capsaicin/infarction

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Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats.

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BACKGROUND Evidence indicated an involvement of afferent nerves in the pathology of acute myocardial infarction. This study was undertaken to clarify the role and mechanisms by which the sensory afferent degeneration exacerbates the myocardial injury in acute myocardial infarction in

Coronary vasospasm and acute myocardial infarction induced by a topical capsaicin patch.

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Capsaicin is the active component of chili peppers, which has been shown to possess several beneficial effects. Currently, the best-known medical use of capsaicin is as a topical painkiller. Drug-induced myocardial infarction is not a common phenomenon and the underlying mechanism has been related

Aggravation of myocardial infarction in the porcine heart by capsaicin-induced depletion of calcitonin gene-related peptide (CGRP).

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The potent vasodilator calcitonin gene-related peptide (CGRP) is stored in a population of C-fiber afferents that are sensitive to capsaicin. CGRP has been suggested to have a beneficial effect in myocardial ischemia. In this study we used capsaicin pretreatment to deplete cardiac C-fiber peptide

Capsaicin, arterial hypertensive crisis and acute myocardial infarction associated with high levels of thyroid stimulating hormone.

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Chili peppers are rich in capsaicin. The potent vasodilator calcitonin gene-related peptide (CGRP) is stored in a population of C-fiber afferents that are sensitive to capsaicin. CGRP and peptides released from cardiac C fibers have a beneficial effect in myocardial ischemia and reperfusion. It has

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine.

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Early cardioprotection can be achieved by a brief ischaemia of noncardiac tissues. Our study examined whether a brief ischaemia of the small intestine induces both early and delayed cardioprotection in the rabbit and assessed the possible mechanism involved in the activation of capsaicin-sensitive

[Protective effect of capsaicin on against myocardial ischemia-reperfusion injury of rat in vivo].

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OBJECTIVE To explore whether the capsaicin offers protective effect and possible mechanism on against myocardial ischemia-reperfusion injury of rat in vivo. METHODS Ligating the left anterior descending coronary artery for 45 min and loosing it for 120 min were performed to establish the rat model

Mechanisms underlying capsaicin effects in canine coronary artery: implications for coronary spasm.

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OBJECTIVE The TRPV1, transient receptor potential vanilloid type 1, agonist capsaicin is considered to be beneficial for cardiovascular health because it dilates coronary arteries through an endothelial-dependent mechanism and may slow atheroma progression. However, recent reports indicate that high

Serotonin-Mediated Cardiac Analgesia via Ah-Type Baroreceptor Activation Contributes to Silent Angina and Asymptomatic Infarction.

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Silent angina is a critical phenomenon in the clinic and is more commonly associated with women patients suffering from myocardial ischemia. Its underlying cause remains mysterious in medicine. With our recent discovery of female-specific Ah-type baroreceptor neurons (BRNs), we hypothesize that

Neural control of blood pressure: focusing on capsaicin-sensitive sensory nerves.

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Hypertension is a major risk factor leading to devastating cardiovascular events such as myocardial infarction, stroke, heart failure, and renal failure. Despite intensive research in this area, mechanisms underlying essential hypertension remain to be defined. Accumulating evidence indicates that

A case of acute myocardial infarction due to the use of cayenne pepper pills.

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The use of weight loss pills containing cayenne pepper has ever been increasing. The main component of cayenne pepper pills is capsaicin. There are conflicting data about the effects of capsaicin on the cardiovascular system. In this paper, we present the case of a 41 year old male patient with no

Acute myocardial infarction and coronary vasospasm associated with the ingestion of cayenne pepper pills in a 25-year-old male.

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Capsaicin, one of the major active components of cayenne pepper pills, is an over-the-counter substance with sympathomimetic activity used commonly by young individuals for weight loss. Here we report the case of a previously healthy young male who developed severe chest pain after using cayenne

Remote cardioprotection by direct peripheral nerve stimulation and topical capsaicin is mediated by circulating humoral factors.

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We have previously shown that remote ischemic preconditioning by limb ischemia (rIPC) or intra-arterial adenosine releases a dialyzable cardioprotective circulating factor(s), the release of which requires an intact neural connection to the limb and is blocked by pretreatment with

Factors mediating remote preconditioning of trauma in the rat heart: central role of the cytochrome p450 epoxygenase pathway in mediating infarct size reduction.

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The present study further identified factors involved in the cardioprotective phenomenon of remote preconditioning of trauma (RPCT) with special emphasis on the role of the epoxyeicosatrienoic acids (EETs) in mediating this phenomenon. Remote preconditioning of trauma was produced by an abdominal

Muscle mechanoreflex and metaboreflex responses after myocardial infarction in rats.

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BACKGROUND During exercise, the sympathetic nervous system is activated and blood pressure and heart rate increase. In heart failure (HF), the muscle metaboreceptor contribution to sympathetic outflow is attenuated and the mechanoreceptor contribution is accentuated. Previous studies suggest that

Degeneration of sensory afferent nerves enhances pulmonary inflammatory alterations in acute myocardial infarction in rats.

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BACKGROUND Evidence suggests proinflammatory changes in the lungs during acute myocardial infarction and a participation of neural mechanisms and substance P in the pathology. This study was undertaken to investigate the role and the mechanisms by which sensory afferent degeneration at neonatal

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