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Journal articles on the topic 'Cardiac receptors. Opioids'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Kunecki, Marcin, Wojciech Płazak, Piotr Podolec, and Krzysztof S. Gołba. "Effects of endogenous cardioprotective mechanisms on ischemia-reperfusion injury." Postępy Higieny i Medycyny Doświadczalnej 71 (January 10, 2017): 20–31. http://dx.doi.org/10.5604/01.3001.0010.3786.

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Ischemic heart disease have been remarked as a leading cause of morbidity and mortality in adults. Early restoration of cardiac perfusion is necessary to restore perfusion of ischemic heart muscle. Effective revascularization reduce mortality by limiting myocardial necrosis at the acute phase of the cardiac infarction. However, reperfusion may induce a cascade of pathophysiological reactions causing the increase of the infarct area of the myocardium This phenomenon known as ischemia-reperfusion injury is responsible for up to 50% of the final infarct size. Sequences of brief episodes of nonlet

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Farias, Martin, Keith E. Jackson, Darice Yoshishige та James L. Caffrey. "Cardiac enkephalins interrupt vagal bradycardia via δ2-opioid receptors in sinoatrial node". American Journal of Physiology-Heart and Circulatory Physiology 284, № 5 (2003): H1693—H1701. http://dx.doi.org/10.1152/ajpheart.00730.2002.

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Local cardiac opioids appear to be important in determining the quality of vagal control of heart rate. Introduction of the endogenous opioid methionine-enkephalin-arginine-phenylalanine (MEAP) into the interstitium of the canine sinoatrial node by microdialysis attenuates vagally mediated bradycardia through a δ-opioid receptor mechanism. The following studies were conducted to test the hypothesis that a δ2-opiate receptor subtype mediates the interruption of vagal transmission. Twenty mongrel dogs were anesthetized and instrumented with microdialysis probes inserted into the sinoatrial node.

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Venkatesan, Priya, Sunit Baxi, Cory Evans, Robert Neff, Xin Wang та David Mendelowitz. "Glycinergic Inputs to Cardiac Vagal Neurons in the Nucleus Ambiguus Are Inhibited by Nociceptin and μ-Selective Opioids". Journal of Neurophysiology 90, № 3 (2003): 1581–88. http://dx.doi.org/10.1152/jn.01117.2002.

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Most parasympathetic regulation of heart rate originates from preganglionic cardiac vagal neurons within the nucleus ambiguus. Little is known regarding the modulation of glycinergic transmission to these neurons. However, the presence of μ-opioid receptors and opioid-receptor-like (ORL1) receptors within the ambiguus, together with the presence of endogenous ligands for both receptor types in the same area, suggests opioids may modulate synaptic transmission to cardiac vagal neurons. This study therefore examined the effects of endomorphin-1 and endomorphin-2 (the μ-selective endogenous pepti

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Bolte, Craig, Gilbert Newman та Jo El J. Schultz. "Hypertensive state, independent of hypertrophy, exhibits an attenuated decrease in systolic function on cardiac κ-opioid receptor stimulation". American Journal of Physiology-Heart and Circulatory Physiology 296, № 4 (2009): H967—H975. http://dx.doi.org/10.1152/ajpheart.00909.2008.

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Opioids/opiates are commonly administered to alleviate pain, unload the heart, or decrease breathlessness in patients with advanced heart failure. As such, it is important to evaluate whether the myocardial opioidergic system is altered in cardiac disease. A hamster model of spontaneous hypertension was investigated before the development of hypertension (1 mo of age) and in the hypertensive state (10 mo of age) to evaluate the effect of prolonged hypertension on myocardial opioidergic activity. Plasma β-endorphin was decreased before the development of hypertension and in the hypertensive sta

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Imai, N., M. Kashiki, P. D. Woolf, and C. S. Liang. "Comparison of cardiovascular effects of mu- and delta-opioid receptor antagonists in dogs with congestive heart failure." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (1994): H912—H917. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h912.

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We have shown previously that right heart failure (RHF) in dogs is associated with activated endogenous opiate systems, and that administration of the opioid receptor antagonist, naloxone, increases arterial pressure, cardiac contractile function and organ blood flows. To study whether the cardiovascular effects of naloxone are mediated via the mu- or delta-opioid receptors, we administered ICI-154,129, a delta-receptor antagonist, and naloxonazine, a mu-receptor antagonist, to 10 conscious dogs with RHF on 2 separate days. Like naloxone, ICI-154,129 increased mean aortic pressure, cardiac out

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Kienbaum, Peter, Norbert Thurauf, Martin C. Michel, Norbert Scherbaum, Markus Gastpar, and Jurgen Peters. "Profound Increase in Epinephrine Concentration in Plasma and Cardiovascular Stimulation after [micro sign]-Opioid Receptor Blockade in Opioid-addicted Patients during Barbiturate-induced Anesthesia for Acute Detoxification." Anesthesiology 88, no. 5 (1998): 1154–61. http://dx.doi.org/10.1097/00000542-199805000-00004.

