Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2015, Volume 83, pp. 88 - 100
Abstract Sick sinus syndrome remains a highly relevant clinical entity, being responsible for the implantation of the majority of electronic pacemakers...
Cardiovascular | Pacemaking | Ion channels | Calcium handling | Arrhythmia | Sinoatrial node | Atrial fibrillation | MOLECULAR-MECHANISM | CARDIAC & CARDIOVASCULAR SYSTEMS | PACEMAKER ACTIVITY | CARDIAC-ARRHYTHMIA | ANGIOTENSIN-II | CELL BIOLOGY | SODIUM-CHANNEL MUTATIONS | TARGETED DISRUPTION | HCN CHANNELS | ION-CHANNEL | ELECTRICAL-ACTIVITY | HEART-RATE | Bradycardia - genetics | Heart Atria - pathology | Humans | MicroRNAs - metabolism | NAV1.5 Voltage-Gated Sodium Channel - metabolism | Bradycardia - metabolism | Ion Transport | NAV1.5 Voltage-Gated Sodium Channel - genetics | Atrial Fibrillation - pathology | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism | Receptors, Purinergic P1 - genetics | Gene Expression Regulation | Connexins - genetics | Renin-Angiotensin System - genetics | Atrial Fibrillation - genetics | Aging - pathology | Connexins - metabolism | Heart Atria - metabolism | Sinoatrial Node - pathology | Atrial Fibrillation - metabolism | Myocytes, Cardiac - pathology | Animals | Bradycardia - pathology | Myocytes, Cardiac - metabolism | Sinoatrial Node - metabolism | Aged | MicroRNAs - genetics | Receptors, Purinergic P1 - metabolism | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - genetics | Aging - metabolism | Sick sinus syndrome
Cardiovascular | Pacemaking | Ion channels | Calcium handling | Arrhythmia | Sinoatrial node | Atrial fibrillation | MOLECULAR-MECHANISM | CARDIAC & CARDIOVASCULAR SYSTEMS | PACEMAKER ACTIVITY | CARDIAC-ARRHYTHMIA | ANGIOTENSIN-II | CELL BIOLOGY | SODIUM-CHANNEL MUTATIONS | TARGETED DISRUPTION | HCN CHANNELS | ION-CHANNEL | ELECTRICAL-ACTIVITY | HEART-RATE | Bradycardia - genetics | Heart Atria - pathology | Humans | MicroRNAs - metabolism | NAV1.5 Voltage-Gated Sodium Channel - metabolism | Bradycardia - metabolism | Ion Transport | NAV1.5 Voltage-Gated Sodium Channel - genetics | Atrial Fibrillation - pathology | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism | Receptors, Purinergic P1 - genetics | Gene Expression Regulation | Connexins - genetics | Renin-Angiotensin System - genetics | Atrial Fibrillation - genetics | Aging - pathology | Connexins - metabolism | Heart Atria - metabolism | Sinoatrial Node - pathology | Atrial Fibrillation - metabolism | Myocytes, Cardiac - pathology | Animals | Bradycardia - pathology | Myocytes, Cardiac - metabolism | Sinoatrial Node - metabolism | Aged | MicroRNAs - genetics | Receptors, Purinergic P1 - metabolism | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - genetics | Aging - metabolism | Sick sinus syndrome
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2017, Volume 312, Issue 1, pp. H106 - H127
Early afterdepolarization (EAD) is known as a cause of ventricular arrhythmias in long QT syndromes. We theoretically investigated how the rapid (I-Kr) and...
