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separate as a fine suspension of solid particles
a precipitated solid substance in suspension or after settling or filtering
fall from clouds; "rain, snow and sleet were falling"; "Vesuvius precipitated its fiery, destructive rage on Herculaneum" (同)come_down, fall
bring about abruptly; "The crisis precipitated by Russias revolution"
fall vertically, sharply, or headlong; "Our economy precipitated into complete ruin"
hurl or throw violently; "The bridge broke and precipitated the train into the river below"

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/30 23:04:56」(JST)

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Chronotropic effects (from chrono-, meaning time, and tropos, "a turn") are those that change the heart rate.

Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate.

A dromotrope affects atrioventricular node (AV node) conduction. A positive dromotrope increases AV nodal conduction, and a negative dromotrope decreases AV nodal conduction. A lusitrope is an agent that affects diastolic relaxation.

Many positive inotropes affect preload and afterload.

Negative chronotropes

Chronotropic variables in systolic myocardial left and right. Left sided systolic chronotropy can be appreciated as Aortic Valve open to close time. Right sided variables are represented by pulmonary valve open to close time. Inverted as diastolic chronotropy, the variables are aortic valve close to open and pulmonic close to open time. Pharmaceutical manipulation of chronotropic properties was perhaps first appreciated by the introduction of digitalis, though it turns out that digitalis has an inotropic effect rather than a chronotropic effect.

Beta blockers such as metoprolol
Acetylcholine
Digoxin
The non-dihydropyridine calcium channel blockers diltiazem and verapamil

Positive chronotropes

Most Adrenergic agonists
Atropine
Dopamine
Epinephrine
Isoproterenol
Theophylline^[1]

References

^ Alboni, P.; Menozzi, C.; Brignole, M.; Paparella, N.; Gaggioli, G.; Lolli, G.; Cappato, R. (1997). "Effects of Permanent Pacemaker and Oral Theophylline in Sick Sinus Syndrome: The THEOPACE Study: A Randomized Controlled Trial". Circulation 96: 260–266. doi:10.1161/01.CIR.96.1.260. PMID 9236443.

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UpToDate Contents

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1. Permanent cardiac pacing: Indications
2. 洞不全症候群の診断および評価 diagnosis and evaluation of the sick sinus syndrome
3. 冠動脈疾患の予後決定のための運動負荷心電図試験 exercise ecg testing to determine prognosis of coronary heart disease
4. 洞徐脈 sinus bradycardia
5. 先天性心疾患における心房性不整脈（房室ブロックを含む） atrial arrhythmias including av block in congenital heart disease

English Journal

Chronotropic and dromotropic responses to localized glutamate microinjections in the rat nucleus ambiguus.

Sampaio KN1, Mauad H1, Michael Spyer K1, Ford TW2.Author information 1Division of Biosciences, Faculty of Life Sciences, University College London, Gower Street, London WC1E 6BT, UK.2Division of Biosciences, Faculty of Life Sciences, University College London, Gower Street, London WC1E 6BT, UK. Electronic address: timothy.ford@nottingham.ac.uk.AbstractThe cardioinhibitory effects of cardiac vagal motoneurons (CVMs) are mediated by activation of postganglionic neurons in the epicardial ganglia which have been shown to exert functionally selective effects on heart rate and atrioventricular conduction in the rat. Here we investigate whether CVMs producing these responses may occupy different rostrocaudal positions within the nucleus ambiguus. Excitation of CVMs was attempted by microinjections of glutamate into the nucleus ambiguus of an arterially perfused preparation in a grid extending over 2mm in the rostrocaudal plane using the obex as a reference point. Microinjections were paired, one made during pacing to measure changes in atrioventricular conduction (P-R interval) independent of changes in heart rate and the other looking for changes in heart period (P-P interval) un-paced. Although evidence of a differential distribution was found in 7 cases, in the majority (13/20), sites producing maximal effects on both variables coincided. Maximal changes in atrioventricular conduction resulted from more rostral sites in 6 cases and from a more caudal site in only one. Overall, the ratio of the change in atrioventricular conduction to the change in heart rate for a given site was significantly greater 1mm rostral to the obex than at either end of the test grid. We conclude that while CVMs controlling atrioventricular conduction are distributed with a peak somewhat rostral to those controlling heart rate in a number of animals, there is a significant overlap and much greater variability in this distribution in the rat than in cats and dogs.
Brain research.Brain Res.2014 Jan 13;1542:93-103. doi: 10.1016/j.brainres.2013.10.035. Epub 2013 Oct 24.
The cardioinhibitory effects of cardiac vagal motoneurons (CVMs) are mediated by activation of postganglionic neurons in the epicardial ganglia which have been shown to exert functionally selective effects on heart rate and atrioventricular conduction in the rat. Here we investigate whether CVMs pro
PMID 24177045

Selective inhibition of the late sodium current has no adverse effect on electrophysiological or contractile function of the normal heart.

