naloxone and Chest-Pain

naloxone has been researched along with Chest-Pain* in 2 studies

Trials

2 trial(s) available for naloxone and Chest-Pain

ArticleYear
High-dose adenosine infusion provokes oscillations of chest pain without correlation to opioid modulation: a double-blind controlled study.
    The journal of pain, 2004, Volume: 5, Issue:9

    Adenosine is a neuromodulator with both excitatory and inhibitory effects in different organs. High-dose adenosine infusion provokes chest pain in patients and healthy volunteers. This study examines the nature of chest pain and whether it is modified by the mu opioid receptor agonist (beta-endorphin) or a nonselective opioid antagonist (naloxone). Ten healthy volunteers with a mean age of 26 +/- 3 years participated in the study. The study was performed during 3 sessions. During every session the subjects were given a high dose of adenosine infusion (140 microg/kg/min) for 22 minutes. After 5 minutes, the subjects were randomized in a double-blind order on 1 of the 3 categories: (1) as placebo, NaCl bolus for 2 minutes followed by NaCl infusion for 15 minutes; (2) beta-endorphin bolus followed by infusion; and (3) naloxone bolus followed by NaCl infusion. Hemodynamic and pain parameters were monitored. During adenosine infusion, all volunteers experienced chest pain with oscillations of pain intensity. The oscillations continued during beta-endorphin and naloxone. There were no significant differences between hemodynamic and pain parameters during beta-endorphin or naloxone compared to adenosine infusion. High-dose infusion of adenosine provokes chest pain with oscillations of algesia and pain-free intervals. Peripheral opioid administration did not influence the adenosine-provoked chest pain.. Adenosine-induced oscillations of pain and pain-free intervals could theoretically be a sign of neuronal reflex activity dependent on spatiotemporal summation of adenosine excitatory and inhibitory properties. This could contribute to the complex nature of angina pectoris. Peripheral opioid receptors might not be involved in the oscillations.

    Topics: Adenosine; Adult; Analgesics; beta-Endorphin; Chest Pain; Double-Blind Method; Humans; Male; Naloxone; Narcotic Antagonists; Periodicity

2004
Effects of naloxone on myocardial ischemic preconditioning in humans.
    Journal of the American College of Cardiology, 1999, Volume: 33, Issue:7

    We attempted to establish whether naloxone, an opioid receptor antagonist, abolishes the adaptation to ischemia observed in humans during coronary angioplasty after repeated balloon inflations.. Experimental studies indicate that myocardial opioid receptors are involved in ischemic preconditioning.. Twenty patients undergoing angioplasty for an isolated stenosis of a major epicardial coronary artery were randomized to receive intravenous infusion of naloxone or placebo during the procedure. Intracoronary electrocardiogram and cardiac pain (using a 100-mm visual analog scale) were determined at the end of the first two balloon inflations. Average peak velocity in the contralateral coronary artery during balloon occlusion, an index of collateral recruitment, was also assessed by using a Doppler guide wire in the six patients of each group with a stenosis on the left anterior descending coronary artery.. In naloxone-treated patients, ST-segment changes and cardiac pain severity during the second inflation were similar to those observed during the first inflation (12+/-6 vs. 11+/-7 mm, p = 0.3, and 58+/-13 vs. 56+/-12 mm, p = 0.3, respectively), whereas in placebo-treated patients, they were significantly less (6+/-3 vs. 13+/-6 mm, p = 0.002 and 31+/-21 vs. 55+/-22 mm, p = 0.008, respectively). In both naloxone- and placebo-treated patients, average peak velocity significantly increased from baseline to the end of the first inflation (p = 0.04 and p = 0.02, respectively), but it did not show any further increase during the second inflation.. The adaptation to ischemia observed in humans after two sequential coronary balloon inflations is abolished by naloxone and is independent of collateral recruitment. Thus, it is due to ischemic preconditioning and is, at least partially, mediated by opioid receptors, suggesting their presence in the human heart.

    Topics: Aged; Angioplasty, Balloon, Coronary; Blood Flow Velocity; Chest Pain; Collateral Circulation; Coronary Vessels; Electrocardiography; Female; Follow-Up Studies; Humans; Ischemic Preconditioning, Myocardial; Male; Middle Aged; Myocardial Ischemia; Naloxone; Narcotic Antagonists; Pain Measurement; Single-Blind Method; Treatment Outcome; Ultrasonography, Interventional

1999