WordNet

(physical chemistry) a sample of matter in which substances in different phases are in equilibrium; "in a static system oil cannot be replaced by water on a surface"; "a system generating hydrogen peroxide"
instrumentality that combines interrelated interacting artifacts designed to work as a coherent entity; "he bought a new stereo system"; "the system consists of a motor and a small computer"
a group of independent but interrelated elements comprising a unified whole; "a vast system of production and distribution and consumption keep the country going" (同)scheme
a complex of methods or rules governing behavior; "they have to operate under a system they oppose"; "that language has a complex system for indicating gender" (同)system of rules
a group of physiologically or anatomically related organs or parts; "the body has a system of organs for digestion"
a procedure or process for obtaining an objective; "they had to devise a system that did not depend on cooperation"
the living body considered as made up of interdependent components forming a unified whole; "exercise helped him get the alcohol out of his system"
any mechanical force that tends to retard or oppose motion
the capacity of an organism to defend itself against harmful environmental agents; "these trees are widely planted because of their resistance to salt and smog"
the action of opposing something that you disapprove or disagree with; "he encountered a general feeling of resistance from many citizens"; "despite opposition from the newspapers he went ahead" (同)opposition
(psychiatry) an unwillingness to bring repressed feelings into conscious awareness
group action in opposition to those in power
the military action of resisting the enemys advance; "the enemy offered little resistance"
the degree of unresponsiveness of a disease-causing microorganism to antibiotics or other drugs (as in penicillin-resistant bacteria)
of or relating to or having vessels that conduct and circulate fluids; "vascular constriction"; "a vascular bundle"
affecting an entire system; "a systemic poison"

PrepTutorEJDIC

〈C〉(関連した部分から成る)『体系』,系統,組織[網],装置 / 〈C〉(教育・政治などの)『制度』,機構;《the~》体制 / 〈C〉(思想・学問などの)『体系』,学説 / 〈C〉(…の)『方法』,方式,やり方《+of doing》 / 〈U〉正しい方針(筋道,順序) / 〈U〉《the~》(身体の)組織,系統 / 〈U〉《the~,one's~》身体,全身
〈U〉〈C〉(…に)『抵抗』(『反抗』)『すること』;(…を)『こらえること』《+『to』(『against』)+『名』(do『ing』)》 / 〈U〉(病気などに対する)『抵抗力』《+『against』(『to』)+『名』》 / 〈U〉〈C〉(またresistance movement)(権力・圧制に対する)抵抗運動,レジスタンス / 〈U〉(空気の)抵抗;(電気の)抵抗
(血液・樹液などを運ぶ)管の,導管の,血管の
(身体・言語のように)体系の,組織の / 全身の,全身的

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/02/13 16:38:57」(JST)

wiki en

Vascular resistance is the resistance to flow that must be overcome to push blood through the circulatory system. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). The systemic vascular resistance may also be referred to as the total peripheral resistance. Vasoconstriction (i.e., decrease in blood vessel diameter) increases SVR, whereas vasodilation (increase in diameter) decreases SVR.

Units for measuring vascular resistance are dyn·s·cm⁻⁵, pascal seconds per cubic metre (Pa·s/m³) or, for ease of deriving it by pressure (measured in mmHg) and cardiac output (measured in l/min), it can be given in mmHg·min/l. This is numerically equivalent to hybrid reference units (HRU), also known as Wood units, frequently used by pediatric cardiologists. To convert from Wood units to MPa·s/m³ you must multiply by 8, or to dyn·s·cm⁻⁵ you must multiply by 80.^[1]

Measurement	Reference Range
Measurement	dyn·s/cm⁵	MPa·s/m³	mmHg·min/l or HRU/Wood units
Systemic vascular resistance	700–1600^[2]	70–160^[3]	9–20^[3]
Pulmonary vascular resistance	20–130^[2]	2–13^[3]	0.25–1.6^[3]

Calculation of resistance

The basic tenet of calculating resistance is that flow is equal to driving pressure divided by resistance.

The systemic vascular resistance can therefore be calculated in units of dyn·s·cm⁻⁵ as

where mean arterial pressure is 2/3 of diastolic blood pressure plus 1/3 of systolic blood pressure (or Diastolic + 1/3(Systolic-Diastolic).

