Quantitative evaluation of ontogenetic change in heart rate and its autonomic regulation in newborn mice with the use of a noninvasive piezoelectric sensor

A reliable basal heart rate (HR) measurement in freely moving newborn mice was accomplished for the first time by using a novel noninvasive piezoelectric transducer (PZT) sensor. The basal HR was ∼320 beats/min at postnatal day (P)0 and increased with age to ∼690 beats/min at P14. Contribution of autonomic control to HR was then assessed. Sympathetic blockade with metoprolol significantly reduced basal HR at both P6 (−236 ± 23 beats/min; mean ± SE) and P12 (−105 ± 8 beats/min), but atropine was without effect, indicating the predominant tonic adrenergic stimulation and absence of vagal control for basal HR in newborn mice. In contrast to stable basal HR during 5-min recording, HR measured by ECG (ECG-HR) was markedly decreased because of the restraint stress of attaching ECG electrodes, with accompanying freezing behavior. ECG-HR lowered and further decreased gradually during 5 min (slow cardiodeceleration) at P0–P3 and rapidly decreased and gradually recovered within 5 min (transient bradycardia) at P9–P14. The response was not uniform in P4–P8 mice: they showed either of these two patterns or sustained bradycardia (9–29%), and the number of mice that showed transient bradycardia increased with age (30–100%) during the period. Studies with autonomic blockade suggest that the slow cardiodeceleration and transient bradycardia are mediated mainly by withdrawal of adrenergic stimulation and phasic vagal activation, respectively, and the autonomic control of HR response to restraint stress is likely to change from the withdrawal of adrenergic stimulation to the phasic vagal activation at different stages during P4–P8 in individual mice. The PZT sensor may offer excellent opportunities to monitor basal HR of small animals noninvasively.

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Intense exercise causes decrease in expression of both endothelial NO synthase and tissue NOx level in hearts

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.279.3.r951 ◽

2000 ◽

Vol 279 (3) ◽

pp. R951-R959 ◽

Cited By ~ 31

Author(s):

Motoyuki Iemitsu ◽

Takashi Miyauchi ◽

Seiji Maeda ◽

Koichi Yuki ◽

Tsutomu Kobayashi ◽

...

Keyword(s):

Nitric Oxide ◽

Heart Rate ◽

Mrna Level ◽

Tissue Level ◽

No Synthase ◽

Adrenergic Stimulation ◽

Intense Exercise ◽

End Products ◽

First Time ◽

Enos Protein

Cardiac myocytes produce nitric oxide (NO). We studied the effects of intense exercise on the expression of NO synthase (NOS) and the tissue level of nitrite (NO2 −)/nitrate (NO3 −) (i.e., NOx), which are stable end products of NO in the heart. Rats ran on a treadmill for 45 min. Immediately after this exercise, the heart was quickly removed. Control rats remained at rest during the same 45-min period. The mRNA level of endothelial NOS (eNOS) in the heart was markedly lower in the exercised rats than in the control rats. Western blot analysis confirmed downregulation of eNOS protein in the heart after exercise. Tissue NOx level in the heart was significantly lower in the exercised rats than in the control rats. The present study revealed for the first time that production of NO in the heart is decreased by intense exercise. Because NO attenuates positive inotropic and chronotropic responses to β1-adrenergic stimulation in the heart, the decrease in cardiac production of NO by intense exercise may contribute to the acceleration of increase in myocardial contractility and heart rate during intense exercise.

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Cardiac autonomic blockade in exercising dogs

Journal of Applied Physiology ◽

10.1152/jappl.1977.42.6.878 ◽

1977 ◽

Vol 42 (6) ◽

pp. 878-883 ◽

Cited By ~ 7

Author(s):

J. M. Atkins ◽

L. D. Horwitz

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Autonomic Control ◽

Cardiac Denervation ◽

Autonomic Blockade ◽

Myocardial Contractile Force ◽

Myocardial Contractile ◽

Severe Exercise

Pharmacological blockade of autonomic control of the heart was studied in dogs performing mild, moderate, and severe running exercise on a level treadmill. The dogs were studied without drugs, after atropine, after propranolol, and after both atropine and propranolol. As compared with results without drugs, cardiac denervation resulted in elevated resting heart rate (+45 beats/min) but reduced heart rate during moderate (-17 beats/min) and severe exercise (-47 beats/min); no change in cardiac output at rest or during mild exercise but decreases (-23% and -25%) during moderate and severe exercise; and reduced first derivatives of left ventricular pressure at rest (-24%) and during exercise (-35, -41, and -52% for mild, moderate, and severe loads, respectively). Cardiac denervation did not alter end-diastolic left ventricular diameter but significantly increased end-systolic diameter during exercise. It is concluded that blockade of autonomic control of the heart diminishes cardiac output during exercise by reducing heart rate and myocardial contractile force but does not alter cardiac output at rest.