Long QT syndrome | Early afterdepolarization | Computer simulation | Mathematical model | Bifurcation analysis | early afterdepolarization | CHRONIC HEART-FAILURE | TRIGGERED ACTIVITY | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | long QT syndrome | CARDIAC-ARRHYTHMIAS | LONG-QT SYNDROME | bifurcation analysis | INTRACELLULAR NA+ | L-TYPE CA2 | SINOATRIAL NODE PACEMAKING | BIOLOGICAL PACEMAKER | NA+/CA2+ EXCHANGER | mathematical model | computer simulation | PERIPHERAL VASCULAR DISEASE | CURRENT I-F | Models, Theoretical | Heart Ventricles - cytology | Heart Conduction System - metabolism | Calcium - metabolism | Models, Cardiovascular | Humans | Sodium - metabolism | Delayed Rectifier Potassium Channels - metabolism | Action Potentials | Long QT Syndrome - metabolism | Sodium-Potassium-Exchanging ATPase - metabolism | Bradycardia - metabolism | Membrane Potentials | Sodium-Calcium Exchanger - metabolism | Myocytes, Cardiac - metabolism | Sarcoplasmic Reticulum - metabolism | Calcium Channels, L-Type - metabolism | Physiological aspects | Models | Arrhythmia | Mathematical analysis | Methods | Heart cells
Long QT syndrome | Early afterdepolarization | Computer simulation | Mathematical model | Bifurcation analysis | early afterdepolarization | CHRONIC HEART-FAILURE | TRIGGERED ACTIVITY | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | long QT syndrome | CARDIAC-ARRHYTHMIAS | LONG-QT SYNDROME | bifurcation analysis | INTRACELLULAR NA+ | L-TYPE CA2 | SINOATRIAL NODE PACEMAKING | BIOLOGICAL PACEMAKER | NA+/CA2+ EXCHANGER | mathematical model | computer simulation | PERIPHERAL VASCULAR DISEASE | CURRENT I-F | Models, Theoretical | Heart Ventricles - cytology | Heart Conduction System - metabolism | Calcium - metabolism | Models, Cardiovascular | Humans | Sodium - metabolism | Delayed Rectifier Potassium Channels - metabolism | Action Potentials | Long QT Syndrome - metabolism | Sodium-Potassium-Exchanging ATPase - metabolism | Bradycardia - metabolism | Membrane Potentials | Sodium-Calcium Exchanger - metabolism | Myocytes, Cardiac - metabolism | Sarcoplasmic Reticulum - metabolism | Calcium Channels, L-Type - metabolism | Physiological aspects | Models | Arrhythmia | Mathematical analysis | Methods | Heart cells
Journal Article
Scientific Reports, ISSN 2045-2322, 06/2016, Volume 6, Issue 1, p. 26992
Injury severity in blast induced Traumatic Brain Injury (bTBI) increases with blast overpressure (BOP) and impulse in dose-dependent manner. Pure primary blast...
BARRIER DYSFUNCTION | NERVOUS-SYSTEM | OXIDATIVE STRESS | ACETYL-L-CARNITINE | SHELL SHOCK | TRAUMATIC BRAIN-INJURY | ANESTHETIZED RAT | MULTIDISCIPLINARY SCIENCES | INDUCED NEUROTRAUMA | COMBAT VETERANS | SHOCK-WAVE | Lung Injury - pathology | NADPH Oxidases - metabolism | Blast Injuries - metabolism | Male | Explosions | Nitrosative Stress | Aldehydes - metabolism | Rats, Sprague-Dawley | Tyrosine - analogs & derivatives | Blast Injuries - pathology | Blood-Brain Barrier - metabolism | Blood-Brain Barrier - pathology | Brain - blood supply | Tyrosine - metabolism | Animals | Bradycardia - metabolism | Brain Injuries, Traumatic - metabolism | Brain Injuries, Traumatic - pathology | Bradycardia - pathology | Lung Injury - metabolism | Microvessels - enzymology | Nitric Oxide Synthase Type II - metabolism
BARRIER DYSFUNCTION | NERVOUS-SYSTEM | OXIDATIVE STRESS | ACETYL-L-CARNITINE | SHELL SHOCK | TRAUMATIC BRAIN-INJURY | ANESTHETIZED RAT | MULTIDISCIPLINARY SCIENCES | INDUCED NEUROTRAUMA | COMBAT VETERANS | SHOCK-WAVE | Lung Injury - pathology | NADPH Oxidases - metabolism | Blast Injuries - metabolism | Male | Explosions | Nitrosative Stress | Aldehydes - metabolism | Rats, Sprague-Dawley | Tyrosine - analogs & derivatives | Blast Injuries - pathology | Blood-Brain Barrier - metabolism | Blood-Brain Barrier - pathology | Brain - blood supply | Tyrosine - metabolism | Animals | Bradycardia - metabolism | Brain Injuries, Traumatic - metabolism | Brain Injuries, Traumatic - pathology | Bradycardia - pathology | Lung Injury - metabolism | Microvessels - enzymology | Nitric Oxide Synthase Type II - metabolism
Journal Article
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Exercise training reduces resting heart rate via downregulation of the funny channel HCN4
Nature Communications, ISSN 2041-1723, 05/2014, Volume 5, Issue 1, p. 3775
Endurance athletes exhibit sinus bradycardia, that is a slow resting heart rate, associated with a higher incidence of sinus node (pacemaker) disease and...
