coronary vasospasm/hypoxia

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Hypoxia-reoxygenation triggers coronary vasospasm in isolated bovine coronary arteries via tyrosine nitration of prostacyclin synthase.

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The role of peroxynitrite in hypoxia-reoxygenation-induced coronary vasospasm was investigated in isolated bovine coronary arteries. Hypoxia-reoxygenation selectively blunted prostacyclin (PGI2)-dependent vasorelaxation and elicited a sustained vasoconstriction that was blocked by a cyclooxygenase

Trandolapril plus verapamil inhibits the coronary vasospasm induced by hypoxia following ischemia-reperfusion injury in dogs.

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1. Dogs were exposed to hypoxemia followed by a coronary angiogram at three different times: under control conditions, after ischemia-reperfusion injury, then 30 min later. 2. In the study group, the dogs were treated with trandolapril (0.05 mg/kg) and verapamil (0.1 mg/ kg) just prior to the final

Vasoconstrictor and vasodilator effects of hypoxia.

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Hypoxia has marked effects on artery calibre, which reflects important physiological control mechanisms that are altered in disease states. Hypoxia modifies the release of mediators, especially from the endothelium, and influences smooth muscle membrane potential and Ca2+ regulation. In this review,

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

Effect of hypoxia on endothelium-dependent relaxation of porcine coronary arteries and veins.

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In isolated transverse strips of porcine coronary artery and rings of coronary vein both mild (pO2 = 70 +/- 2.6 mmHg) and severe (pO2 = 17.4 +/- 0.8 mmHg) hypoxia (30 min duration) produced a transient contraction depending on the severity of hypoxia. Hypoxia did not influence the contraction evoked

Mechanisms responsible for coronary vasospasm.

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Studies have been conducted on isolated segments of the left circumflex coronary artery of the dog to gain information on the mechanism or mechanisms of vasospasm. Coronary arteries contain both postjunctional alpha 1- and beta 1-adrenoceptors, and both are accessible to norepinephrine released from

Mechanisms of coronary vasospasm: role of endothelium.

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Studies in recent years have demonstrated that coronary vasospasm (Prinzmetal's Angina) is a consequence of endothelial cell damage. Normal endothelium, in response to increases in shear stress, or to platelet products and other agonists, releases endothelium-derived relaxing factor(s) (EDRF) with

Inhibitory effect of lidoflazine on contractions of isolated canine coronary arteries caused by norepinephrine, 5-hydroxytryptamine, high potassium, anoxia and ergonovine maleate.

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Experiments were performed on isolated coronary arteries to determine whether or not lidoflazine, an agent reported to be beneficial in the treatment of angina pectoris, is effective in antagonizing coronary vasoconstriction. Segments of canine circumflex and right coronary arteries were suspended

Animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction. A study on hemodynamics, EKG, coronary angiography, biochemistry and pathology.

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An animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction (CAS-CATH-AMI) was obtained by injecting ergonovine(0.22 mg/kg) directly into the left coronary artery (LCA) of 17 dogs under general anesthesia. Various parameters of the experimental group were compared with

Coronary artery spasm following on-pump coronary artery bypass grafting with 20 months follow-up.

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We report on a 69-year-old woman who demonstrated native coronary artery and grafted vessel spasm following on-pump coronary artery bypass grafting (CABG). Despite intraaortic balloon pump (IABP) insertion, electrocardiogram (ECG) abnormalities did not disappear. Emergency coronary angiography (CAG)

The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking.

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A reduced oxygen supply to the heart causes coronary vasodilatation in the first instance. But if the hypoxia is severe or prolonged, the dilatation passes off and coronary vasospasm develops leading to a vicious circle with a further reduction of myocardial oxygenation. The spasm is associated with

Preconditioning improves cardioplegia-related coronary microvascular smooth muscle hypercontractility: role of KATP channels.

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OBJECTIVE The effect of preconditioning before hyperkalemic cardioplegia on the coronary smooth muscle remains to be elucidated. We tested the hypothesis that hypoxic preconditioning could protect coronary smooth muscle against subsequent hyperkalemic cardioplegia-induced coronary vasospasm and that

Non-infarctual ST elevation and acute cardiopulmonary failure in carbon monoxide poisoning: a case report.

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Carbon monoxide is produced by the incomplete combustion of organic fuel. In the United States, it is responsible for about 500 deaths annually. Increased carboxyhemoglobin concentration and hypoxia disrupt cardiac myocyte integrity and cause dysrhythmias, acute cardiac failure and

Systemic anaphylaxis--separation of cardiac reactions from respiratory and peripheral vascular events.

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An anaphylactic reaction in the isolated perfused heart is characterized by a drastic coronary constriction, arrhythmias, and an impairment of contractility. In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to ascertain

Spasm of the coronary arteries: causes and consequences (the scientist's viewpoint).

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Both beta 1- and alpha 1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the beta 1-adrenoceptors, whereas constriction prevails in the

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