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Background Acute displacement of opioids from their receptors by administration of large doses of opioid antagonists during general anesthesia is a new approach for detoxification of patients addicted to opioids. The authors tested the hypothesis that mu-opioid receptor blockade by naloxone induces cardiovascular stimulation mediated by the sympathoadrenal system. Methods Heart rate, cardiac index, and intravascular pressures were measured in 10 patients addicted to opioids (drug history; mean +/- SD, 71 +/- 51 months) during a program of methadone substitution (96 +/- 57 mg/day). Cardiovascul

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Lishmanov, Yu B., L. N. Maslov, N. Yu Naryzhnaya, et al. "ENDOGENOUS OPIOID SYSTEM AS A MEDIATOR OF ACUTE AND LONG-TERM ADAPTATION TO STRESS. PROSPECTS FOR CLINICAL USE OF OPIOID PEPTIDES." Annals of the Russian academy of medical sciences 67, no. 6 (2012): 73–82. http://dx.doi.org/10.15690/vramn.v67i6.287.

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It has been well established that opioid peptides (OPs) affect various hormonal systems. Opioids exhibit stress-limiting and gastro-protective effects in stressed animals, acting via μ- and δ-opioid receptors (OR). Peripheral μ-OR stimulation by endogenous and exogenous opioids increases cardiac tolerance to pathological consequences of stress. Enhancement of prostacyclin synthesis, decrease of thromboxane production as well as suppression of lipid peroxidation can be directly responsible for cardioprotective effects of OPs in stressed animals. Adaptive responses are accompanied by increased O

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Fu, Liang-Wu, and John C. Longhurst. "Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 1 (2013): H76—H85. http://dx.doi.org/10.1152/ajpheart.00091.2013.

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Thinly myelinated Aδ-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) sensory nerve fibers are activated during myocardial ischemia to transmit the sensation of angina pectoris. Although recent observations showed that myocardial ischemia increases the concentrations of opioid peptides and that the stimulation of peripheral opioid receptors inhibits chemically induced visceral and somatic nociception, the role of opioids in cardiac spinal afferent signaling during myocardial ischemia has not been studied. The present study tested the hypothesis that peripheral opioid receptors modul

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Periyasamy, S. M. "Inhibition of cardiac sarcolemmal Na+/H+ antiporter by opioids." Canadian Journal of Physiology and Pharmacology 70, no. 7 (1992): 1048–56. http://dx.doi.org/10.1139/y92-144.

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In our routine screening of chemicals that would inhibit cardiac sarcolemmal Na+/H+ antiporter, we discovered that some of the opioids produced inhibition of cardiac sarcolemmal Na+/H+ antiporter in micromolar concentrations. Using U-50,488H, a selective κ-opioid agonist, we characterized the nature of interaction between opioids and the Na+/H+ antiporter. The inhibitory effect of U-50,488H on Na+/H+ antiporter was immediate and reversible, and was not mediated through the interaction with the opioid receptors but due to the direct interaction of U-50.488H with the Na+/H+ antiporter. The kinet

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McLaughlin, P. J. "Regulation of DNA synthesis of myocardial and epicardial cells in developing rat heart by [Met5]enkephalin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 1 (1996): R122—R129. http://dx.doi.org/10.1152/ajpregu.1996.271.1.r122.

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Endogenous opioids serve as negative growth factors in neural and nonneural tissues in addition to being neuromodulators. This study investigated the hypothesis that native opioid peptides are inhibitory growth factors in heart development. DNA synthesis of ventricular myocardial and epicardial cells in 1-day-old rats was examined. Administration of a variety of opioids and peptides revealed that [Met5]enkephalin had the greatest inhibitory effect on DNA synthesis; peptides related to mu-, delta-, kappa-, epsilon-, and sigma-receptors had no influence on cell proliferation, even at concentrati

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Streicher, John M., та Edward J. Bilsky. "Peripherally Acting μ-Opioid Receptor Antagonists for the Treatment of Opioid-Related Side Effects: Mechanism of Action and Clinical Implications". Journal of Pharmacy Practice 31, № 6 (2017): 658–69. http://dx.doi.org/10.1177/0897190017732263.

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Opioid receptors are distributed throughout the central and peripheral nervous systems and on many nonneuronal cells. Therefore, opioid administration induces effects beyond analgesia. In the enteric nervous system (ENS), stimulation of µ-opioid receptors triggers several inhibitory responses that can culminate in opioid-induced bowel dysfunction (OBD) and its most common side effect, opioid-induced constipation (OIC). OIC negatively affects patients’ quality of life (QOL), ability to work, and pain management. Although laxatives are a common first-line OIC therapy, most have limited efficacy

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Zatta, Amanda J., Hajime Kin, Darice Yoshishige, et al. "Evidence that cardioprotection by postconditioning involves preservation of myocardial opioid content and selective opioid receptor activation." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 3 (2008): H1444—H1451. http://dx.doi.org/10.1152/ajpheart.01279.2006.

