β-Receptor-mediated increase in venous return in humans

1987 ◽  
Vol 65 (8) ◽  
pp. 1658-1665 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Richard A. Reeves
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Positive Inotropic Effect ◽  
Venous Return ◽  
Left Ventricular ◽  
Receptor Stimulation ◽  
Selective Blockade ◽  
Healthy Humans ◽  
Β Receptor ◽  
Stimulation Of

To assess the involvement of β1 and β2-receptors in the regulation of venous return in humans, changes in left ventricular end-diastolic (LVED) dimension were determined during β-receptor stimulation either by exogenous catecholamines or by increased endogenous sympathetic activity after hydralazine, after placebo and during nonselective versus β1 -selective blockade. Taking changes in heart rate and LV emptying into account, the three β-agonists (isoproterenol, terbutaline, and epinephrine) as well as hydralazine increased venous return as inferred from LVED dimension. After hydralazine, nonselective and β1-selective blockade were equally effective in blunting the increases in venous return, in heart rate, and in positive inotropic response. β1-Selective blockade did not affect the increase in heart rate caused by epinephrine and partially inhibited the positive inotropic effect and the increase in venous return. Nonselective blockade not only blocked the increase in venous return owing to epinephrine but actually led to a decrease, as evidenced by a decrease in LVED dimension despite the marked bradycardia and high afterload with this combination. The present findings in healthy humans indicate that stimulation of both β1- and β2-receptors increases venous return, heart rate, and myocardial contractility. β1-Receptors appeal to predominate in the response to neuronal sympathetic activity.

Takotsubo Cardiomyopathy: Its Possible Impact during Adult Donor Care

2011 ◽  
Vol 21 (4) ◽  
pp. 344-349
Author(s):  
David J. Powner ◽  
Hanh Truong
Keyword(s):  
Calcium Channels ◽  
Brain Death ◽  
Takotsubo Cardiomyopathy ◽  
Cardiac Contractility ◽  
Circulatory Support ◽  
Receptor Stimulation ◽  
Treatment Methods ◽  
Biochemical Processes ◽  
Β Receptor ◽  
Stimulation Of

Takotsubo cardiomyopathy, the syndrome caused by an extreme release and circulation of catecholamines, shares several histopathological and clinical similarities with cardiac changes after brain death noted in animal investigations and human observation. Overwhelming stimulation of myocardial inotropic β receptors may alter their responsiveness and induce other biochemical processes, producing reduced cardiac contractility. Treatment methods in Takotsubo cardiomyopathy that use extracorporeal circulatory support and medications that do not rely on β-receptor stimulation and preemptive blockade of β receptors or calcium channels before brain death may be relevant to donor care.

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

2004 ◽  
Vol 287 (4) ◽  
pp. H1658-H1662 ◽  
Author(s):  
N. Charkoudian ◽  
E. A. Martin ◽  
F. A. Dinenno ◽  
J. H. Eisenach ◽  
N. M. Dietz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Healthy Humans ◽  
Rapid Changes

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10° head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased ∼2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: −3.1 ± 0.6 and −3.3 ± 1.0 versus −5.0 ± 0.6 units·beat−1·mmHg−1 ( P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

Cardiac function in goats exposed to carbon monoxide

1979 ◽  
Vol 47 (2) ◽  
pp. 429-434 ◽  
Author(s):  
W. E. James ◽  
C. E. Tucker ◽  
R. F. Grover
Keyword(s):  
Heart Rate ◽  
Carbon Monoxide ◽  
Cardiac Index ◽  
Sympathetic Activity ◽  
Myocardial Function ◽  
Statistical Significance ◽  
Hemoglobin Concentration ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium

To investigate the possibility that prolonged carbon monoxide (CO) exposure would depress myocardial function, six chronically instrumented, unsedated goats were exposed to 160--200 ppm CO for 2 wk, resulting in a mean carboxyhemoglobin saturation of 20%. Cardiac index and stroke volume remained unchanged during and after exposure. Hematocrit and hemoglobin concentration started increasing on the 10th day of exposure, this increase reached statistical significance (P less than 0.05) on the 6th postexposure day. Contractility (Vmax) of the left ventricular myocardium and heart rate were unchanged during exposure to CO, but both were significantly (P less than 0.05) decreased at some time during the 1st wk after removal from CO. If there was a decrease in intrinsic myocardial function during CO exposure, it may have been masked by increased sympathetic activity. The mechanism(s) that might produce the decrease in heart rate and contractility after removal from CO are not obvious. Possible explanations are discussed.