ATRIAL | SINUS | MULTIDISCIPLINARY SCIENCES | ATRIOVENTRICULAR NODE | FUNCTIONAL ROLES | FOLLOW-UP | CA2+-ACTIVATED K+ CHANNEL | BRADYCARDIA | EXPRESSION | SINOATRIAL NODE | CLINICAL-SIGNIFICANCE | Up-Regulation | Bradycardia - genetics | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism | Down-Regulation | Heart Rate - genetics | Rats | Repressor Proteins - genetics | MicroRNAs - metabolism | RNA, Messenger - metabolism | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Animals | Bradycardia - metabolism | Adaptation, Physiological - genetics | Sinoatrial Node - metabolism | Mice | MicroRNAs - genetics | In Vitro Techniques | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - genetics | Physical Conditioning, Animal | Repressor Proteins - metabolism
ATRIAL | SINUS | MULTIDISCIPLINARY SCIENCES | ATRIOVENTRICULAR NODE | FUNCTIONAL ROLES | FOLLOW-UP | CA2+-ACTIVATED K+ CHANNEL | BRADYCARDIA | EXPRESSION | SINOATRIAL NODE | CLINICAL-SIGNIFICANCE | Up-Regulation | Bradycardia - genetics | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism | Down-Regulation | Heart Rate - genetics | Rats | Repressor Proteins - genetics | MicroRNAs - metabolism | RNA, Messenger - metabolism | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Animals | Bradycardia - metabolism | Adaptation, Physiological - genetics | Sinoatrial Node - metabolism | Mice | MicroRNAs - genetics | In Vitro Techniques | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - genetics | Physical Conditioning, Animal | Repressor Proteins - metabolism
Journal Article
Nature, ISSN 0028-0836, 02/2003, Volume 421, Issue 6923, pp. 634 - 639
Mutations in ion channels involved in the generation and termination of action potentials constitute a family of molecular defects that underlie fatal cardiac...
SODIUM-CALCIUM EXCHANGE | CHANNELS | VENTRICULAR MYOCYTES | SPECTRIN | GENE | MULTIDISCIPLINARY SCIENCES | Bradycardia - genetics | Calcium Channels - metabolism | Humans | Male | Death, Sudden, Cardiac - etiology | Bradycardia - complications | Long QT Syndrome - physiopathology | Action Potentials | Bradycardia - metabolism | Sodium-Calcium Exchanger - metabolism | Myocardium - metabolism | Electrocardiography | Inositol 1,4,5-Trisphosphate Receptors | Female | Calcium Signaling | Heart - physiopathology | Heart Rate | Bradycardia - physiopathology | Long QT Syndrome - classification | Myocardium - pathology | Ankyrins - physiology | Mutation - genetics | Long QT Syndrome - metabolism | Sodium-Potassium-Exchanging ATPase - metabolism | Patch-Clamp Techniques | Phenotype | Animals | Pedigree | Ankyrins - genetics | Long QT Syndrome - genetics | Protein Binding | Heterozygote | Mice | Receptors, Cytoplasmic and Nuclear - metabolism | Cardiovascular disease | Mutation
SODIUM-CALCIUM EXCHANGE | CHANNELS | VENTRICULAR MYOCYTES | SPECTRIN | GENE | MULTIDISCIPLINARY SCIENCES | Bradycardia - genetics | Calcium Channels - metabolism | Humans | Male | Death, Sudden, Cardiac - etiology | Bradycardia - complications | Long QT Syndrome - physiopathology | Action Potentials | Bradycardia - metabolism | Sodium-Calcium Exchanger - metabolism | Myocardium - metabolism | Electrocardiography | Inositol 1,4,5-Trisphosphate Receptors | Female | Calcium Signaling | Heart - physiopathology | Heart Rate | Bradycardia - physiopathology | Long QT Syndrome - classification | Myocardium - pathology | Ankyrins - physiology | Mutation - genetics | Long QT Syndrome - metabolism | Sodium-Potassium-Exchanging ATPase - metabolism | Patch-Clamp Techniques | Phenotype | Animals | Pedigree | Ankyrins - genetics | Long QT Syndrome - genetics | Protein Binding | Heterozygote | Mice | Receptors, Cytoplasmic and Nuclear - metabolism | Cardiovascular disease | Mutation
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 2016, Volume 310, Issue 3, pp. C193 - C204
The extracellular calcium-sensing receptor CaSR is expressed in blood vessels where its role is not completely understood. In this study, we tested the...
