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of or relating to a cavity or chamber in the body (especially one of the upper chambers of the heart)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/03/30 14:57:58」(JST)

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In anatomy, the atrium (plural: atria) is a portion of the blood collection chamber of the heart. It is also sometimes called the auricle, although in the technical sense, the auricle is a separate part of the main atrium^[1] known as the atrial appendages. The atrium is a chamber in which blood enters the heart, as opposed to the ventricle, where it is pushed out of the organ. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system. In fish, the circulatory system is very simple: a two-chambered heart including one atrium and one ventricle. In other vertebrate groups, the circulatory system is much more complicated. Their circulatory systems are divided into two types: a three-chambered heart, with two atria and one ventricle, or a four-chambered heart, with two atria and two ventricles. The atrium receives blood as it returns to the heart to complete a circulating cycle, whereas the ventricle pumps blood out of the heart to start a new cycle.^[2]^[3]

Atria

Structure[edit]

Main articles: Left atrium and Right atrium

Humans have a four-chambered heart consisting of the right atrium, left atrium, right ventricle, and left ventricle. The right atrium receives deoxygenated blood from the superior vena cava, inferior vena cava and coronary sinus. The left atrium receives oxygenated blood from the left and right pulmonary veins.^[4] The atria do not have valves at their inlets.^[5] As a result, a venous pulsation is normal and can be detected in the jugular vein as the jugular venous pressure.^[6]^[7] Internally, there is the rough musculae pectinati and crista terminalis, which act as a boundary inside the atrium and the smooth walled part derived from the sinus venosus.^[8] There is also a fossa ovalis in the interatrial septum, which is used in the fetal period as a means of bypassing the lung.The atrium is depolarized by calcium.

There are two atria, one on either side of the heart. On the right side is the atrium that holds blood that is deoxygenated. It sends blood to the right ventricle, which sends it to the lungs for oxygen. After it comes back, it is sent to the left atrium. The blood is pumped from the left atrium and sent to the left ventricle where it is sent to the aorta, which takes it to the rest of the body.^[9]

Function[edit]

In human physiology, the atria facilitate circulation primarily by allowing uninterrupted venous flow to the heart during ventricular systole.^[10]^[11] By being partially empty and distensible, atria prevent the interruption of venous flow to the heart that would occur during ventricular systole if the veins ended at the inlet valves of the heart. In normal physiologic states, the output of the heart is pulsatile, and the venous inflow to the heart is continuous and non-pulsatile. But without functioning atria, venous flow becomes pulsatile, and the overall circulation rate decreases significantly.^[12]^[13]

Atria have four essential characteristics that cause them to promote continuous venous flow. (1) There are no atrial inlet valves to interrupt blood flow during atrial systole. (2) The atrial systole contractions are incomplete and thus do not contract to the extent that would block flow from the veins through the atria into the ventricles. During atrial systole, blood not only empties from the atria to the ventricles, but blood continues to flow uninterrupted from the veins right through the atria into the ventricles. (3) The atrial contractions must be gentle enough so that the force of contraction does not exert significant back pressure that would impede venous flow. (4) The "let go" of the atria must be timed so that they relax before the start of ventricular contraction, to be able to accept venous flow without interruption.^[14]^[15]

By preventing the inertia of interrupted venous flow that would otherwise occur at each ventricular systole, atria allow approximately 75% more cardiac output than would otherwise occur. The fact that atrial contraction is 15% of the amount of the succeeding ventricular ejection has led to a misplaced emphasis on their role in pumping up the ventricles (the so-called "atrial kick"), whereas the key benefit of atria is in preventing circulatory inertia and allowing uninterrupted venous flow to the heart.^[16]^[17]

References[edit]

