scholarly journals INFLUENCE OF FENTANYL ON THE CHRONOTROPIC RESPONSE OF ISOLATED RABBIT ATRIA TO CHOLINERGIC AND ADRENERGIC STIMULATION

1978 ◽  
Vol 28 (1) ◽  
pp. 105-114
Author(s):  
Yoshio HATANO ◽  
Noboru TODA
Keyword(s):  
Adrenergic Stimulation ◽  
Chronotropic Response ◽  
Rabbit Atria

The effect of pH on rabbit atrial response to histamine

1976 ◽  
Vol 54 (2) ◽  
pp. 118-127 ◽  
Author(s):  
M. J. Hughes ◽  
I. A. Coret
Keyword(s):  
Histamine Receptor ◽  
Maximum Response ◽  
Force Of Contraction ◽  
Histamine Concentration ◽  
Adenyl Cyclase Activity ◽  
Chronotropic Response ◽  
Spontaneous Rate ◽  
Histamine Response ◽  
Ph Range ◽  
Rabbit Atria

The chronotropic response of isolated rabbit atria in normal Tyrode's medium increases monotonically with increasing doses of histamine (9 × 10−7–9 × 10−4 M). Plots of the inverse of response against the inverse of concentration were linear; and from these plots were derived values for the theoretical maximum response at 'infinite' dose and for the histamine concentration required to evoke a half maximum response. Alteration of pH by changing [HCO3−] at constant pCO2, [Na+] and osmolality did not appreciably affect the response to histamine in the range pH 7.0–7.6. However, at pH below 7.0 the magnitude of histamine response was reduced at all concentrations of histamine tested. In the pH range 7.0–7.6, additions of NaHCO3 at constant pCO2 increased the spontaneous rate of rabbit atria (in the absence of histamine); however, there was little effect of changing pH (in this range) by altering [HCO3−] at constant pCO2 when [Na+] and osmolality were kept constant. Immersion in solutions at pH's less than 7.0 led to decline in spontaneous rate and force of contraction. It is probable that depression of adenyl cyclase activity rather than a specific change in ionization of histamine receptor is responsible for a decreased response to histamine at pH 6.9.

Chronotropic response of spontaneously beating rabbit atria to hyperosmotic media

1977 ◽  
Vol 233 (2) ◽  
pp. H228-H233 ◽  
Author(s):  
L. A. Roberts ◽  
M. J. Hughes
Keyword(s):  
Rate Control ◽  
Passive Tension ◽  
Force Of Contraction ◽  
Tyrode Solution ◽  
Chronotropic Response ◽  
Wide Range ◽  
Osmotic Agent ◽  
Hyperosmolar Solutions ◽  
Rabbit Atria ◽  
Plateau Level

Spontaneously beating rabbit atria responded to hyperosmotic Tyrode bathing media with an increase in rate, force of contraction, and passive tension dependent on the level of osmolality and the osmotic agent employed. The positive chronotropic response reached a maximum within a few minutes and then declined to a lower, maintained plateau level. The plateau change in rate was similar whether the osmotic agent added to Tyrode solution was sucrose, mannitol or NaCl. For these agents, the response increased linearly with osmotic pressure of the bathing media from 300 to 500 mosmol/kg H2O, then progressively decreased approaching zero (plateau rate = control) at about 700 mosmol/kg H2O. The chronotropic response to urea in Tyrode solution, though less than for the other three agents, progressively increased over the entire range of osmolalities tested (from 300 to 700 mosmol/kg H2O). The inotropic response was positive for all agents from 300 to 600 mosmol/kg H2O. Passive tension of atria increased with added NaCl, sucrose, or mannitol, but not with urea. Propranolol did not alter the atrial response to hyperosmolality. Thus, we find that the chronotropic response of atria to hyperosmolar solutions is positive over a wide range of agents and osmolalities, in contrast to earlier reports of a direct negative chronotropic effect.

scholarly journals Long-term effect of dietary α-linolenic acid or decosahexaenoic acid on incorporation of decosahexaenoic acid in membranes and its influence on rat heart in vivo