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Opioids introduced at reperfusion (R) following ischemia (I) reduce infarct size much like postconditioning, suggesting the hypothesis that postconditioning increases cardiac opioids and activates local opioid receptors. Anesthetized male rats subjected to 30 min regional I and 3 h R were postconditioned with three cycles of 10 s R and 10 s reocclusion at onset of R. Naloxone (NL), its peripherally restricted analog naloxone methiodide, δ-opioid receptor (DOR) antagonist naltrindole (NTI), κ-opioid receptor antagonist norbinaltorphimine (NorBNI), and μ-opioid receptor (MOR) antagonist H-D-Phe-

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Leffler, Andreas, Georg Frank, Katrin Kistner та ін. "Local Anesthetic-like Inhibition of Voltage-gated Na+Channels by the Partial μ-opioid Receptor Agonist Buprenorphine". Anesthesiology 116, № 6 (2012): 1335–46. http://dx.doi.org/10.1097/aln.0b013e3182557917.

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Background Opioids induce analgesia mainly by inhibiting synaptic transmission via G protein-coupled opioid receptors. In addition to analgesia, buprenorphine induces a pronounced antihyperalgesia and is an effective adjuvant to local anesthetics. These properties only partially apply to other opioids, and thus targets other than opioid receptors are likely to be employed. Here we asked if buprenorphine inhibits voltage-gated Na(+) channels. Methods Na(+) currents were examined by whole cell patch clamp recordings on different recombinant Na(+) channel α-subunits. The effect of buprenorphine o

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Tjen-A-Looi, Stephanie C., Peng Li, Min Li та John C. Longhurst. "Modulation of cardiopulmonary depressor reflex in nucleus ambiguus by electroacupuncture: roles of opioids and γ-aminobutyric acid". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, № 7 (2012): R833—R844. http://dx.doi.org/10.1152/ajpregu.00440.2011.

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Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) elicits depressor cardiovascular reflex responses, including decreases in blood pressure and heart rate mediated in part by the brain stem parasympathetic cardiac neurons in the nucleus ambiguus (NAmb). The present study examined NAmb neurotransmitter mechanisms underlying the influence of electroacupuncture (EA) on the PBG-induced hypotension and bradycardia. We hypothesized that somatic stimulation during EA modulates PBG responses through opioid and γ-aminobutyric acid (GABA) modulation in the NAmb. Anesthetized and ventila

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Roychoudhury, Priodarshi, Astha Koolwal Kapoor, Declan Walsh, Henry Cortes, and Hance Clarke. "State of the science: cannabis and cannabinoids in palliative medicine—the potential." BMJ Supportive & Palliative Care 11, no. 3 (2021): 299–302. http://dx.doi.org/10.1136/bmjspcare-2021-002888.

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Cannabinoids are chemicals derived naturally from the cannabis plant or are synthetically manufactured. They interact directly with cannabinoid receptors or share chemical similarity with endocannabinoids (or both). Within palliative medicine, cannabinoid receptors (CB1 and CB2) may modulate some cancer symptoms: appetite, chemotherapy-induced nausea and vomiting, and mood, pain and sleep disorders. Opioid and cannabinoid receptors have overlapping neuroanatomical receptor distribution, particularly at the dorsal horn, dorsal striatum and locus coeruleus. They have a favourable safety profile

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Farias, Martin, Keith Jackson, Michael Johnson, and James L. Caffrey. "Cardiac enkephalins attenuate vagal bradycardia: interactions with NOS-1-cGMP systems in canine sinoatrial node." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (2003): H2001—H2012. http://dx.doi.org/10.1152/ajpheart.00275.2003.

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Endogenous opioids and nitric oxide (NO) are recognized modulators of cardiac function. Enkephalins and inhibitors of NO synthase (NOS) both produce similar interruptions in the vagal control of heart rate. This study was conducted to test the hypothesis that NO systems within the canine sinoatrial (SA) node facilitate local vagal transmission and that the endogenous enkephalin methionine-enkephalin-arginine-phenylalanine (MEAP) attenuates vagal bradycardia by interrupting the NOS-cGMP pathway. Microdialysis probes were inserted into the SA node, and they were perfused with nonselective ( Nω-n

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Pearce, William. "Hypoxic regulation of the fetal cerebral circulation." Journal of Applied Physiology 100, no. 2 (2006): 731–38. http://dx.doi.org/10.1152/japplphysiol.00990.2005.