The pulmonary vascular resistance can therefore be calculated in units of dyn·s·cm⁻⁵ as

where the pressures are measured in units of millimetres of mercury (mmHg) and the cardiac output is measured in units of litres per minute (L/min). The pulmonary artery wedged pressure (also called pulmonary artery occlusion pressure or PAOP) is a measurement in which one of the pulmonary arteries is occluded, and the pressure downstream from the occlusion is measured in order to approximately sample the left atrial pressure.^[4] Therefore the numerator of the above equation is the pressure difference between the input to the pulmonary blood circuit (where the heart's right ventricle connects to the pulmonary trunk) and the output of the circuit (which is the input to the left atrium of the heart). The above equation contains a numerical constant to compensate for the units used, but is conceptually equivalent to the following:

where R is the pulmonary vascular resistance (fluid resistance), ΔP is the pressure difference across the pulmonary circuit, and Q is the rate of blood flow through it.

As an example: If Systolic pressure: 120 mmHg, Diastolic pressure: 80 mmHg, Right atrial mean pressure: 3 mmHg, Cardiac output: 5 l/min, Then Mean Arterial Pressure would be: (2 Diastolic pressure + Systolic pressure)/3 = 93.3 mmHg, and Systemic vascular resistance: (93 - 3) / 5 = 18 Wood Units. Or Systemic vascular resistance: 18 x 80 = 1440 dyn·s/cm5. These values are in the normal limits.

Determinants of vascular resistance

The major determinant of vascular resistance is small arteriolar (known as resistance arterioles) tone. These vessels are from 450 µm down to 100 µm in diameter. (As a comparison, the diameter of a capillary is about 3 to 4 µm.)

Another determinant of vascular resistance is the pre-capillary arterioles. These arterioles are less than 100 µm in diameter. They are sometimes known as autoregulatory vessels since they can dynamically change in diameter to increase or reduce blood flow.

Any change in the viscosity of blood (such as due to a change in hematocrit) would also affect the measured vascular resistance.

Regulation of vascular resistance

There are many factors that alter the vascular resistance. Many of the platelet-derived substances, including serotonin, are vasodilatory when the endothelium is intact and are vasoconstrictive when the endothelium is damaged.

Cholinergic stimulation causes release of endothelium-derived relaxing factor (EDRF) (later it was discovered that EDRF was nitric oxide) from intact endothelium, causing vasodilation. If the endothelium is damaged, cholinergic stimulation causes vasoconstriction.

Role of adenosine

Adenosine probably doesn't play a role in maintaining the vascular resistance in the resting state. However, it causes vasodilation and decreased vascular resistance during hypoxia. Adenosine is formed in the myocardial cells during hypoxia, ischemia, or vigorous work, due to the breakdown of high-energy phosphate compounds (e.g., adenosine monophosphate, AMP). Most of the adenosine that is produced leaves the cell and acts as a direct vasodilator on the vascular wall. Because adenosine acts as a direct vasodilator, it is not dependent on an intact endothelium to cause vasodilation.

Adenosine causes vasodilation in the small and medium sized resistance arterioles (less than 100 µm in diameter). When adenosine is administered it can cause a coronary steal phenomenon,^[5] where the vessels in healthy tissue dilate as much as the ischemic tissue and more blood is shunted away from the ischemic tissue that needs it most. This is the principle behind adenosine stress testing.

Adenosine is quickly broken down by adenosine deaminase, which is present in red cells and the vessel wall.

Coronary vascular resistance

The regulation of tone in the coronary arteries is a complex subject. There are a number of mechanisms for regulating coronary vascular tone, including metabolic demands (i.e.: hypoxia), neurologic control, and endothelial factors (i.e.: EDRF, endothelin).

Local metabolic control (based on metabolic demand) is the most important mechanism of control of coronary flow. Decreased tissue oxygen content and increased tissue CO₂ content act as vasodilators. Acidosis acts as a direct coronary vasodilator and also potentiates the actions of adenosine on the coronary vasculature.

References

^ Fuster, V.; Alexander, R.W.; O'Rourke, R.A. (2004) Hurst's the heart, book 1. 11th Edition, McGraw-Hill Professional, Medical Pub. Division. Page 513. ISBN 978-0-07-143224-5.
^ ^a ^b Table 30-1 in: Trudie A Goers; Washington University School of Medicine Department of Surgery; Klingensmith, Mary E; Li Ern Chen; Sean C Glasgow (2008). The Washington manual of surgery. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 0-7817-7447-0.
^ ^a ^b ^c ^d Derived from values in dyn·s/cm⁵
^ University of Virginia Health System."The Physiology: Pulmonary Artery Catheters"
^ Masugata H, Peters B, Lafitte S, et al. (2003). "Assessment of adenosine-induced coronary steal in the setting of coronary occlusion based on the extent of opacification defects by myocardial contrast echocardiography". Angiology 54 (4): 443–8. doi:10.1177/000331970305400408. PMID 12934764.