2007 ◽  
Vol 293 (4) ◽  
pp. H2296-H2304 ◽  
Author(s):  
Adey Ayalew-Pervanchon ◽  
Delphine Rousseau ◽  
Daniel Moreau ◽  
Patrick Assayag ◽  
Pierre Weill ◽  
...  
Keyword(s):  
Linolenic Acid ◽  
Dietary Intakes ◽  
Adrenergic Stimulation ◽  
Adult Rats ◽  
Chronotropic Response ◽  
Cardiac Membrane ◽  
Male Wistar Rats ◽  
Dha Enrichment

The present study was designed to evaluate whether long-term intake of dietary α-linolenic acid (ALA), supplied as whole grain-extruded linseed, can increase endogenous production of n-3 long-chain polyunsaturated fatty acids (FAs) in healthy adult rats and influence the heart rate (HR) and adrenergic response in the same way as docosahexaenoic acid (DHA)-rich diets. DHA enrichment was evaluated using FA analysis of tissue phospholipids after 8, 16, 24, and 32 wk of feeding in male Wistar rats randomly assigned to three dietary groups ( n = 8 in each group): a reference fat diet (RFD), an ALA-rich (ALA) diet, and a DHA-rich (DHA) diet. At 1 wk before the animals were killed, under anesthesia, HR was measured from ECG recordings during an adrenergic stimulation challenge ( n = 8). There was a significant increase of DHA in the cardiac membrane in the ALA group compared with the RFD group. DHA content in the cardiac membrane was ∼10% in the ALA group vs. 20% in the DHA group and 4% in the RFD group. The cardiac FA profile was established after 2 mo and remained essentially unchanged thereafter. Regardless of the diet, DHA in the heart decreased with age. Nevertheless, DHA content in the heart remained at >15% in the DHA group and remained greater in older rats fed the ALA diet than in younger RFD-fed rats. Basal HR decreased in the ALA group (395 ± 24.9 beats/min) to a level between that of the DHA and RFD groups (375 ± 26.4 and 407 ± 36.7 beats/min, respectively). Both n-3 dietary intakes contribute to enhancement of the chronotropic response to adrenergic agonist stimulation. Regulation of HR by neurohumoral mediators may be controlled by lower content of DHA, e.g., by a dietary supply of extruded linseed (ALA).

Autonomic nervous control of heart rate in muskrats during exercise in air and under water.

1996 ◽  
Vol 199 (7) ◽  
pp. 1563-1568 ◽  
Author(s):  
P E Signore ◽  
D R Jones
Keyword(s):  
Heart Rate ◽  
Neural Control ◽  
Cardiac Response ◽  
Resting Heart Rate ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Pronounced Increase ◽  
Chronotropic Response ◽  
Autonomic Nervous ◽  
Parasympathetic Tone

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.

Cardiovascular responsiveness to beta-adrenergic stimulation and blockade in chronic hypoxia

1975 ◽  
Vol 228 (2) ◽  
pp. 477-481 ◽  
Author(s):  
JT Maher ◽  
SC Manchanda ◽  
A Cymerman ◽  
DL Wolfe ◽  
LH Hartley
Keyword(s):  
Heart Rate ◽  
Chronic Hypoxia ◽  
Fold Increase ◽  
Initial Increase ◽  
Plasma Norepinephrine ◽  
Adrenergic Stimulation ◽  
Chronotropic Response ◽  
Beta Adrenoceptor ◽  
Arterial Ph ◽  
The Mean

Previous studies have shown that exposure to high altitude results in an initial increase in heart rate, followed by a return to sea-level values within several days; circulating catecholamines rise progressively during this time. Nine conscious dogs were studied in normoxia (N) and after 10 days' exposure to 445 torr (CH). The mean (plus or minus SE) hematocrit was higher in CH (50 plus or minus 2 vs. 42 plus or minus 1%) while Pa-o2 (53 plus or minus 1 vs. 97 plus or minus 2 torr) and PaCO2 (27 plus or minus 1 vs. 35 plus or minus 1 torr) were lower than in N. A 3.5-fold increase in plasma norepinephrine above the N value was found in CH. Arterial pH, heart rate (HR), and mean femoral arterial pressure (MAP) did not differ significantly in N and CH. Isoproterenol (ISO), 0.5 mug/kg iv, produced an average increase in HR of 92 plus or minus 9 beats/min in N, but only 66 plus or minus 8 beats/min in CH (P smaller than .02). Reduction in MAP after ISO were similar. Pretreatment with propranolol, 0.15 mg/kg iv, reduced HR equally in N and CH without affecting MAP, but diminished the HR response to ISO significantly more in CH than in N. The attenuated chronotropic response to beta-adrenoceptor stimulation following chronic hypobaric hypoxia suggests a relative cardiac refractoriness secondary to an increased level of sympathetic activity.