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Fetal cerebrovascular responses to acute hypoxia are fundamentally different from those observed in the adult cerebral circulation. The magnitude of hypoxic vasodilatation in the fetal brain increases with postnatal age although fetal cerebrovascular responses to acute hypoxia can be complicated by age-dependent depressions of blood pressure and ventilation. Acute hypoxia promotes adenosine release, which depresses fetal cerebral oxygen consumption through action of adenosine on neuronal A1 receptors and vasodilatation through activation of A2 receptors on cerebral arteries. The vascular effec

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Dehe, Lukas, Mohammed Shaqura, Michael Nordine, et al. "Chronic Naltrexone Therapy Is Associated with Improved Cardiac Function in Volume Overloaded Rats." Cardiovascular Drugs and Therapy 35, no. 4 (2021): 733–43. http://dx.doi.org/10.1007/s10557-020-07132-4.

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Abstract Purpose Myocardial opioid receptors were demonstrated in animals and humans and seem to colocalize with membranous and sarcolemmal calcium channels of the excitation–contraction coupling in the left ventricle (LV). Therefore, this study investigated whether blockade of the cardiac opioid system by naltrexone would affect cardiac function and neurohumoral parameters in Wistar rats with volume overload-induced heart failure. Methods Volume overload in Wistar rats was induced by an aortocaval fistula (ACF). Left ventricular cardiac opioid receptors were identified by immunohistochemistry

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Huh, Joon, Garrett J. Gross, Hiroshi Nagase та Bruce T. Liang. "Protection of cardiac myocytes via δ1-opioid receptors, protein kinase C, and mitochondrial KATP channels". American Journal of Physiology-Heart and Circulatory Physiology 280, № 1 (2001): H377—H383. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h377.

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The objective of the present study was to investigate the role of δ1-opioid receptors in mediating cardioprotection in isolated chick cardiac myocytes and to investigate whether protein kinase C and mitochondrial ATP-sensitive K+(KATP) channels act downstream of the δ1-opioid receptor in mediating this beneficial effect. A 5-min preexposure to the selective δ1-opioid receptor agonist (−)-TAN-67 (1 μM) resulted in less myocyte injury during the subsequent prolonged ischemia compared with untreated myocytes. 7-Benzylidenenaltrexone, a selective δ1-opioid receptor antagonist, completely blocked t

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Sigg, Daniel C., James A. Coles, Peter R. Oeltgen та Paul A. Iaizzo. "Role of δ-opioid receptor agonists on infarct size reduction in swine". American Journal of Physiology-Heart and Circulatory Physiology 282, № 6 (2002): H1953—H1960. http://dx.doi.org/10.1152/ajpheart.01045.2001.

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Opioids are involved in cardiac ischemic preconditioning. Important species differences in cellular signaling mechanisms, antiarrhythmic, and antistunning effects have been described. The role of the δ-opioid receptor activation in swine remains unknown. Forty minutes before a 45-min occlusion and 180-min reperfusion of the left anterior descending coronary artery, open-chest, pentobarbital-anesthetized swine received either 1) saline (controls); 2) [d-Ala2,d-Leu5]enkephalin (DADLE); 3) [d-Pen2,5]enkephalin (DPDPE); 4) deltorphin-D, a novel δ2-opioid agonist; or 5) ischemic preconditioning (IP

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Xiao, Guo-Sheng, Jing-Jun Zhou, Guan-Ying Wang, Chun-Mei Cao, Gui-Rong Li, and Tak-Ming Wong. "In Vitro Electrophysiologic Effects of Morphine in Rabbit Ventricular Myocytes." Anesthesiology 103, no. 2 (2005): 280–86. http://dx.doi.org/10.1097/00000542-200508000-00011.

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Background Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results Morphine at

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Panneerselvam, Mathivadhani, Yasuo M. Tsutsumi, Jacqueline A. Bonds та ін. "Dark chocolate receptors: epicatechin-induced cardiac protection is dependent on δ-opioid receptor stimulation". American Journal of Physiology-Heart and Circulatory Physiology 299, № 5 (2010): H1604—H1609. http://dx.doi.org/10.1152/ajpheart.00073.2010.

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Epicatechin, a flavonoid, is a well-known antioxidant linked to a variety of protective effects in both humans and animals. In particular, its role in protection against cardiovascular disease has been demonstrated by epidemiologic studies. Low-dose epicatechin, which does not have significant antioxidant activity, is also protective; however, the mechanism by which low-dose epicatechin induces this effect is unknown. Our laboratory tested the hypothesis that low-dose epicatechin mediates cardiac protection via opioid receptor activation. C57BL/6 mice were randomly assigned to 1 of 10 groups:

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Zhang, Ye, Michael G. Irwin, and Tak Ming Wong. "Remifentanil Preconditioning Protects against Ischemic Injury in the Intact Rat Heart." Anesthesiology 101, no. 4 (2004): 918–23. http://dx.doi.org/10.1097/00000542-200410000-00017.