G protein-coupled receptor | CaSR | PULMONARY VEINS | SMALL ARTERIES | PHYSIOLOGY | blood pressure regulation | calcium-sensing receptor | CELL BIOLOGY | ENDOTHELIAL-CELLS | IMAGE-ANALYSIS | NITRIC-OXIDE | GENE-EXPRESSION | SMOOTH-MUSCLE-CELLS | blood vessel tone regulation | CARDIAC FIBROSIS | vascular smooth muscle cells | TRANSGENIC MICE | Bradycardia - genetics | Muscle, Smooth, Vascular - metabolism | Receptors, G-Protein-Coupled - metabolism | Blood Pressure - genetics | Calcium - metabolism | Aorta - metabolism | Mice, 129 Strain | Hypotension - genetics | Muscle, Smooth, Vascular - physiopathology | Dose-Response Relationship, Drug | Vasodilation - genetics | Ventricular Remodeling | Bradycardia - metabolism | Hypotension - physiopathology | Blood Pressure - drug effects | Muscle, Smooth, Vascular - drug effects | Vasoconstriction - genetics | Vasoconstrictor Agents - pharmacology | Heart Rate | Genetic Predisposition to Disease | Vasodilator Agents - pharmacology | Mice, Inbred C57BL | Bradycardia - physiopathology | Mesenteric Arteries - metabolism | Vasoconstriction - drug effects | Mice, Knockout | Phenotype | Animals | Hypotension - metabolism | Receptors, G-Protein-Coupled - deficiency | Calcium Signaling - drug effects | Myocytes, Cardiac - metabolism | Receptors, G-Protein-Coupled - genetics | Vasodilation - drug effects | Calcium Signaling - genetics | Call for Papers
G protein-coupled receptor | CaSR | PULMONARY VEINS | SMALL ARTERIES | PHYSIOLOGY | blood pressure regulation | calcium-sensing receptor | CELL BIOLOGY | ENDOTHELIAL-CELLS | IMAGE-ANALYSIS | NITRIC-OXIDE | GENE-EXPRESSION | SMOOTH-MUSCLE-CELLS | blood vessel tone regulation | CARDIAC FIBROSIS | vascular smooth muscle cells | TRANSGENIC MICE | Bradycardia - genetics | Muscle, Smooth, Vascular - metabolism | Receptors, G-Protein-Coupled - metabolism | Blood Pressure - genetics | Calcium - metabolism | Aorta - metabolism | Mice, 129 Strain | Hypotension - genetics | Muscle, Smooth, Vascular - physiopathology | Dose-Response Relationship, Drug | Vasodilation - genetics | Ventricular Remodeling | Bradycardia - metabolism | Hypotension - physiopathology | Blood Pressure - drug effects | Muscle, Smooth, Vascular - drug effects | Vasoconstriction - genetics | Vasoconstrictor Agents - pharmacology | Heart Rate | Genetic Predisposition to Disease | Vasodilator Agents - pharmacology | Mice, Inbred C57BL | Bradycardia - physiopathology | Mesenteric Arteries - metabolism | Vasoconstriction - drug effects | Mice, Knockout | Phenotype | Animals | Hypotension - metabolism | Receptors, G-Protein-Coupled - deficiency | Calcium Signaling - drug effects | Myocytes, Cardiac - metabolism | Receptors, G-Protein-Coupled - genetics | Vasodilation - drug effects | Calcium Signaling - genetics | Call for Papers
Journal Article
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, ISSN 0363-6135, 02/2012, Volume 302, Issue 3, pp. H770 - H781
Song J, Gao E, Wang J, Zhang XQ, Chan TO, Koch WJ, Shang X, Joseph JI, Peterson BZ, Feldman AM, Cheung JY. Constitutive overexpression of phosphomimetic...
