Effects of reserpine on circulation of the rat after microwave irradiation

1962 ◽  
Vol 202 (6) ◽  
pp. 1171-1174 ◽  
Author(s):  
Theodore Cooper ◽  
Teresa Pinakatt ◽  
Max Jellinek ◽  
Alfred W. Richardson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Continuous Wave ◽  
Peripheral Resistance ◽  
Thermal Response ◽  
Cardiac Response ◽  
Tissue Temperature ◽  
White Rats

Hyperthermia of 40.5 C was induced in anesthetized white rats by microwave exposure (2,450-Mc continuous wave, .08 w/cm2). Thermal response was accompanied by increased cardiac output, stroke volume, cardiac work, and heart rate. Blood pressure and total peripheral resistance decreased. Administration of reserpine as a single dose of 2.5 mg/kg body wt. 1 day before the experiment depleted the myocardial norepinephrine, but did not eliminate the accelerated heart rate and increase of cardiac output during hyperthermia. Hyperthermia after reserpine did not alter significantly the stroke volume and blood pressure, and the peripheral resistance decreased. These data suggest that the circulatory adaptation to microwave hyperthermia is mediated not only through the sympathetic nervous system, but by other mechanisms such as direct cardiac response to the increased tissue temperature.

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.

Cardiovascular changes during acceleration stress in dogs

1960 ◽  
Vol 15 (6) ◽  
pp. 1065-1068 ◽  
Author(s):  
Edward J. Hershgold ◽  
Sheldon H. Steiner
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Technical Assistance ◽  
Peripheral Resistance ◽  
Cardiovascular Changes ◽  
Positive Acceleration ◽  
Acceleration Stress ◽  
Circulatory Disturbances

Dogs were accelerated on the Wright-Patterson AFB human centrifuge in positive and transverse vectors. Cardiac output, blood pressure and heart rate were measured, and stroke volume and peripheral resistance calculated. In positive (headward) acceleration, the cardiac output and stroke volume were reduced; the peripheral resistance was increased. In the transverse vectors, the cardiac output was stable or increased; stroke volume was stable, and peripheral resistance was reduced. The results suggest that the circulatory disturbances associated with positive acceleration may limit tolerance to acceleration and that these may be avoided in transverse acceleration. Note: (With the Technical Assistance of Peter Grenell) Submitted on December 3, 1959

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.

Cardiovascular changes associated with thermal polypnea in the chicken

1964 ◽  
Vol 207 (6) ◽  
pp. 1349-1353 ◽  
Author(s):  
G. C. Whittow ◽  
P. D. Sturkie ◽  
G. Stein
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Respiratory Rate ◽  
Peripheral Resistance ◽  
Flow Through ◽  
Skin Temperatures ◽  
Increased Blood Flow

The effect of hyperthermia on the respiratory rate, cardiac output, blood pressure, arterial hematocrit, and the skin temperatures of the extremities of unanesthetized hens has been investigated. During hyperthermia, the respiratory rate increased to a maximal value and then declined. There was also an increase in cardiac output, followed by a decrease, but the peak cardiac output occurred at a rectal temperature which was significantly higher than that at which the peak respiratory rate was recorded. The increase in cardiac output was the result of an increase in both stroke volume and heart rate. The diminution of cardiac output seemed to be related to a decrease in the stroke volume at high levels of heart rate. The decrease in blood pressure and total peripheral resistance was attributed partly to an increased blood flow through the extremities.

Effects of euglycaemic and hypoglycaemic hyperinsulinaemia on sympathetic and parasympathetic regulation of haemodynamics in healthy subjects

2003 ◽  
Vol 105 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Tomi LAITINEN ◽  
Hanna HUOPIO ◽  
Ilkka VAUHKONEN ◽  
Cyril CAMARO ◽  
Juha HARTIKAINEN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Plasma Adrenaline ◽  
Parasympathetic Regulation

