Operant conditioning of heart rate in curarized rats: hemodynamic changes

1975 ◽  
Vol 228 (3) ◽  
pp. 870-874 ◽  
Author(s):  
JA Gliner ◽  
SM Horvath ◽  
RR Wolfe
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Operant Conditioning ◽  
Peripheral Resistance ◽  
Experimental Period ◽  
The Other ◽  
Control Group ◽  
Physiological Effects ◽  
Hemodynamic Changes ◽  
Heart Rate Conditioning

Three groups of curarized rats were subjected to operant heart rate conditioning with use of a shock-avoidance procedure while cardiac output, mean arterial pressure, and total peripheral resistance were measured. Heart rate changes in the control group remained constant during the entire 90-min experimental period, while cardiac output decreased significantly. Those rats that were reinforced for increasing their heart rate had a small but statistically significant increase in heart rate, but cardiac output decreased to approximately the same extent as in the control group. The group reinforced for decreasing their heart rate demonstrated a large, significant decrease in heart rate and an even larger drop in cardiac output, which was significantly greater than that of either of the other two groups. Operant conditioning of a single facet of the cardiovascular system resulted in significantly larger changes in other cardiovascular parameters, which may have been partly masked by the physiological effects of d-tubocurarine. Therefore, only when these other measures of cardiovascular function are taken into consideration can interpretation of operant heart rate conditioning become meaningful.

Autonomic Cardiovascular Dysregulation at Rest and During Stress in Chronically Low Blood Pressure

2019 ◽  
Vol 33 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Stefan Duschek ◽  
Alexandra Hoffmann ◽  
Casandra I. Montoro ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Control Group ◽  
Low Blood Pressure

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.

Cardioinhibitory effect of atrial peptide in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. R610-R616 ◽  
Author(s):  
D. E. Allen ◽  
M. Gellai
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Atropine Sulfate ◽  
Plasma Extravasation ◽  
Hemodynamic Changes ◽  
Volume Depletion ◽  
Fluid Losses ◽  
Opposite Response

The hemodynamic and renal excretory responses to 150-min atriopeptin II (AP II) infusion (330 ng X kg-1 X min-1) were assessed in five chronically instrumented rats with (FR protocol) and without (NR protocol) replaced urinary fluid losses. The observed changes were compared with those obtained by vehicle in the same rats. The hypotension seen with AP II infusion (120-min value: -27 +/- 2%, FR and NR responses combined) was due solely to a decreased cardiac output (CO; 120-min combined value: -34 +/- 3%). Total peripheral resistance remained unchanged or slightly elevated. A drop in stroke volume plus a later-developing (by 75-90 min) decrease in heart rate contributed to the CO decline. This latter bradycardic component, the opposite response to that typically produced reflexly by hypotension, was reversed by atropine sulfate treatment at 120 min and may thus be neural in origin. The finding of similar hemodynamic changes in the FR and NR rats and the lack of a significant effect of AP II on hematocrit suggest that volume depletion or a plasma extravasation were not contributors to the cardioinhibitory effect of the peptide.

Platelet Antiaggregation And Hemodynamic Effects Of Adenosine And Prostaglandin E1

1981 ◽  
Author(s):  
T N Masters ◽  
G G V Born ◽  
F Robicsek
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Prostaglandin E1 ◽  
Canine Model ◽  
Ascending Aorta ◽  
The Other ◽  
Systemic Resistance ◽  
Hemodynamic Effects ◽  
Hemodynamic Changes ◽  
Counter Model