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Background Opioid receptors mediate cardiac ischemic preconditioning. Remifentanil is a new, potent ultra-short-acting phenylpiperidine opioid used in high doses for anesthesia. The authors hypothesize that pretreatment with this drug confers cardioprotection. Methods Male Sprague-Dawley rats were anesthetized and the chest was opened. All animals were subjected to 30 min of occlusion of the left coronary artery and 2 h of reperfusion. Before the 30-min occlusion, rats received either preconditioning by ischemia (ischemic preconditioning, 5-min occlusion, 5-min reperfusion x 3) or pretreatment

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Ventura, C., M. C. Capogrossi, H. A. Spurgeon, and E. G. Lakatta. "Kappa-opioid peptide receptor stimulation increases cytosolic pH and myofilament responsiveness to Ca2+ in cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 5 (1991): H1671—H1674. http://dx.doi.org/10.1152/ajpheart.1991.261.5.h1671.

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Although kappa- and delta-opioid receptors on mammalian cardiac myocytes have been discovered recently, the intracellular effects that result from stimulation of these receptors remain unknown. We examine the effects of a rapid and brief exposure to a kappa-opioid receptor agonist on intracellular Ca2+, pH, and cell length in individual isolated rat ventricular cells. The specific kappa-agonist trans-dl-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]- benzene-acetamide (U-50488H) (methane sulfonate salt) caused a transient increase in cytosolic pH (pHi) measured from the change in SNARF

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Espinoza, M., R. Riquelme, A. M. Germain, J. Tevah, J. T. Parer, and A. J. Llanos. "Role of endogenous opioids in the cardiovascular responses to asphyxia in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 5 (1989): R1063—R1068. http://dx.doi.org/10.1152/ajpregu.1989.256.5.r1063.

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Intravenous administration of the opioid receptor antagonist naloxone to asphyxiated fetal sheep increases the arterial blood pressure. We examined the hypothesis that endogenous opioids modify the cardiac output distribution during asphyxia due to changes in the vascular resistance of some fetal organs. Thirteen fetal sheep (0.8-0.9 of gestation) were chronically catheterized. Fetal asphyxia was induced by reducing the uterine blood flow with an inflatable occluder around the common internal iliac artery to approximately 50% of control for 40 min. Naloxone solution or the solvent alone was ad

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Villemagne, Patricia S., Robert F. Dannals, Hayden T. Ravert, and James J. Frost. "PET imaging of human cardiac opioid receptors." European Journal of Nuclear Medicine and Molecular Imaging 29, no. 10 (2002): 1385–88. http://dx.doi.org/10.1007/s00259-002-0897-z.

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Treskatsch, S., M. Shaqura, C. Spies, M. Schäfer, and S. A. Mousa. "Cardiac opioid receptors as potential targets for local opioid regulation." European Journal of Anaesthesiology 27 (June 2010): 72. http://dx.doi.org/10.1097/00003643-201006121-00230.

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Graf, Bernhard M., Martin N. Vicenzi, Eike Martin, Zeljko J. Bosnjak, and David F. Stowe. "Ketamine Has Stereospecific Effects in the Isolated Perfused Guinea Pig Heart." Anesthesiology 82, no. 6 (1995): 1426–37. http://dx.doi.org/10.1097/00000542-199506000-00014.

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Background S(+)-Ketamine is judged to produce more potent anesthesia than either the racemate or the R(-) ketamine isomer because of differential activation of specific cerebral receptors. Other than central nervous system effects, the most important side effects of ketamine occur in the cardiovascular system. We examined the direct cardiac effects of the isomers and the racemate of ketamine in the isolated perfused guinea pig heart. Methods Twenty-three guinea pig hearts were perfused by the Langendorff technique with modified 37 degrees C Krebs-Ringer's solution (97% oxygen and 3% carbon dio

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Zhang, Shi-zhong, Ning-fu Wang, Jian Xu та ін. "κ-Opioid Receptors Mediate Cardioprotection by Remote Preconditioning". Anesthesiology 105, № 3 (2006): 550–56. http://dx.doi.org/10.1097/00000542-200609000-00019.

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Background Remote preconditioning is known to be cardioprotective, but the exact mechanism has not been fully elucidated. The objective of the current study was to investigate the role of kappa-opioid receptors in cardioprotection by remote preconditioning and reveal possible underlying mechanisms. Methods Remote preconditioning was induced in anesthetized male Sprague-Dawley rats by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. Myocardial ischemia-reperfusion was achieved by ligation of the left anterior descending coronary artery for 30 min and the

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Cassell, Robert J., Krishna K. Sharma, Hongyu Su, et al. "The Meta-Position of Phe4 in Leu-Enkephalin Regulates Potency, Selectivity, Functional Activity, and Signaling Bias at the Delta and Mu Opioid Receptors." Molecules 24, no. 24 (2019): 4542. http://dx.doi.org/10.3390/molecules24244542.