^ http://www.drugs.com/dict/auricles-of-atria.html
^ http://www.healthsystem.virginia.edu/uvahealth/adult_cardiac/anatomy.cfm
^ http://www.ivy-rose.co.uk/HumanBody/Blood/Heart_Structure.php
^ http://www.ivy-rose.co.uk/HumanBody/Blood/Heart_Structure.php
^ http://www.americanheart.org/presenter.jhtml?identifier=4598
^ http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm
^ http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A622#A629
^ http://www.med.unc.edu/embryo_images/unit-cardev/cardev_htms/cardev040.htm
^ Human heart anatomy diagram. Retrieved on 2010-07-02.
^ Anderson, RM. The Gross Physiology of the Cardiovascular System (2nd ed., 2012). See "Chapter 1: Normal Physiology."
^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.
^ The Determinants of Cardiac Output (video produced by University of Arizona Biomedical Communications; demonstration of atrial effect begings at 13:43).
^ http://cardiac-output.info (See discussion of atrial effect in text Chapter 1.)
^ Anderson, RM. The Gross Physiology of the Cardiovascular System (2nd ed.) See "Chapter 1: Normal Physiology."
^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.
^ The Gross Physiology of the Cardiovascular System at 11.
^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.

UpToDate Contents

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1. 発作性心房細動 paroxysmal atrial fibrillation
2. 新規発症した心房細動の管理 management of new onset atrial fibrillation
3. 非弁膜症性心房細動における塞栓予防のための抗血栓治療 antithrombotic therapy to prevent embolization in nonvalvular atrial fibrillation
4. 心房細動の概要 overview of atrial fibrillation
5. 心房粗動の評価および管理の概要 overview of the evaluation and management of atrial flutter

English Journal

Atrial natriuretic peptide gene variants and circulating levels: implications in cardiovascular diseases.

Rubattu S, Sciarretta S1, Volpe M.Author information 1†IRCCS Neuromed, Pozzilli (Isernia), Italy.AbstractANP (atrial natriuretic peptide), discovered 30 years ago in rat cardiac atria, has been extensively investigated with regard to physiology, pathophysiology, cardiovascular disease therapeutics and molecular genetic aspects. Besides its diuretic, natriuretic and vasorelaxant effects, novel properties of this hormone have been described. Thus anti-hypertrophic, anti-fibrotic, anti-proliferative and anti-inflammatory actions suggest that ANP contributes not only to haemodynamic homoeostasis and adjustments, but has also a role in cardiovascular remodelling. Circulating ANP levels represent a valuable biomarker in cardiovascular diseases. ANP structure is highly conserved among species, indicating a key role in cardiovascular health. Thus an abnormal ANP structure may contribute to an increased risk of disease due to altered functions at either the vascular or cardiac level. Among others, the 2238T>C exon 3 variant has been associated with endothelial cell damage and dysfunction and with an increased risk of acute cardiovascular events, a frameshift mutation within exon 3 has been related to increased risk of atrial fibrillation, and ANP gene variants have been linked to increased risk of hypertension in different ethnic groups. On the other hand, the rs5068 variant, falling within the 3' UTR and associated with higher circulating ANP levels, has been shown to have a beneficial cardioprotective and metabolic effect. Dissecting out the disease mechanisms dependent on specific ANP molecular variants may reveal information useful in the clinical setting for diagnostic, prognostic and therapeutic purposes. Furthermore, insights from molecular genetic analysis of ANP may well integrate advancing knowledge on the role of ANP as a significant biomarker in patients affected by cardiovascular diseases.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul 1;127(1):1-13. doi: 10.1042/CS20130427.
ANP (atrial natriuretic peptide), discovered 30 years ago in rat cardiac atria, has been extensively investigated with regard to physiology, pathophysiology, cardiovascular disease therapeutics and molecular genetic aspects. Besides its diuretic, natriuretic and vasorelaxant effects, novel properti
PMID 24611929

Acute mercury toxicity modulates cytochrome P450, soluble epoxide hydrolase and their associated arachidonic acid metabolites in C57Bl/6 mouse heart.