The efficacy of using adenosine (ADEN) or prostaglandin E1 to prevent platelet loss during cardiopulmonary bypass (CPB) was tested in experiments conducted with a simulated CPB circuit with cardiotomy suction. The hemodynamic effects of the compounds were tested in a canine model to ascertain hemodynamic tolerance of platelet-salvaging concentrations. Platelet concentrations were determined with a Coulter Counter Model S-Plus in 3 separate groups each composed of 10 experiments in which ADEN (1 mM) and PGE1 (0.5 and 1.0 pM) were added to the bypass circuit to determine platelet protection. It was found that PGE1 at both concentrations was effective in salvaging platelets (0.5 μM-70% and 1.0 μM- 95%) and ADEN at 1 mM salvaged approximately 45%. Hemodynamic effects of PGE1 and ADEN were studied in heparinized (3 mg/Kg) mongrel dogs weighing between 20-27 Kg which were artificially ventilated and catheters placed to measure LV and arterial pressures and dP/dT. Via a left thoracotomy a 15 mm Statham Blood Flowmeter Probe placed around the ascending aorta measured Cardiac Output (CO). ADEN, in seven increasing doses (range: 0.45-3.40 mg/Kg/min), was infused for 2 min with 5 min between doses. In two groups of 10 dogs each, PGE1 was infused with two dose ranges: 0.40-3.00 and 2.0-15.0 μg/Kg/min. PGE1 was infused in seven increasing doses in each range and hemodynamic changes recorded during 3 min of infusion. Hemodynamically, ADEN reduced heart rate and systemic resistance progressively as dose increased. The unchanging CO accompanied by reduced dP/dT and LV pressure suggests the myocardium is not directly affected. PGE1 on the other hand, continually reduced CO and dP/dT with increasing doses, but with the smallest dose reduced arterial pressure 20% which remained unchanged with increasing doses. PGE1 therefore appears to directly depress the myocardium with maximal resistance changes occurring with the smallest doses. Platelet salvaging concentrations for ADEN were within acceptable limits, whereas PGE1 was not.

V1 vs. combined V1+V2 vasopressin blockade after hemorrhage in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1325-H1329
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Conscious Dogs ◽  
Hemodynamic Changes ◽  
Significant Difference ◽  
V2 Antagonist

We examined the hypothesis that V2-like receptors might contribute to the hemodynamic response seen after blockade of the vasoconstrictor (V1) effect of arginine vasopressin (AVP) in nonhypotensive hemorrhage. Seven chronically instrumented dogs were bled 15 ml/kg within 15 min on two different days, at least 3 days apart, and then injected either with the V1 antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-methyl)tyrosine]AVP [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg] or with the combined V1+V2 antagonist [1(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-ethyl)-D-tyrosine)4-valine]AVP [d(CH2)5-D-Tyr-(Et)VAVP (10 micrograms/kg)]. Mean arterial pressure, heart rate, and cardiac output (electromagnetic flowmeter) were measured before as well as after hemorrhage and for 10 min after antagonist administration. Both antagonists given after hemorrhage significantly decreased mean arterial pressure as well as total peripheral resistance and increased cardiac output. The V1 antagonist also increased heart rate significantly. No significant hemodynamic changes were measured in another group of six dogs in the absence of antagonist treatment. Although hemodynamic changes tended to be greater with the V1 antagonist than with the combined V1+V2 antagonist, a significant difference between the two analogues was established only for heart rate. These results indicate that in hemorrhage interaction with V2-like receptors plays only a modest role in the hemodynamic changes after V1 blockade in conscious dogs, contrary to what was found in dehydration.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

IMMEDIATE HEMODYNAMIC EFFECTS OF ISOPROTERENOL

1963 ◽  
Vol 41 (1) ◽  
pp. 1949-1953 ◽  
Author(s):  
Margaret Beznák ◽  
P. Hacker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Subcutaneous Injection ◽  
Direct Action ◽  
Peripheral Resistance ◽  
Oxygen Demand ◽  
Hemodynamic Effects ◽  
Hemodynamic Changes ◽  
Histological Damage

Subcutaneous injection of 40 mg/kg isoproterenol is followed within 2 minutes by a fall in blood pressure and peripheral resistance, by tachycardia, and by an increase in cardiac output. It seems likely that these hemodynamic changes are a consequence of a direct action of isoproterenol on the myocardium. Isoproterenol also causes a significant increase in the oxygen consumption of the rats. The increased oxygen demand of the tissues may play a role in maintaining the hemodynamic changes for periods of more than an hour after isoproterenol. Signs of histological damage in the myocardium begin to appear without affecting the function of the cardiovascular system, as measured by the tests used.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

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