Enhanced chronotropic and inotropic responses of rat myocardium to cholinergic stimulus with aging

1992 ◽  
Vol 70 (12) ◽  
pp. 1618-1624 ◽  
Author(s):  
Na Su ◽  
Njanoor Narayanan
Keyword(s):  
Muscarinic Receptor ◽  
Heart Function ◽  
Specific Binding ◽  
Adrenergic Stimulation ◽  
Chronotropic Response ◽  
Related Difference ◽  
Age Related ◽  
Rat Hearts ◽  
Inotropic Responses ◽  
The Impact

The ability of the heart to respond to adrenergic stimulation diminishes with aging, and this may be one of the factors contributing to the age-associated decline in cardiac stress responsiveness. On the other hand, little is known about the impact of aging on the responsiveness of the heart to cholinergic stimulation. In this study, we determined the chronotropic and inotropic responses of the isolated, Langendorff-perfused hearts from adult (6–8 months) and aged (28–30 months) rats to cholinergic agonists so as to assess age-related alterations in postsynaptic cholinergic control of heart function. The results showed the following. (i) In isolated perfused spontaneously beating rat hearts, the negative chronotropic response to acetylcholine (10−9–10−5 M) was up to 4-fold greater in the aged compared with adult hearts; this age-related difference was less marked (2-fold) but not abolished in the presence of a maximally effective concentration (5 μM) of the cholinesterase inhibitor eserine. (ii) The cholinesterase-resistant agonist carbachol (10−9–2.5 × 10−6 M) elicited a 2- to 3-fold greater negative chronotropic response in the aged compared with adult hearts. (iii) In isolated perfused, electrically paced (4 Hz) rat hearts, carbachol (10−9–10−3 M) elicited a concentration-dependent negative inotropic response, which was 2-fold greater in the aged compared with adult heart at all carbachol concentrations, (iv) Acetylcholinesterase activities (micromoles per gram per hour) were 50–60% lower in the aged atria (83 ± 21) and ventricles (24 ± 6) than in adult atria (210 ± 20) and ventricles (47 ± 7). (v) No significant age-related difference was observed in the specific binding of (–)-[3H]quinuclidinyl benzilate to muscarinic receptor sites in atria or ventricles. These findings demonstrate a striking enhancement in the responses of the heart to cholinergic stimulus with aging, which can be attributed in part, but not solely to age-associated decline in cholinesterase activity. Age-associated alterations in muscarinic receptor linked events may also underlie the cholinergic hypersensitivity of the aging heart.Key words: aging, muscarinic receptor, cardiac performance in vitro, cholineresterase activity.

Differences in automaticity between Purkinje strands from right and left dog ventricle

1980 ◽  
Vol 239 (2) ◽  
pp. H247-H251
Author(s):  
J. Reiser ◽  
G. J. Anderson
Keyword(s):  
Intrinsic Rate ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Purkinje Fibers ◽  
Chronotropic Response ◽  
Cycle Lengths ◽  
Left And Right ◽  
Ventricular Conduction

Previous in situ studies have implicated differences in the pacemaker rates between the left and right ventricular conduction system. Our studies were conducted to characterize automaticity in peripheral right and left canine Purkinje fibers in vitro. Standard microelectrode techniques were utilized. In paired right (RPF) and left (LPF) canine Purkinje fibers, control intrinsic rate (IR) was found to be higher in LPF (24.8 +/- 1.7 beats/min) than in RPF (11.5 +/- 1.5 beats/min, P less than 0.01). Following overdrive stimulation at various cycle lengths, LPF consistently showed earlier escape beats. In low K0+ (1.35 mM), IR increased comparably in both RPF and LPF. However, high K0+ (5.4 mM) resulted in a greater reducton of the IR in RPF (-78%) than in LPF (-58%). After epinephrine (10(-6) M) the IR of LPF > RPF although the chronotropic response was more pronounced in RPF. Adrenergic stimulation preceded by beta-adrenergic blockade did not produce significant differences in the intrinsic rate between RPF and LPF. These findings indicate that automaticity in right and left Purkinje strands is functionally dissimilar.