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Autonomic control of heart rate during forced activity and digestion in the snakeBoa constrictor

Journal of Experimental Biology ◽

10.1242/jeb.204.20.3553 ◽

2001 ◽

Vol 204 (20) ◽

pp. 3553-3560 ◽

Cited By ~ 2

Author(s):

Tobias Wang ◽

E. W. Taylor ◽

Denis Andrade ◽

Augusto S. Abe

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiovascular Responses ◽

Autonomic Control ◽

Boa Constrictor ◽

Adrenergic Antagonist ◽

Autonomic Blockade ◽

The Mean ◽

Positive Chronotropic Effect ◽

Mean Heart Rate

SUMMARYReptiles, particularly snakes, exhibit large and quantitatively similar increments in metabolic rate during muscular exercise and following a meal, when they are apparently inactive. The cardiovascular responses are similar during these two states, but the underlying autonomic control of the heart remains unknown. We describe both adrenergic and cholinergic tonus on the heart during rest, during enforced activity and during digestion (24–36 h after ingestion of 30 % of their body mass) in the snake Boa constrictor. The snakes were equipped with an arterial catheter for measurements of blood pressure and heart rate, and autonomic tonus was determined following infusion of the β-adrenergic antagonist propranolol (3 mg kg–1) and the muscarinic cholinoceptor antagonist atropine (3 mg kg–1).The mean heart rate of fasting animals at rest was 26.4±1.4 min–1, and this increased to 36.1±1.4 min–1 (means ± s.e.m.; N=8) following double autonomic block (atropine and propranolol). The calculated cholinergic and adrenergic tones were 60.1±9.3 % and 19.8±2.2 %, respectively. Heart rate increased to 61.4±1.5 min–1 during enforced activity, and this response was significantly reduced by propranolol (maximum values of 35.8±1.6 min–1), but unaffected by atropine. The cholinergic and adrenergic tones were 2.6±2.2 and 41.3±1.9 % during activity, respectively. Double autonomic block virtually abolished tachycardia associated with enforced activity (heart rate increased significantly from 36.1±1.4 to 37.6±1.3 min–1), indicating that non-adrenergic, non-cholinergic effectors are not involved in regulating heart rate during activity. Blood pressure also increased during activity.Digestion was accompanied by an increase in heart rate from 25.6±1.3 to 47.7±2.2 min–1 (N=8). In these animals, heart rate decreased to 44.2±2.7 min–1 following propranolol infusion and increased to 53.9±1.8 min–1 after infusion of atropine, resulting in small cholinergic and adrenergic tones (6.0±3.5 and 11.1±1.1 %, respectively). The heart rate of digesting snakes was 47.0±1.0 min–1 after double autonomic blockade, which is significantly higher than the value of 36.1±1.4 min–1 in double-blocked fasting animals at rest. Therefore, it appears that some other factor exerts a positive chronotropic effect during digestion, and we propose that this factor may be a circulating regulatory peptide, possibly liberated from the gastrointestinal system in response to the presence of food.

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Mathematical modeling autonomic control of heart rate and mean blood pressure in autonomic blockade and hypertension

Clinical Physiology of Circulation ◽

10.24022/1814-6910-2017-14-4-202-210 ◽

2017 ◽

Vol 14 (4) ◽

pp. 202-210

Author(s):

Yu.M. Ishbulatov ◽

A.S. Karavaev ◽

A.R. Kiselev ◽

S.A. Mironov ◽

V.A. Shvarts ◽

...

Keyword(s):

Mathematical Modeling ◽

Blood Pressure ◽

Heart Rate ◽

Autonomic Control ◽

Mean Blood Pressure ◽

Autonomic Blockade

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Trigeminal Depressor Response during Percutaneous Microcompression of the Trigeminal Ganglion for Trigeminal Neuralgia

Neurosurgery ◽

10.1227/00006123-198812000-00010 ◽

1988 ◽

Vol 23 (6) ◽

pp. 745-748 ◽

Cited By ~ 63

Author(s):

Jeffrey A. Brown ◽

Mark C. Preul

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Trigeminal Neuralgia ◽

Arterial Blood Pressure ◽

Trigeminal Ganglion ◽

Depressor Response ◽

Arterial Blood ◽

First Time ◽

Transient Bradycardia ◽

Intravenous Atropine

Abstract Percutaneous microcompression of the trigeminal ganglion for trigeminal neuralgia was performed 23 times on 21 patients. Significant abrupt drops in heart rate and blood pressure (P < 0.0002) occurred when the needle entered the foramen ovale or upon balloon advancement or inflation. In 16 of 23 (70%) procedures, the heart rate fell abruptly to 60 or less, by a mean of 38%. Mean arterial blood pressure decreased transiently by 31% during 12 of 23 (55%) procedures. Our findings of transient bradycardia and hypotension upon mechanical stimulation or compression of the mandibular nerve or trigeminal ganglion show for the first time the presence of a trigeminal depressor response in humans. We recommend that heart rate and arterial blood pressure be monitored continuously during percutaneous microcompression of the trigeminal ganglion. Intravenous atropine should be available for immediate use, and an external pacemaker should be fitted preoperatively.

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