Stimulation of metabotropic glutamate receptors in the dorsomedial hypothalamus elevates heart rate in rats

1996 ◽  
Vol 270 (5) ◽  
pp. R1115-R1121 ◽  
Author(s):  
J. DiMicco ◽  
A. J. Monroe
Keyword(s):  
Heart Rate ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Cardiovascular Effects ◽  
Nmda Receptor Antagonist ◽  
Dorsomedial Hypothalamus ◽  
Metabotropic Glutamate ◽  
Selective Blockade ◽  
Stimulation Of

This study examined the potential role of metabotropic glutamate receptors (mGluRs) in the dorsomedial hypothalamus (DMH) by assessing the cardiovascular effects of microinjecting the agonist trans-1-aminocyclopentane-1, 3- dicarboxylate (tACPD) into this region in urethan-anesthetized rats. Dose-related tachycardia was observed after unilateral microinjection of 1S 3R-tACPD (10-200 pmol/50nl) but not after injection of 1R, 3S-tACPD, which has been reported to have little or no activity at mGluRs. Microinjection of dihydroxyphenylglycine, an agonist at mGluRs linked to phosphoinositide hydrolysis, resulted in increases in heart rate that correlated closely in magnitude to those seen after injection of the same dose of 1S, 3R-tACPD. Coinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2- amino-5-phosphonopentanoic acid, given at doses shown to elicit selective blockade of NMDA ionotropic glutamate receptors, reduced the increase in heart rate evoked by 100 pmol 1S, 3R-tACPD alone. Thus the DMH contains functional mGluRs, and stimulation of these receptors activates the same sympathoexcitatory mechanism characterized previously to provoke dose-related tachycardia.

Autonomic Balance in Cardiac Control

1958 ◽  
Vol 192 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Stimulus Frequency ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Sympathetic Stimulation ◽  
Vagus Nerves ◽  
Ventricular Performance ◽  
Anesthetized Dogs ◽  
Stimulation Of

Stimulation of the sympathetic nerves to the heart in anesthetized dogs produced tachycardia and changes in left ventricular performance, including alterations in both pressures and dimensions. Stimulation of the vagus nerves in dogs predominately induced a bradycardia. When the heart rate was controlled by an artificial pacemaker, sympathetic stimulation produced changes in ventricular performance. By adjustments in stimulus frequency, the effects of vagal and sympathetic stimulation on heart rate could be balanced, but complete cancellation of effects was impossible because the vagus had a more powerful effect on heart rate and the sympathetic nerves had a greater influence on mechanical performance.

Similarity of cardiovascular responses to exercise and to diencephalic stimulation

1960 ◽  
Vol 198 (6) ◽  
pp. 1139-1142 ◽  
Author(s):  
Orville A. Smith ◽  
Robert F. Rushmer ◽  
Earl P. Lasher
Keyword(s):  
Heart Rate ◽  
Third Ventricle ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
The Third ◽  
Stimulating Electrodes ◽  
Stimulation Of

Devices to measure left ventricular pressure, diameter and heart rate in animals with closed chests were placed on the hearts of dogs. After recovery from this operation the dogs were trained to exercise on a treadmill and the cardiovascular responses to this exercise were recorded. Stimulating electrodes were then stereotaxically placed in the diencephalon. In some dogs the electrodes were chronically implanted, and the stimulation was carried out after recovery from this second operation. In other animals stimulation was carried out immediately while they were under chloralose anesthesia. Stimulation of the H1 and H2 fields of Forel and the periventricular gray of the third ventricle resulted in cardiovascular responses similar to those which result from exercise.

Ca2+dependence of positive inotropic responses of guinea pig isolated cardiac preparations to cAMP-generating and cAMP-independent agonists

1984 ◽  
Vol 62 (1) ◽  
pp. 105-108 ◽  
Author(s):  
L. F. Yao ◽  
K. M. MacLeod ◽  
J. H. McNeill
Keyword(s):  
Guinea Pig ◽  
Papillary Muscles ◽  
Similar Magnitude ◽  
Myocardial Cells ◽  
Receptor Stimulation ◽  
Histamine Response ◽  
Β Receptor ◽  
Inotropic Responses ◽  
Stimulation Of