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As tool compounds to study cardiac ischemia, the endogenous δ-opioid receptors (δOR) agonist Leu5-enkephalin and the more metabolically stable synthetic peptide (d-Ala2, d-Leu5)-enkephalin are frequently employed. However, both peptides have similar pharmacological profiles that restrict detailed investigation of the cellular mechanism of the δOR’s protective role during ischemic events. Thus, a need remains for δOR peptides with improved selectivity and unique signaling properties for investigating the specific roles for δOR signaling in cardiac ischemia. To this end, we explored substitution

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Frithiof, R., and M. Rundgren. "Activation of central opioid receptors determines the timing of hypotension during acute hemorrhage-induced hypovolemia in conscious sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (2006): R987—R996. http://dx.doi.org/10.1152/ajpregu.00070.2006.

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After an initial compensatory phase, hemorrhage reduces blood pressure due to a widespread reduction of sympathetic nerve activity (decompensatory phase). Here, we investigate the influence of intracerebroventricular naloxone (opioid-receptor antagonist) and morphine (opioid-receptor agonist) on the two phases of hemorrhage, central and peripheral hemodynamics, and release of vasopressin and renin in chronically instrumented conscious sheep. Adult ewes were bled (0.7 ml·kg−1·min−1) from a jugular vein until mean arterial blood pressure (MAP) reached 50 mmHg. Starting 30 min before and continui

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Barbosa, Joana, Juliana Faria, Fernanda Garcez, et al. "Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats." Pharmaceuticals 14, no. 2 (2021): 97. http://dx.doi.org/10.3390/ph14020097.

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Tramadol and tapentadol, two structurally related synthetic opioid analgesics, are widely prescribed due to the enhanced therapeutic profiles resulting from the synergistic combination between μ-opioid receptor (MOR) activation and monoamine reuptake inhibition. However, the number of adverse reactions has been growing along with their increasing use and misuse. The potential toxicological mechanisms for these drugs are not completely understood, especially for tapentadol, owing to its shorter market history. Therefore, in the present study, we aimed to comparatively assess the putative lung,

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Zhang, Li, Hui Guo, Fang Yuan, et al. "Limb remote ischemia per-conditioning protects the heart against ischemia–reperfusion injury through the opioid system in rats." Canadian Journal of Physiology and Pharmacology 96, no. 1 (2018): 68–75. http://dx.doi.org/10.1139/cjpp-2016-0585.

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Remote ischemia per-conditioning (RPerC) has been demonstrated to have cardiac protection, but the underlying mechanism remains unclear. This study aimed to investigate the mechanism underlying cardiac protection of RPerC. Adult male Sprague–Dawley rats were used in this study. Cardiac ischemia/reperfusion (I/R) was induced by 30 min of occlusion and 3 h of reperfusion of the left anterior descending coronary artery. RPerC were performed by 5 min of occlusion of the right femoral artery followed by 5 min of reperfusion for three times during cardiac ischemia. The hemodynamics, left ventricular

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Kurachi, Y. "G protein regulation of cardiac muscarinic potassium channel." American Journal of Physiology-Cell Physiology 269, no. 4 (1995): C821—C830. http://dx.doi.org/10.1152/ajpcell.1995.269.4.c821.

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Several ion channels can be regulated by G proteins in a “membrane-delimited” manner. The cardiac muscarinic K+ (KACh) channel, which is responsible for the acetylcholine (ACh) or adenosine-induced deceleration of heart beat and atrioventricular conduction, is the prototype of this type of receptor-dependent regulation of ion channels. Because similar transduction mechanisms are utilized by various membrane receptors, such as somatostatin, 5-hydroxytryptamine-1, alpha 2-adrenergic, mu-and delta-opioid, D2-dopamine, and gamma-aminobutyric acid B receptors, in neuronal, hormone-secreting, renal,

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LEE, H. THOMAS, and CHARLES W. EMALA. "Protein Kinase C and Gi/o Proteins Are Involved in Adenosine- and Ischemic Preconditioning—Mediated Renal Protection." Journal of the American Society of Nephrology 12, no. 2 (2001): 233–40. http://dx.doi.org/10.1681/asn.v122233.

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Abstract. Renal ischemic reperfusion (IR) injury is a significant clinical problem in anesthesia and surgery. Recently, it was demonstrated that both renal ischemic preconditioning (IPC) and systemic adenosine pretreatment protect against renal IR injury. In cardiac IPC, pertussis toxin-sensitive G-proteins (i.e., Gi/o), protein kinase C (PKC), and ATP-sensitive potassium (K+ATP) channels are implicated in this protective signaling pathway. The aim of this study was to elucidate the signaling pathways that are responsible for renal protection mediated by both IPC and adenosine pretreatment. In

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Klopfenstein, H. S., and D. W. Mathias. "Influence of naloxone on response to acute cardiac tamponade in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 2 (1990): H512—H517. http://dx.doi.org/10.1152/ajpheart.1990.259.2.h512.