POSTINFARCTION MYOCYTES | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | PHOSPHORYLATION | NA+-CA2+ EXCHANGER | DILATED CARDIOMYOPATHY | intracellular Ca2+ and Na+ regulation | FXYD proteins | NA+-K+-ATPASE | ALTERS CONTRACTILITY | in vivo catheterization | RAT CARDIAC MYOCYTES | RABBIT VENTRICULAR MYOCYTES | TRANSIENTS | PERIPHERAL VASCULAR DISEASE | SODIUM-CALCIUM EXCHANGE | beta-adrenergic responsiveness | Potassium - metabolism | Bradycardia - genetics | Action Potentials - genetics | Calcium - metabolism | Myocardial Contraction - physiology | Male | Sodium-Calcium Exchanger - genetics | Sodium - metabolism | Phosphoproteins - metabolism | Arrhythmias, Cardiac - physiopathology | Bradycardia - metabolism | Sodium-Calcium Exchanger - metabolism | Gene Expression - physiology | Female | Membrane Proteins - metabolism | Receptors, Adrenergic, beta - metabolism | Arrhythmias, Cardiac - genetics | Heart Failure - mortality | Arrhythmias, Cardiac - metabolism | Bradycardia - mortality | Myocytes, Cardiac - cytology | Membrane Proteins - genetics | Calcium Channels, L-Type - physiology | Heart Failure - genetics | Mice, Transgenic | Heart Failure - metabolism | Phosphoproteins - genetics | Mice, Inbred Strains | Action Potentials - physiology | Animals | Myocytes, Cardiac - physiology | Mice | Cardiac Excitation and Contraction | β-adrenergic responsiveness
POSTINFARCTION MYOCYTES | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | PHOSPHORYLATION | NA+-CA2+ EXCHANGER | DILATED CARDIOMYOPATHY | intracellular Ca2+ and Na+ regulation | FXYD proteins | NA+-K+-ATPASE | ALTERS CONTRACTILITY | in vivo catheterization | RAT CARDIAC MYOCYTES | RABBIT VENTRICULAR MYOCYTES | TRANSIENTS | PERIPHERAL VASCULAR DISEASE | SODIUM-CALCIUM EXCHANGE | beta-adrenergic responsiveness | Potassium - metabolism | Bradycardia - genetics | Action Potentials - genetics | Calcium - metabolism | Myocardial Contraction - physiology | Male | Sodium-Calcium Exchanger - genetics | Sodium - metabolism | Phosphoproteins - metabolism | Arrhythmias, Cardiac - physiopathology | Bradycardia - metabolism | Sodium-Calcium Exchanger - metabolism | Gene Expression - physiology | Female | Membrane Proteins - metabolism | Receptors, Adrenergic, beta - metabolism | Arrhythmias, Cardiac - genetics | Heart Failure - mortality | Arrhythmias, Cardiac - metabolism | Bradycardia - mortality | Myocytes, Cardiac - cytology | Membrane Proteins - genetics | Calcium Channels, L-Type - physiology | Heart Failure - genetics | Mice, Transgenic | Heart Failure - metabolism | Phosphoproteins - genetics | Mice, Inbred Strains | Action Potentials - physiology | Animals | Myocytes, Cardiac - physiology | Mice | Cardiac Excitation and Contraction | β-adrenergic responsiveness
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2008, Volume 294, Issue 2, pp. 1036 - 1047
Virtually every mammalian cell, including cardiomyocytes, possesses an intrinsic circadian clock. The role of this transcriptionally based molecular mechanism...