Literature

1. Grossman W, Baim D. Grossman's Cardiac Catheterization, Angiography, and Intervention, Sixth Edition. Page 172, Tabe 8.1 ISBN 0-683-30741-X

2. Heart information: Systemic vascular resistance

UpToDate Contents

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English Journal

A new strategy for treating hypertension by blocking the activity of the brain renin-angiotensin system with aminopeptidase A inhibitors.

Gao J1, Marc Y, Iturrioz X1, Leroux V1, Balavoine F2, Llorens-Cortes C1.Author information 1*Laboratory of Central Neuropeptides in the Regulation of Body Fluid Homeostasis and Cardiovascular Functions, CIRB, Collège de France, INSERM U1050, Paris, F-75231, France.2†Quantum Genomics, Massy, F-91300, France.AbstractHypertension affects one-third of the adult population and is a growing problem due to the increasing incidence of obesity and diabetes. Brain RAS (renin-angiotensin system) hyperactivity has been implicated in the development and maintenance of hypertension in several types of experimental and genetic hypertension animal models. We have identified in the brain RAS that APA (aminopeptidase A) and APN (aminopeptidase N), two membrane-bound zinc metalloproteases, are involved in the metabolism of AngII (angiotensin II) and AngIII (angiotensin III) respectively. The present review summarizes the main findings suggesting that AngIII plays a predominant role in the brain RAS in the control of BP (blood pressure). We first explored the organization of the APA active site by site-directed mutagenesis and molecular modelling. The development and the use in vivo of specific and selective APA and APN inhibitors EC33 and PC18 respectively, has allowed the demonstration that brain AngIII generated by APA is one of the main effector peptides of the brain RAS, exerting a tonic stimulatory control over BP in conscious hypertensive rats. This identified brain APA as a potential therapeutic target for the treatment of hypertension, which has led to the development of potent orally active APA inhibitors, such as RB150. RB150 administered orally in hypertensive DOCA (deoxycorticosteroneacetate)-salt rats or SHRs (spontaneously hypertensive rats) crosses the intestinal, hepatic and blood-brain barriers, enters the brain, generates two active molecules of EC33 which inhibit brain APA activity, block the formation of brain AngIII and normalize BP for several hours. The decrease in BP involves two different mechanisms: a decrease in vasopressin release into the bloodstream, which in turn increases diuresis resulting in a blood volume reduction that participates in the decrease in BP and/or a decrease in sympathetic tone, decreasing vascular resistance. RB150 constitutes the prototype of a new class of centrally acting antihypertensive agents and is currently being evaluated in a Phase Ib clinical trial.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Aug 1;127(3):135-48. doi: 10.1042/CS20130396.
Hypertension affects one-third of the adult population and is a growing problem due to the increasing incidence of obesity and diabetes. Brain RAS (renin-angiotensin system) hyperactivity has been implicated in the development and maintenance of hypertension in several types of experimental and gen
PMID 24697296

The probiotic Lactobacillus coryniformis CECT5711 reduces the vascular pro-oxidant and pro-inflammatory status in obese mice.