The effects of procedures which diminish Ca2+ influx into myocardial cells on responses of isolated cardiac preparations to cAMP-independent histamine H1 receptor stimulation and cAMP-generating β-receptor stimulation were measured. The histamine response of guinea pig left atria, which appears to be primarily mediated by H1 receptors, was depressed to a greater extent than was the response of this preparation to isoproterenol by decreasing the extracellular Ca2+ concentration, and by the Ca2+ influx blocker D-600. Similarly, while the H1 agonist 2-pyridylethylamine dihydrochloride (PEA) produced increases in tension of a similar magnitude as the partial β-agonist salbutamol in both left atria and in papillary muscles, responses of both preparations to PEA were depressed to a significantly greater extent by decreasing the extracellular Ca2+ concentration than were responses to salbutamol. Overall, both the basal developed force of papillary muscles and the responses of these preparations to H1 and β-receptor stimulation appeared to be less depressed by decreasing the extracellular Ca2+ concentration than were those of left atria. These results indicate that responses mediated via cAMP-independent H1 receptors, like those arising from α-receptor stimulation, are more sensitive to procedures which diminish Ca2+ influx than are responses arising from stimulation of cAMP-generating β-receptors. This may reflect differences in the mechanisms by which stimulation of H1, α-, and β-receptors give rise to positive inotropic responses. In addition, left atria may be more dependent than papillary muscles on extracellular Ca2+ for the support of contraction.

The effect of isoproterenol on isolated muskrat and guinea pig hearts

1986 ◽  
Vol 64 (12) ◽  
pp. 2674-2677 ◽  
Author(s):  
Thomas A. McKean
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adrenergic Stimulation ◽  
Potential Predator ◽  
Opposing Effects ◽  
Sympathetic Effect ◽  
Stimulation Of

Isoproterenol, a β-adrenergic agonist, was given by bolus injection to Langendorff-perfused muskrat and guinea pig hearts. Bolus content ranged from 18 to 29 200 pmol. The hearts responded by increasing left ventricular pressure, heart rate, and release of lactate. The drug threshold was similar for the hearts of the two species but the magnitude of the response differed both at threshold and at saturation doses. The increase in left ventricular pressure and heart rate was greater in guinea pig hearts compared with muskrat hearts. Lactate release was stimulated earlier and increased more in muskrat hearts compared with guinea pig hearts. The weak β-adrenergic stimulation of heart rate and left ventricular pressure in the muskrat may be of benefit when the animal dives to escape a potential predator. Under these conditions of fear, exercise, hypoxia, and diving there would be opposing effects of sympathetic versus vagal stimulation of the myocardium. The sympathetic effect would be to increase myocardial oxygen consumption while the vagal effect would be to reduce it. In the diving mammal the vagal effect predominates and this may be augmented by a blunted rate and pressure response to β-stimulation.

Autonomic responses during acute myocardial infarction in the rat model: implications for arrhythmogenesis

2018 ◽  
Vol 29 (4) ◽  
pp. 339-345 ◽  
Author(s):  
Theofilos M. Kolettis ◽  
Marianthi Kontonika ◽  
Panagiotis Lekkas ◽  
Antonios P. Vlahos ◽  
Giannis G. Baltogiannis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Time Course ◽  
Left Ventricular ◽  
Fluctuation Analysis ◽  
Vagal Activity ◽  
Ventricular Tachyarrhythmias ◽  
Autonomic Responses

AbstractBackgroundAutonomic responses participate in the pathophysiology of acute myocardial infarction, but their precise time course remains unclear. Here, we investigated the autonomic activity and ventricular tachyarrhythmias in conscious, unrestrained rats post-infarction.MethodsThe left coronary artery was ligated in 12 Wistar rats, and six rats were sham operated, followed by 24-h electrocardiographic recording via implanted telemetry transmitters. Sympathetic activity was assessed by detrended fluctuation analysis and vagal activity by time- and frequency-domain analysis of heart rate variability. The duration of the ventricular tachyarrhythmias was measured, and voluntary motion served as a marker of heart failure.ResultsIn sham-operated rats, heart rate and sympathetic activity remained low, whereas vagal activity rose progressively after the fourth hour. Post-ligation, medium-sized antero-septal necrosis was observed, reaching ~20% of the left ventricular volume; tachyarrhythmias were frequent, displaying a bimodal curve, and motion counts were low. Vagal activity decreased early post-ligation, coinciding with a high incidence of tachyarrhythmias, but tended to rise subsequently in rats with higher motion counts. Sympathetic activity increased after the third hour, along with a second tachyarrhythmia peak, and remained elevated throughout the 24-h period.ConclusionsVagal withdrawal, followed by gradual sympathetic activation, may participate in arrhythmogenesis during acute myocardial infarction.

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