Epinephrine | Bradycardia | Carbohydrate | Chronobiology | Fatty acids | OXIDATIVE-PHOSPHORYLATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | PROTEIN | fatty acids | RAT | epinephrine | carbohydrate | BLOOD-PRESSURE | SKELETAL-MUSCLE MITOCHONDRIA | OBESITY | chronobiology | RHYTHMS | ATTENUATION | PERIPHERAL VASCULAR DISEASE | HEART-RATE | DYSFUNCTION | bradycardia | Echocardiography | Oligonucleotide Array Sequence Analysis | Myocardial Contraction - physiology | Circadian Rhythm - genetics | Circadian Rhythm - physiology | Reverse Transcriptase Polymerase Chain Reaction | Telemetry | DNA - genetics | Myocardial Contraction - genetics | Animals | Mitochondria, Heart - physiology | Myocytes, Cardiac - physiology | Perfusion | Gene Expression - physiology | Myocardium - metabolism | Muscle Proteins - metabolism | Electrocardiography | Heart Rate - physiology | DNA - biosynthesis | Signal Transduction - physiology | Mice | In Vitro Techniques
Epinephrine | Bradycardia | Carbohydrate | Chronobiology | Fatty acids | OXIDATIVE-PHOSPHORYLATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | PROTEIN | fatty acids | RAT | epinephrine | carbohydrate | BLOOD-PRESSURE | SKELETAL-MUSCLE MITOCHONDRIA | OBESITY | chronobiology | RHYTHMS | ATTENUATION | PERIPHERAL VASCULAR DISEASE | HEART-RATE | DYSFUNCTION | bradycardia | Echocardiography | Oligonucleotide Array Sequence Analysis | Myocardial Contraction - physiology | Circadian Rhythm - genetics | Circadian Rhythm - physiology | Reverse Transcriptase Polymerase Chain Reaction | Telemetry | DNA - genetics | Myocardial Contraction - genetics | Animals | Mitochondria, Heart - physiology | Myocytes, Cardiac - physiology | Perfusion | Gene Expression - physiology | Myocardium - metabolism | Muscle Proteins - metabolism | Electrocardiography | Heart Rate - physiology | DNA - biosynthesis | Signal Transduction - physiology | Mice | In Vitro Techniques
Journal Article
PLOS ONE, ISSN 1932-6203, 04/2016, Volume 11, Issue 4, p. e0153187
Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as...
POMC NEURONS | VAGUS NERVE-STIMULATION | RETICULARIS-VENTRALIS | NUCLEUS-TRACTUS-SOLITARIUS | CARDIAC VAGAL NEURONS | MULTIDISCIPLINARY SCIENCES | AFFERENT MODULATION | IN-VIVO | MEDULLA-OBLONGATA | STRESS-INDUCED ANALGESIA | BETA-ENDORPHIN | Brain Stem - metabolism | Channelrhodopsins | Melanocyte-Stimulating Hormones - pharmacology | Arcuate Nucleus of Hypothalamus - cytology | Male | Brain Stem - cytology | Brain Stem - drug effects | Bradycardia - metabolism | Arcuate Nucleus of Hypothalamus - drug effects | Female | Neurons - metabolism | Neurons - drug effects | Solitary Nucleus - metabolism | Solitary Nucleus - cytology | Arcuate Nucleus of Hypothalamus - metabolism | Mice, Transgenic | Solitary Nucleus - drug effects | Pro-Opiomelanocortin - metabolism | Analgesia | Microscopy, Confocal | Animals | Naloxone - pharmacology | Narcotic Antagonists - pharmacology | Analgesics, Opioid - metabolism | Respiratory Insufficiency - metabolism | Bradycardia | Chemotherapy | Usage | Opioids | Research | Health aspects | Risk factors | Cancer | Heart | Neurosciences | Peptides | Arrhythmia | Brain stem | Arcuate nucleus | Central nervous system | Position sensing | Solitary tract nucleus | Proopiomelanocortin | Activation | Mental depression | Experiments | Nuclei | Pain | Analgesics | Rodents | Modulation | Physiology | Heart diseases | Pain perception | Narcotics | Opioid receptors | Neurons | Periaqueductal gray area | Melanocortin | Pharmacology | Metabolism | Vectors (Biology) | Latency | Hypotheses | Naloxone | Nucleus ambiguus | Endorphins | In vivo methods and tests | Respiration