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During progressive acute cardiac tamponade (CT) in conscious dogs, cardiac output (CO) falls continuously while arterial blood pressure (BP) is well maintained until an abruptly terminal decline. This response is primarily dependent on alpha-adrenergic mechanisms. During hemorrhagic shock, the opioid receptor blocker naloxone increases CO and BP and improves survival perhaps by reversing an opioid-induced cardiovascular depression. We produced 10 episodes of decompensated CT (DCT; 30% decline in BP) by intrapericardial saline infusion (20 ml/min) in five euvolemic conscious dogs. CT resulted i

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Regalin, Doughlas, Martielo Ivan Gehrcke, Felipe Comassetto, et al. "Seric Concentration of Troponin I and Electrocardiographic Tracing in Dogs Submitted to Long-Term Sedation during 24 Hours." Acta Scientiae Veterinariae 45, no. 1 (2017): 8. http://dx.doi.org/10.22456/1679-9216.80771.

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Background: General anesthetics and sedatives are commonly used for long-term sedation in veterinary medicine; however, they can lead to cardiac suppression. Cardiac troponin I is a biomarker used to detect myocardial pathology, monitor treatment, and assess outcomes in veterinary patients. The aim of this study was to evaluate the serum concentration of troponin I (cTnI), the electrocardiographic (ECG) tracing, and the ventricular stroke work index in dogs undergoing two long-term sedation protocols over 24 h.Materials, Methods & Results: Twelve healthy mongrel dogs with an average weight

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Davis, Shavsha, Shekhar H. Deo, Matthew Barlow, Darice Yoshishige, Martin Farias та James L. Caffrey. "The monosialosyl ganglioside GM-1 reduces the vagolytic efficacy of δ2-opioid receptor stimulation". American Journal of Physiology-Heart and Circulatory Physiology 291, № 5 (2006): H2318—H2326. http://dx.doi.org/10.1152/ajpheart.00455.2006.

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The cardiac enkephalin, methionine-enkephalin-arginine-phenylalanine (MEAP), alters vagally induced bradycardia when introduced by microdialysis into the sinoatrial (SA) node. The responses to MEAP are bimodal; lower doses enhance bradycardia and higher doses suppress bradycardia. The opposing vagotonic and vagolytic effects are mediated, respectively, by δ1 and δ2 phenotypes of the same receptor. Stimulation of the δ1 receptor reduced the subsequent δ2 responses. Experiments were conducted to test the hypothesis that the δ-receptor interactions were mediated by the monosialosyl ganglioside GM

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Zhang, Ye, Michael G. Irwin, Tak Ming Wong, Mai Chen та Chun-Mei Cao. "Remifentanil Preconditioning Confers Cardioprotection via Cardiac κ- and δ-Opioid Receptors". Anesthesiology 102, № 2 (2005): 371–78. http://dx.doi.org/10.1097/00000542-200502000-00020.

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Background Remifentanil preconditioning (RPC) reduces the infarct size in anesthetized rat hearts, and this effect seems to be mediated by all three types of opioid receptors (ORs). Because there is evidence of only kappa- and delta- but not mu-ORs in the rat heart, the authors investigated whether RPC confers cardioprotection via cardiac kappa- and delta-OR as well as via extracardiac mu-OR agonist activity. The authors also investigated the involvement of signaling mechanisms, namely protein kinase C and mitochondrial adenosine triphosphate-sensitive potassium (KATP) channels. Methods The he

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Ventura, Carlo, Luciana Bastagli, Pasquale Bernardi, Claudio M. Caldarera, and Carlo Guarnieri. "Opioid receptors in rat cardiac sarcolemma: effect of phenylephrine and isoproterenol." Biochimica et Biophysica Acta (BBA) - Biomembranes 987, no. 1 (1989): 69–74. http://dx.doi.org/10.1016/0005-2736(89)90456-2.

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Sheikh, Maaz, Navid Ahmed, Himali Gandhi, and On Chen. "Report of ventricular fibrillation in a 44-year-old man using kratom." BMJ Case Reports 14, no. 3 (2021): e237837. http://dx.doi.org/10.1136/bcr-2020-237837.

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Kratom is an unregulated kappa-opioid receptor agonist available for order on the internet that is used as a remedy for chronic pain. We present a case of a middle-aged man who suffered a cardiac arrest in the setting of kratom ingestion.

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Liang, Bruce T., and Garrett J. Gross. "Direct Preconditioning of Cardiac Myocytes via Opioid Receptors and K ATP Channels." Circulation Research 84, no. 12 (1999): 1396–400. http://dx.doi.org/10.1161/01.res.84.12.1396.

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Huang, Ming-He, Hui-Qun Wang, William R. Roeske та ін. "Mediating δ-opioid-initiated heart protection via the β2-adrenergic receptor: role of the intrinsic cardiac adrenergic cell". American Journal of Physiology-Heart and Circulatory Physiology 293, № 1 (2007): H376—H384. http://dx.doi.org/10.1152/ajpheart.01195.2006.