Amara IE1, Elshenawy OH1, Abdelrady M1, El-Kadi AO2.Author information 1Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, T6G 2E1, AB, Canada.2Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, T6G 2E1, AB, Canada; College of Pharmacy, Qatar University, Doha, Qatar. Electronic address: aelkadi@ualberta.ca.AbstractMercury exposure is associated with increased risk of cardiovascular disease and profound cardiotoxicity. However, the correlation between Hg(2+)-mediated toxicity and alteration in cardiac cytochrome P450s (Cyp) and their dependent arachidonic acid metabolites has never been investigated. Therefore, we investigated the effect of acute mercury toxicity on the expression of Cyp-epoxygenases and Cyp-ω-hydroxylases and their associated arachidonic acid metabolites in mice hearts. In addition, we examined the expression and activity of soluble epoxide hydrolase (sEH) as a key player in arachidonic acid metabolism pathway. Mercury toxicity was induced by a single intraperitoneal injection (IP) of 2.5mg/kg of mercuric chloride (HgCl2). Our results showed that mercury treatment caused a significant induction of the cardiac hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP); in addition to Cyp1a1, Cyp1b1, Cyp2b9, Cyp2b10, Cyp2b19, Cyp2c29, Cyp2c38, Cyp4a10, Cyp4a12, Cyp4a14, Cyp4f13, Cyp4f15, Cyp4f16 and Cyp4f18 gene expression. Moreover, Hg(2+) significantly increased sEH protein expression and activity levels in hearts of mercury-treated mice, with a consequent decrease in 14,15-, and 11,12-epoxyeicosatrienoic acids (EETs) levels. Whereas the formation of 14,15-, 11,12-, 8,9-dihydroxyeicosatrienoic acids (DHETs) was significantly increased. In conclusion, acute Hg(2+) toxicity modulates the expression of several Cyp and sEH enzymes with a consequent decrease in the cardioprotective EETs which could represent a novel mechanism by which mercury causes progressive cardiotoxicity. Furthermore, inhibiting sEH might represent a novel therapeutic approach to prevent Hg(2+)-induced hypertrophy.
Toxicology letters.Toxicol Lett.2014 Apr 7;226(1):53-62. doi: 10.1016/j.toxlet.2014.01.025. Epub 2014 Jan 25.
Mercury exposure is associated with increased risk of cardiovascular disease and profound cardiotoxicity. However, the correlation between Hg(2+)-mediated toxicity and alteration in cardiac cytochrome P450s (Cyp) and their dependent arachidonic acid metabolites has never been investigated. Therefore
PMID 24472606

Clinical Predictors of Long-Term Outcomes in Patients With Critical Limb Ischemia Who have Undergone Endovascular Therapy.

Chang SH1, Tsai YJ, Chou HH, Wu TY, Hsieh CA, Cheng ST, Huang HL.Author information 11Section of Cardiology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.AbstractClinical predictors of long-term outcomes in patients with critical limb ischemia (CLI) treated with endovascular therapy (EVT) remain unclear. In this study, clinical predictors of long-term outcomes in EVT-treated patients with CLI were investigated. In this prospective, observational study, we analyzed a total of 253 Taiwanese patients with CLI with 314 limbs who underwent EVT between 2005 and 2012. Cox models were used to estimate hazard ratios of death, limb loss, and sustained clinical success (SCS). Multivariate analysis showed that age, atrial fibrillation (AF), end-stage renal disease (ESRD), and albumin were significant predictors of mortality. Patients with coronary artery disease and low albumin levels had a significant risk of major limb amputation, while AF, ESRD, and albumin were significant, independent predictors of SCS. In addition to previously reported predictors, we showed that AF and malnutrition can be used to predict long-term outcome in EVT-treated patients with CLI.
Angiology.Angiology.2014 Apr;65(4):315-22. doi: 10.1177/0003319713515544. Epub 2013 Dec 19.
Clinical predictors of long-term outcomes in patients with critical limb ischemia (CLI) treated with endovascular therapy (EVT) remain unclear. In this study, clinical predictors of long-term outcomes in EVT-treated patients with CLI were investigated. In this prospective, observational study, we an
PMID 24357434

Japanese Journal

DOWN-REGULATION OF L-TYPE CA2+ CURRENT IN LEFT ATRIAL MYOCYTES OF RATS DURING EXPERIMENTAL CARDIAC HYPERTROPHY

Zhang Chunpeng,Okamoto Yosuke,Ohba Takayoshi,Ishibashi Kazuyuki,Yamamoto Hiroshi,Ono Kyoichi,Yamamoto Fumio
秋田医学 39(2), 61-71, 2013-02-00
NAID 110009575393