POMC NEURONS | VAGUS NERVE-STIMULATION | RETICULARIS-VENTRALIS | NUCLEUS-TRACTUS-SOLITARIUS | CARDIAC VAGAL NEURONS | MULTIDISCIPLINARY SCIENCES | AFFERENT MODULATION | IN-VIVO | MEDULLA-OBLONGATA | STRESS-INDUCED ANALGESIA | BETA-ENDORPHIN | Brain Stem - metabolism | Channelrhodopsins | Melanocyte-Stimulating Hormones - pharmacology | Arcuate Nucleus of Hypothalamus - cytology | Male | Brain Stem - cytology | Brain Stem - drug effects | Bradycardia - metabolism | Arcuate Nucleus of Hypothalamus - drug effects | Female | Neurons - metabolism | Neurons - drug effects | Solitary Nucleus - metabolism | Solitary Nucleus - cytology | Arcuate Nucleus of Hypothalamus - metabolism | Mice, Transgenic | Solitary Nucleus - drug effects | Pro-Opiomelanocortin - metabolism | Analgesia | Microscopy, Confocal | Animals | Naloxone - pharmacology | Narcotic Antagonists - pharmacology | Analgesics, Opioid - metabolism | Respiratory Insufficiency - metabolism | Bradycardia | Chemotherapy | Usage | Opioids | Research | Health aspects | Risk factors | Cancer | Heart | Neurosciences | Peptides | Arrhythmia | Brain stem | Arcuate nucleus | Central nervous system | Position sensing | Solitary tract nucleus | Proopiomelanocortin | Activation | Mental depression | Experiments | Nuclei | Pain | Analgesics | Rodents | Modulation | Physiology | Heart diseases | Pain perception | Narcotics | Opioid receptors | Neurons | Periaqueductal gray area | Melanocortin | Pharmacology | Metabolism | Vectors (Biology) | Latency | Hypotheses | Naloxone | Nucleus ambiguus | Endorphins | In vivo methods and tests | Respiration
Journal Article
Medical Hypotheses, ISSN 0306-9877, 10/2018, Volume 119, pp. 63 - 67
Relative bradycardia is the term used to describe the mechanism where there is dissociation between pulse and temperature. This finding is important to...
MEDICINE, RESEARCH & EXPERIMENTAL | INDUCED SYSTEMIC INFLAMMATION | SMOOTH-MUSCLE | CYCLOSPORINE-A | ROSTRAL VENTROLATERAL MEDULLA | HEART-RATE-VARIABILITY | NITRIC-OXIDE SYNTHASE | IN-VIVO | ENDOTOXIN TOLERANCE | SEPTIC SHOCK | SEPSIS | Models, Theoretical | Tumor Necrosis Factor-alpha - metabolism | Heart Rate | Temperature | Cytokines - metabolism | Bradycardia - diagnosis | Comorbidity | Endothelin-1 - metabolism | Humans | Bradycardia - therapy | NADPH Oxidases - metabolism | Neurotransmitter Agents - metabolism | Pulse | Lipopolysaccharides - metabolism | Treatment Outcome | Inflammation | Sepsis - physiopathology | Immune System | Sinoatrial Node | Autonomic Nervous System | Nitric Oxide - metabolism | Interleukin-6 - metabolism | Medical colleges | Medical research | Bradycardia | Heart beat | College graduates | Medicine, Experimental
MEDICINE, RESEARCH & EXPERIMENTAL | INDUCED SYSTEMIC INFLAMMATION | SMOOTH-MUSCLE | CYCLOSPORINE-A | ROSTRAL VENTROLATERAL MEDULLA | HEART-RATE-VARIABILITY | NITRIC-OXIDE SYNTHASE | IN-VIVO | ENDOTOXIN TOLERANCE | SEPTIC SHOCK | SEPSIS | Models, Theoretical | Tumor Necrosis Factor-alpha - metabolism | Heart Rate | Temperature | Cytokines - metabolism | Bradycardia - diagnosis | Comorbidity | Endothelin-1 - metabolism | Humans | Bradycardia - therapy | NADPH Oxidases - metabolism | Neurotransmitter Agents - metabolism | Pulse | Lipopolysaccharides - metabolism | Treatment Outcome | Inflammation | Sepsis - physiopathology | Immune System | Sinoatrial Node | Autonomic Nervous System | Nitric Oxide - metabolism | Interleukin-6 - metabolism | Medical colleges | Medical research | Bradycardia | Heart beat | College graduates | Medicine, Experimental
Journal Article
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, ISSN 0363-6119, 06/2009, Volume 296, Issue 6, pp. 1783 - 1796
The medullary 5-HT system has potent effects on heart rate and breathing in adults. We asked whether this system mitigates the respiratory instability and...