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Stimulation of cardiac β2-adrenergic receptor (β2-AR) or δ-opioid receptor (DOR) exerts a similar degree of cardioprotection against myocardial ischemia in experimental models. We hypothesized that δ-opioid-initiated cardioprotection is mediated by the intrinsic cardiac adrenergic (ICA) cell via enhanced epinephrine release. Using immunohistochemical and in situ hybridization methods, we detected in situ tyrosine hydroxylase (TH) mRNA and TH immunoreactivity that was colocalized with DOR immunoreactivity in ICA cells in human and rat hearts. Western blot analysis detected DOR protein in ICA ce

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Patel, Hemal H., Brian P. Head, Heidi N. Petersen та ін. "Protection of adult rat cardiac myocytes from ischemic cell death: role of caveolar microdomains and δ-opioid receptors". American Journal of Physiology-Heart and Circulatory Physiology 291, № 1 (2006): H344—H350. http://dx.doi.org/10.1152/ajpheart.01100.2005.

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The role of caveolae, membrane microenvironments enriched in signaling molecules, in myocardial ischemia is poorly defined. In the current study, we used cardiac myocytes prepared from adult rats to test the hypothesis that opioid receptors (OR), which are capable of producing cardiac protection in vivo, promote cardiac protection in cardiac myocytes in a caveolae-dependent manner. We determined protein expression and localization of δ-OR (DOR) using coimmunohistochemistry, caveolar fractionation, and immunoprecipitations. DOR colocalized in fractions with caveolin-3 (Cav-3), a structural comp

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Singh, Vinita, and Donald Harvey. "3447 Effects of intranasal ketamine on uncontrolled cancer related pain." Journal of Clinical and Translational Science 3, s1 (2019): 40–42. http://dx.doi.org/10.1017/cts.2019.99.

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OBJECTIVES/SPECIFIC AIMS: If intranasal ketamine can be utilized for pain control in cancer patients, this could provide them with superior analgesia and better quality of life, without the risk of significant respiratory depression associated with opioid medications. We seek to obtain preliminary data via a clinical trial addressing safety, feasibility, and utility of this novel technique for the treatment of persistent uncontrolled cancer pain. These findings would be an important initial step towards testing the effectiveness of intranasal ketamine as a non-opioid medication for cancer pain

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Xiao, R. P., S. Pepe, H. A. Spurgeon, M. C. Capogrossi, and E. G. Lakatta. "Opioid peptide receptor stimulation reverses beta-adrenergic effects in rat heart cells." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (1997): H797—H805. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h797.

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Opioid peptide receptor (OPR) agonists are co-released with the beta-adrenergic receptor (beta-AR) agonist norepinephrine (NE) from nerve terminals in the heart during sympathetic stimulation. Whereas recent studies indicate that OPR and beta-AR coexist on the surface of cardiac myocytes, whether significant "cross talk" occurs between OPR and beta-AR signaling cascades within heart cells is unknown. In the present study we demonstrate a marked effect of delta-OPR stimulation to modulate beta-adrenergic responses in single isolated rat ventricular myocytes. Nanomolar concentrations (10(-8) M)

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Kuzume, Koh, Roger A. Wolff, Kazuhiko Amakawa, Kazuyo Kuzume, and Donna M. Van Winkle. "Sustained exogenous administration of Met5-enkephalin protects against infarction in vivo." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (2003): H2463—H2470. http://dx.doi.org/10.1152/ajpheart.00341.2003.

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The opioid antagonist naloxone abolishes infarct limitation by myocardial ischemic preconditioning, suggesting that one or more endogenous opioid peptides can mediate cardiac protection against ischemic damage. We tested the hypothesis that the naturally occurring opioid peptide Met5-enkephalin (ME) modulates myocardial infarct size in vivo. Experiments were conducted in barbiturate-anesthetized open-chest rabbits subjected to regional myocardial ischemia-reperfusion. ME was administered via osmotic minipump for 24 h. Infarct size was assessed with tetrazolium and is expressed as a percentage

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Maslov, Leonid N., Yury B. Lishmanov, Peter R. Oeltgen та ін. "Activation of peripheral δ2 opioid receptors increases cardiac tolerance to ischemia/reperfusion injury". Life Sciences 84, № 19-20 (2009): 657–63. http://dx.doi.org/10.1016/j.lfs.2009.02.016.

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Rhee, H. M., and J. D. D. Lapp. "Are Opioid Receptors Involved in the Brady cardiac and Hypotensive Action of Clonidine?" American Journal of Hypertension 1, no. 3 Pt 3 (1988): 249S—254S. http://dx.doi.org/10.1093/ajh/1.3.249s.

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Prokudina, E. S., N. V. Naryzhnaya, E. A. Nesterov, S. Yu Tsibulnikov, and L. N. Maslov. "Continuous Normobaric Hypoxia Improved Cardiac Bioenergetics after Ischemia/Reperfusion: Role of Opioid Receptors." Bulletin of Experimental Biology and Medicine 169, no. 1 (2020): 13–17. http://dx.doi.org/10.1007/s10517-020-04814-9.

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