicotinamide coenzymes in heart and coronary blood during myocardial infarction.

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Ingia / Ingia

[Effect of nicotinamide on the components of the cardiac tissue respiratory chain in experimental myocardial infarct].

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Ingia / Ingia

Effect of administration of vitamin A, ascorbic acid and nicotinamide adenine dinucleotide + flavin adenine dinucleotide on severity of myocardial infarction induced by isoproterenol in rats.

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Ingia / Ingia

[Effect of membrane protectors on the diastolic function of the heart in patients with acute myocardial infarction].

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Ingia / Ingia

Apexcardiography was employed to make a noninvasive assessment of left ventricular diastolic function in 80 patients with extensive myocardial infarction. In half the patients, there were impairments in cardiac diastole as manifested by its altered phase structure and some changed parameters

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