Cardiac function and chronotropic sensitivity to beta-adrenergic stimulation in sepsis

1986 ◽  
Vol 251 (2) ◽  
pp. H405-H412 ◽  
Author(s):  
L. W. Smith ◽  
S. L. Winbery ◽  
L. A. Barker ◽  
K. H. McDonough
Keyword(s):  
Heart Rate ◽  
Myocardial Function ◽  
Cardiovascular Response ◽  
Maximal Heart Rate ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Chronotropic Response ◽  
Arterial Blood ◽  
Perfused Hearts ◽  
Right Atria

An organism's cardiovascular response to sepsis is at least partly dependent on hormonal and neural modulation of myocardial function. We have investigated both intrinsic myocardial performance and one aspect of myocardial sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, studied with the isolated, perfused working heart preparation, was depressed over a range of preloads in septic animals, whereas heart rate was elevated. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied chronotropic responses to isoproterenol in both Langendorff perfused hearts and in isolated right atria. In langendorff perfused hearts from septic animals, basal rates were significantly increased and lower concentrations of isoproterenol elicited greater increases in heart rate. In isolated right atria from septic animals, basal rates were also elevated and the EC50 for the chronotropic response to isoproterenol was significantly less than in atria from control animals. The maximal heart rate response to isoproterenol was not significantly different from control. These results indicate that in sepsis, despite apparently adequate in vivo cardiac performance, intrinsic myocardial function is depressed, but chronotropic sensitivity to beta-adrenergic stimulation is increased.

Enhanced beta-adrenergic-mediated cardiovascular responses in endurance athletes

1996 ◽  
Vol 80 (2) ◽  
pp. 516-521 ◽  
Author(s):  
M. G. Hopkins ◽  
R. J. Spina ◽  
A. A. Ehsani
Keyword(s):  
Maximal Exercise ◽  
Systolic Function ◽  
Volume Overload ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Endurance Athletes ◽  
Inotropic Response ◽  
Adrenergic Stimulation ◽  
Ventricular Systolic Function ◽  
Chronotropic Response

To determine whether the adaptive increase in left ventricular systolic function in the trained state is mediated by enhanced responses to beta-adrenergic stimulation, we studied eight male endurance athletes [age 27 +/- 1.8 yr; maximal O2 uptake (VO2max) 60 +/- 0.9 (SE) ml x kg-1 x min-1] and eight sedentary men (age 27 +/- 1.4 yr; VO2max 43.1 +/- 1.7 ml x kg-1 x min-1). Left ventricular function was evaluated with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile in the basal state, after parasympathetic blockade by atropine, and during infusion of dobutamine. Cardiac output and stroke volume, determined with the acetylene rebreathing technique, during maximal exercise were significantly higher in the endurance athletes than in the sedentary men (28.9 +/- 1.7 vs. 23 +/- 1.23 1/min, P = 0.019, and 162 +/- 12 vs. 125 +/- 7 ml/min, P = 0.029). Endurance athletes showed physiological volume overload-left ventricular hypertrophy and greater enhancements of left ventricular systolic function and filling dynamics in response to dobutamine than did the sedentary men as reflected in 1) a steeper slope of the fractional shortening-end-systolic wall stress relationship (-0.986 +/- 0.16 vs. -0.508 +/- 0.054, P = 0.014, athletes vs. controls) and 2) a higher early-to-late transmitral diastolic Doppler velocity ratio (2.14 +/- 0.14 vs. 1.74 +/- 0.12, P = 0.016) at a comparable heart rate. Although endurance athletes had a significantly greater inotropic response to dobutamine, they demonstrated a markedly attenuated chronotropic response to beta1-adrenergic stimulation compared with sedentary subjects. Our findings suggest that, even with a blunted chronotropic response, endurance-trained young men show an augmented inotropic response to a beta1-adrenergic agonist that, along with physiological volume overload hypertrophy and increased diastolic filling, can contribute to a larger stroke volume during maximal exercise in the trained state.

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