Toral M1, Gómez-Guzmán M1, Jiménez R, Romero M, Sánchez M1, Utrilla MP, Garrido-Mesa N2, Rodríguez-Cabezas ME, Olivares M3, Gálvez J, Duarte J.Author information 1*Department of Pharmacology, School of Pharmacy, University of Granada, Granada, Spain.2‡CIBER-EHD, Department of Pharmacology, Center for Biomedical Research, University of Granada, Granada, Spain.3§Research Department of Biosearch, Granada, Spain.AbstractObesity is associated with intestine dysbiosis and is characterized by a low-grade inflammatory status, which affects vascular function. In the present study, we evaluated the effects of a probiotic with immunomodulatory properties, Lactobacillus coryniformis CECT5711, in obese mice fed on an HFD (high-fat diet). The probiotic treatment was given for 12 weeks, and it did not affect the weight evolution, although it reduced basal glycaemia and insulin resistance. L. coryniformis administration to HFD-induced obese mice induced marked changes in microbiota composition and reduced the metabolic endotoxaemia as it decreased the LPS (lipopolysaccharide) plasma level, which was associated with a significant improvement in gut barrier disruption. Furthermore, it lowered TNFα (tumour necrosis factor α) expression in liver, improving the inflammatory status, and thus the glucose metabolism. Additionally, the probiotic reversed the endothelial dysfunction observed in obese mice when endothelium- and NO (nitric oxide)-dependent vasodilatation induced by acetylcholine in aortic rings was studied. It also restored the increased vessel superoxide levels observed in obese mice, by reducing NADPH oxidase activity and increasing antioxidant enzymes. Moreover, chronic probiotic administration for 2 weeks also improved endothelial dysfunction and vascular oxidative stress induced by in vivo administration of LPS in control mice fed on a standard chow diet. The results of the present study demonstrate an endothelial-protective effect of L. coryniformis CECT5711 in obese mice by increasing NO bioavailability, suggesting the therapeutic potential of this gut microbiota manipulation to prevent vasculopathy in obesity.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul;127(1):33-45. doi: 10.1042/CS20130339.
Obesity is associated with intestine dysbiosis and is characterized by a low-grade inflammatory status, which affects vascular function. In the present study, we evaluated the effects of a probiotic with immunomodulatory properties, Lactobacillus coryniformis CECT5711, in obese mice fed on an HFD (h
PMID 24410749

Ischemic heart disease and the mediterranean diet.

Whayne TF Jr.Author information Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, 326 Wethington Building, 900 South Limestone Street, Lexington, KY, 40536-0200, USA, twhayn0@uky.edu.AbstractLifestyle modification is primary in cardiovascular (CV) disease prevention. A major contribution is the Mediterranean diet (MedDiet), defined by two of seven components. Italian investigators determined a significant decrease in peripheral arterial disease of 56 % for a high score. Multiple specific CV risk factors are also favorably modified by the MedDiet. This includes beneficial effect on inflammation, vascular endothelium, and insulin resistance. There is also evidence that coronary heart disease, diabetes mellitus, and metabolic syndrome are decreased. Benefit appears to extend to new migrants in France. The economics of dietary adherence are favorable with decreased total lifetime health costs. Although mixed nuts appear to be a major factor in the MedDiet, special emphasis goes to extra virgin olive oil. Benefit also extends to other noncommunicable diseases with a decrease in cancer, Parkinson's disease, and Alzheimer's disease. Further quantitation of benefit and understanding of mechanisms involved in dietary benefit is essential.
Current cardiology reports.Curr Cardiol Rep.2014 Jun;16(6):491. doi: 10.1007/s11886-014-0491-6.
Lifestyle modification is primary in cardiovascular (CV) disease prevention. A major contribution is the Mediterranean diet (MedDiet), defined by two of seven components. Italian investigators determined a significant decrease in peripheral arterial disease of 56 % for a high score. Multiple specif
PMID 24743900

Japanese Journal

Low-Dose β-Blocker in Combination With Milrinone Safely Improves Cardiac Function and Eliminates Pulsus Alternans in Patients With Acute Decompensated Heart Failure

KOBAYASHI Shigeki,SUSA Takehisa,TANAKA Takeo,MURAKAMI Wakako,FUKUTA Seiko,OKUDA Shinichi,DOI Masahiro,WADA Yasuaki,NAO Tomoko,YAMADA Jutaro,OKAMURA Takayuki,YANO Masafumi,MATSUZAKI Masunori
Circulation journal : official journal of the Japanese Circulation Society 76(7), 1646-1653, 2012-06-25
… Low-dose landiolol (1.5μg·kg-1·min-1) significantly reduced HR by 11% without changing blood pressure (BP) and CI, whereas higher doses (≥3.0μg·kg-1·min-1) tended to decrease BP and CI while increasing PCWP and systemic vascular resistance. …
NAID 10030503344

〈Review〉Kidney and Hypertension

Arima Shuji
Acta Medica Kinki University 37(1), 1-8, 2012-06
… [Abstract]　The kidney plays an important role in the control of systemic blood pressure by regulating the composition of body fluid and electrolytes and by producing and releasing various vasoactive substances. … an increased pre-glomerular vascular resistance, a decreased whole kidney ultrafiltration and an increased tubular sodium reabsorption. …
NAID 80022703765