Fernandes S, Hoyer K, Liu G, Wang WQ, Dhalla AK, Belardinelli L, Rajamani S.Author information Department of Biology, Cardiovascular Therapeutic Area, Gilead Sciences, Fremont, CA.AbstractInhibition of cardiac late Na current (INa,L) decreases sodium-dependent calcium overload in diseased hearts. Because INa,L is small in the absence of disease, its inhibition is not expected to significantly alter function of the normal heart. To test this hypothesis, we determined the effects of GS-458967 (GS967), a novel selective inhibitor of INa,L (IC50 = 0.13µM), on cardiac function and hemodynamics. The bradycardic agent ivabradine and the Na channel blocker flecainide were used for comparison. A single per os administration of GS967 (5 mg/kg) had no effect on blood pressure or heart rate (HR) in unanesthetized rats. In anesthetized rats, GS967 (0.6±0.1 µM plasma concentration) had no significant effect on HR, PR or QRS electrocardiogram intervals, or contraction. Flecainide (8 mg/kg) slowed HR by 23±3% (p<0.001), prolonged the PR and QRS intervals by 42±8% and 64±12% (p<0.001) and had a significant negative inotropic effect. Ivabradine (3 mg/kg) slowed HR by 36±6% (p<0.001). In rat and rabbit isolated perfused hearts, GS967 (0.1-3 µM) had no significant effects on HR, QRS interval, or contractile function. The results show that selective inhibition of cardiac INa,L is not associated with chronotropic, dromotropic, inotropic, or hemodynamic changes.
Journal of cardiovascular pharmacology.J Cardiovasc Pharmacol.2014 Jan 8. [Epub ahead of print]
Inhibition of cardiac late Na current (INa,L) decreases sodium-dependent calcium overload in diseased hearts. Because INa,L is small in the absence of disease, its inhibition is not expected to significantly alter function of the normal heart. To test this hypothesis, we determined the effects of GS
PMID 24406487

Exercise-Induced Muscle Vasodilatation and Treadmill Exercise Test Responses in Individuals without Overt Heart Disease.

Nunes RA, Giampaoli V, de Freitas HF, da Costa Pereira A, Araújo F, Correia GF, Rondon MU, Negrão CE, Mansur AJ.Author information Heart Institute (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.AbstractBackground: The beneficial effects of exercise on cardiovascular health may be related to the improvement in several physiologic pathways, including peripheral vascular function. The aim of this study was to evaluate the relationship between cardiovascular responses during the treadmill exercise test and exercise-induced muscle vasodilatation in individuals without overt heart disease. Methods: The study included 796 asymptomatic subjects (431 females and 365 males) without overt heart disease. We evaluated the heart rate (chronotropic reserve and heart rate recovery), blood pressure (maximum systolic and diastolic blood pressure as well as systolic blood pressure recovery) and exercise capacity during symptom-limited treadmill exercise testing. Exercise-induced muscle vasodilatation was studied with venous occlusion plethysmography and estimated by forearm blood flow and vascular conductance responses during a 3-min handgrip maneuver. Results: Forearm blood flow increase during the handgrip exercise was positively associated with heart rate recovery during treadmill exercise testing (p < 0.001). Forearm vascular conductance increase during the handgrip exercise was inversely associated with exercise diastolic blood pressure during exercise treadmill testing (p = 0.038). No significant association was found between exercise capacity and exercise-induced muscle vasodilation. Conclusion: In a sample of individuals without overt heart disease, exercise-induced muscle vasodilatation was associated with heart rate and blood pressure responses during treadmill exercise testing, but was not associated with exercise capacity. These findings suggest that favorable hemodynamic and chronotropic responses are associated with better vasodilator capacity, but exercise capacity does not predict muscle vasodilatation. © 2013 S. Karger AG, Basel.
Cardiology.Cardiology.2014;127(1):38-44. doi: 10.1159/000355157. Epub 2013 Nov 1.
Background: The beneficial effects of exercise on cardiovascular health may be related to the improvement in several physiologic pathways, including peripheral vascular function. The aim of this study was to evaluate the relationship between cardiovascular responses during the treadmill exercise tes
PMID 24192918

Japanese Journal

特発性間質性肺炎患者の運動に伴う心拍数,経皮的酸素飽和度の変化と身体機能の関係

日本呼吸ケア・リハビリテーション学会誌 = The journal of the Japan Society for Respiratory Care and Rehabilitation 26(3), 485-490, 2017-04
NAID 40021212903

僧帽弁形成術後の僧帽弁前尖収縮期前方運動に対してシベンゾリン静脈内投与が有効であった一例

Cardiovascular Anesthesia 21(1), 69-74, 2017
NAID 130006069670

Pharmacological characterization of <i>microminipig</i> as a model to assess the drug-induced cardiovascular responses for non-clinical toxicity and/or safety pharmacology studies