coronary vasospasm/arginine

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Coronary artery spasm in the rat induced by hypothalamic stimulation.

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Anesthetized rats were sterotaxically implanted with electrodes and electrically stimulated in the lateral hypothalamus. During elevation of the S-T segment on simultaneous precordial electrocardiograms, the heart was perfused with glutaraldehyde-paraformaldehyde fixative and the major coronary

Coronary artery spasm: involvement of small intramyocardial branches.

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A study was conducted to determine if the small (resistance) vessels of the coronary circulation could undergo spasm comparable to that of the major conductance (epicardial) arteries which in the rat measure 275-300 micron in diameter. This information may be relevant to the growing evidence of

Resolution of nebivolol-induced coronary vasospasm by intracoronary nitroglycerin during a coronary angiogram.

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Nebivolol is a novel beta1-selective beta-blocker with vasodilator properties mediated through activation of the l-arginine-nitric oxide pathway. There is no published report of coronary artery spasm associated with nebivolol. We describe a 64-year-old female patient who developed unstable angina

Coronary artery spasm related to thiol oxidation and senescence marker protein-30 in aging.

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BACKGROUND Senescence marker protein-30 (SMP30) decreases with aging, and SMP30 knockout (KO) mice show a short life with increased oxidant stress. OBJECTIVE We assessed the effect of oxidant stress with SMP30 deficiency in coronary artery spasm and clarify its underlying mechanisms. RESULTS We

Coronary vasospasm induced in transgenic mouse with increased phospholipase C-δ1 activity.

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BACKGROUND We reported that phospholipase C (PLC)-δ1 activity was enhanced 3-fold in patients with coronary spastic angina. We detected variant PLC-δ1 with replacement of arginine 257 by histidine (R257H) showing increased enzymatic activity. We tested the hypothesis that increased PLC-δ1 activity

Enhanced activity of variant phospholipase C-delta1 protein (R257H) detected in patients with coronary artery spasm.

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BACKGROUND We recently demonstrated that phospholipase C (PLC)-delta1 activity in cultured skin fibroblasts obtained from patients with coronary spastic angina (CSA) is enhanced. We tested the hypothesis that structural abnormality in PLC-delta1 isoform is a cause of the enhanced

Antianginal effects of FK409, a new spontaneous NO releaser.

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1. The aim of this study was to compare antianginal effects of (+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamide (FK409), a new spontaneous nitric oxide releaser, with those of isosorbide dinitrate (ISDN). We used two types of rat angina model; methacholine- and arginine vasopressin

Recombinant gene transfer of endothelial nitric oxide synthase augments coronary artery relaxations during hypoxia.

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BACKGROUND Coronary arteries respond to hypoxia with transient relaxations, which increases coronary blood flow, in part, by release of nitric oxide. We hypothesized that increased expression of nitric oxide synthase might further augment blood vessel relaxation during hypoxia. The present study

Unmasking of thrombin vasoconstriction in isolated perfused dog hearts after intracoronary infusion of air embolus.

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Effects of intracoronary thrombin and acetylcholine administration on coronary vascular reactivity were studied in isolated perfused (Langendorff) dog hearts before and after air embolus treatment. Under constant flow condition with control coronary perfusion pressure of 71.4 +/- 5.4 mm Hg (mean +/-

Attenuation of lipopolysaccharide-induced hyperreactivity of human internal mammary arteries by melatonin.

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Reactive oxygen species (ROS) are thought to be important mediators in ischaemia/reperfusion injury following coronary vasospasm. The most ubiquitous action of melatonin is that of a free radical scavenger. Therefore, we investigated the action of melatonin by monitoring changes in the tone on ring

Nitric oxide-mediated flow-dependent dilation is impaired in coronary arteries in patients with coronary spastic angina.

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OBJECTIVE This study sought to examine whether flow-dependent dilation is impaired at the site of coronary artery spasm in patients with coronary spastic angina. BACKGROUND Physiologic stimuli such as exercise and exposure to cold have been shown to cause an increase in coronary blood flow, leading

Basal release of endothelium-derived nitric oxide at site of spasm in patients with variant angina.

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OBJECTIVE The aim of this study was to investigate the basal release of nitric oxide at spastic sites in patients with variant angina. BACKGROUND We previously reported that endothelium-dependent dilator responses to acetylcholine, substance P and bradykinin are preserved at the site of coronary

Endothelium-dependent contraction of canine coronary artery is enhanced by crystalloid cardioplegic solution.

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Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution enhances endothelium-dependent contraction of coronary arteries. Segments of canine coronary arteries (n = 8 in each group) were preserved in cold (4 degrees C) crystalloid cardioplegic solution (group 1)

Left Main Coronary Spasm: an Extremely Rare Entity with Possible Life-Threatening Complications.

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Coronary artery spasm is a known cause of acute coronary syndrome. However, left main coronary spasm is an extremely rare entity and can present in different ways depending on the duration and severity of the spasm. We present a 44-year-old female patient who presented with transient ST elevation in

Endothelial nitric oxide synthase T-786C mutation, a reversible etiology of Prinzmetal's angina pectoris.

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Because the endothelial nitric oxide synthase (eNOS) T-786C polymorphism is associated with reduced nitric oxide production and coronary artery spasm in Japanese patients, we speculated that it might be reversibly associated with Prinzmetal's variant angina in white Americans. Polymerase chain

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