Chemoreflex | Neonate | SIDS | Breathing | Hering-breuer | PHYSIOLOGY | UNANESTHETIZED RATS | breathing | CO2 | AWAKE RATS | INFANT-DEATH-SYNDROME | neonate | MEDULLARY RAPHE NEURONS | chemoreflex | CO2 RESPONSE | CONSCIOUS RATS | NEWBORN PIGLETS | NUCLEUS AMBIGUUS | CARDIAC VAGAL NEURONS | Hering-Breuer | SEROTONERGIC NEURONS | Adaptation, Physiological | Neurons - pathology | Age Factors | Apnea - metabolism | Humans | Brain Stem - metabolism | Body Weight - drug effects | Reflex - drug effects | Infant | Apnea - physiopathology | Brain Stem - drug effects | Hypoxia - metabolism | Respiratory Mechanics - drug effects | Heart Rate - drug effects | Serotonin Agents - toxicity | Bradycardia - metabolism | Brain Stem - pathology | Neurons - metabolism | Neurons - drug effects | Infant, Newborn | Hypercapnia - metabolism | Animals, Newborn | Asphyxia - physiopathology | Hypercapnia - physiopathology | Respiration Disorders - chemically induced | Pulmonary Ventilation - drug effects | Respiration Disorders - physiopathology | Bradycardia - physiopathology | Rats | 5,7-Dihydroxytryptamine - toxicity | Respiration Disorders - metabolism | Bradycardia - chemically induced | Animals | Asphyxia - metabolism | Oxygen Consumption - drug effects | Serotonin - metabolism | Sudden Infant Death | Hypoxia - physiopathology | Brain Stem - physiopathology | Energy Metabolism - drug effects | Index Medicus | Neurohumoral Control of Cardiovascular Function
Chemoreflex | Neonate | SIDS | Breathing | Hering-breuer | PHYSIOLOGY | UNANESTHETIZED RATS | breathing | CO2 | AWAKE RATS | INFANT-DEATH-SYNDROME | neonate | MEDULLARY RAPHE NEURONS | chemoreflex | CO2 RESPONSE | CONSCIOUS RATS | NEWBORN PIGLETS | NUCLEUS AMBIGUUS | CARDIAC VAGAL NEURONS | Hering-Breuer | SEROTONERGIC NEURONS | Adaptation, Physiological | Neurons - pathology | Age Factors | Apnea - metabolism | Humans | Brain Stem - metabolism | Body Weight - drug effects | Reflex - drug effects | Infant | Apnea - physiopathology | Brain Stem - drug effects | Hypoxia - metabolism | Respiratory Mechanics - drug effects | Heart Rate - drug effects | Serotonin Agents - toxicity | Bradycardia - metabolism | Brain Stem - pathology | Neurons - metabolism | Neurons - drug effects | Infant, Newborn | Hypercapnia - metabolism | Animals, Newborn | Asphyxia - physiopathology | Hypercapnia - physiopathology | Respiration Disorders - chemically induced | Pulmonary Ventilation - drug effects | Respiration Disorders - physiopathology | Bradycardia - physiopathology | Rats | 5,7-Dihydroxytryptamine - toxicity | Respiration Disorders - metabolism | Bradycardia - chemically induced | Animals | Asphyxia - metabolism | Oxygen Consumption - drug effects | Serotonin - metabolism | Sudden Infant Death | Hypoxia - physiopathology | Brain Stem - physiopathology | Energy Metabolism - drug effects | Index Medicus | Neurohumoral Control of Cardiovascular Function
Journal Article