The effects of hypoglycaemia during hyperinsulinaemia, occurring under various pathophysiological conditions, on the cardiovascular regulatory system and vasculature are largely unknown. The aim of the present study was to investigate regulatory and haemodynamic responses to acute hyperinsulinaemia and consequent hypoglycaemia in 18 healthy subjects. Blood sampling and 5 min ECG and blood pressure recordings were performed at baseline and during the euglycaemic and hypoglycaemic phases of a hyperinsulinaemic clamp. Heart rate variability (HRV) and blood pressure variability (BPV) were assessed by using power spectral analysis, and baroreflex sensitivity (BRS) was assessed using the cross-spectral method. Stroke volume was assessed from the non-invasive blood pressure signal by the arterial pulse contour method. Euglycaemic hyperinsulinaemia did not change plasma catecholamine concentrations, HRV, BPV, BRS, heart rate, blood pressure, stroke volume, cardiac output or peripheral resistance. However, hyperinsulinaemic hypoglycaemia resulted in an 11.7-fold increase in the plasma adrenaline concentration (from 0.19±0.03 to 1.68±0.32 nmol/l; P<0.001), and a modest 1.3-fold increase in the plasma noradrenaline concentration (from 1.74±0.22 to 2.02±0.19 nmol/l; P<0.05) compared with baseline. Furthermore, we observed significant decreases in diastolic blood pressure (from 68±3 to 60±3 mmHg; P<0.05) and peripheral resistance (from 24.1±1.2 to 18.5±1.1 mmHg·min-1·l-1; P<0.01). Stroke volume and cardiac output increased markedly from the euglycaemic to the hypoglycaemic period only (P<0.01 for both). Hypoglycaemia did not influence HRV, BPV or BRS. Our findings indicate that hyperinsulinaemic hypoglycaemia is characterized by a significant increase in the plasma adrenaline concentration and by decreases in peripheral resistance and blood pressure. Counter-regulation during hyperinsulinaemic hypoglycaemia involves selective adrenomedullary sympathetic activation, and does not influence cardiac parasympathetic regulation or baroreflex control of heart rate.

scholarly journals Development of cardiovascular responses to hypoxia in larvae of the frog Xenopus laevis

1996 ◽  
Vol 271 (4) ◽  
pp. R912-R917 ◽  
Author(s):  
R. Fritsche ◽  
W. Burggren
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Xenopus Laevis ◽  
Stroke Volume ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Inhibitory Effect ◽  
Show Evidence

Cardiovascular responses (blood pressure, heart rate, stroke volume, cardiac output, and peripheral vascular resistance) to acute hypoxia (Po2 = 70 mmHg) in developing larvae of Xenopus laevis from Nieuwkoop-Faber (NF) stage 45 and up to newly metamorphosed froglets were investigated. The results revealed two distinct response patterns to acute hypoxia in "early" (NF stages 45-48 and 49-51) and "late" (NF stages 52-53, 54-57, and 58-62) larval Xenopus. The early larvae responded to acute hypoxia with a significantly decreased stroke volume, cardiac output, and blood pressure. Peripheral resistance increased, whereas no change in heart rate occurred. In late larvae, stroke volume and blood pressure increased during acute hypoxia, but an offsetting bradycardia prevented major changes in cardiac output. We conclude that, up to stage 51 of development, hypoxia exerts a direct inhibitory effect on the heart and smooth muscle of the blood vessels, with no Frank-Starling relationship apparent. Older larvae show evidence of both intrinsic and extrinsic regulation of the cardiovascular system in response to acute hypoxia, suggesting that there is a specific point in larval development when cardiovascular regulation during hypoxia is expressed.

Cardiovascular response to graded exercise in the sympathectomized-vagotomized dog

1963 ◽  
Vol 204 (2) ◽  
pp. 291-296 ◽  
Author(s):  
Edmundo Ashkar ◽  
William F. Hamilton
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Stroke Volume ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Graded Exercise ◽  
Oxygen Difference

Seven dogs who ran well on a motor-driven treadmill were completely sympathectomized (including adrenal denervation) and subjected to unilateral vagotomy below the recurrent laryngeal branch. After recovery and retraining, a terminal experiment was performed in which, after completing the vagotomy, direct Fick determinations of cardiac output and continuous recordings of mean arterial pressure, heart rate, and oxygen consumption were made at rest and during increasing exercise The results were compared with those described by Barger et al. ( Am. J. Physiol. 184: 613, 1956) for normal dogs running at smaller speeds and grades. The heart rate of the operated dogs increased from 117 to 134. Barger's normal dogs doubled their heart rate. The A-V oxygen difference increased with work slightly less than Barger's normal dogs but the scatter in both groups was wide, as was the case with the stroke volume. The resting cardiac output was nearly normal in the operated dogs but increased only 34% with exercise, as against 200–300% in Barger's normals. Oxygen consumption increased about twofold as against the expected normal of three- to sevenfold. Peripheral resistance in both groups went down about 40%. The blood pressure in the normal increased substantially while that in the operated dogs fell about 20% to an average of 60 mm Hg.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

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.

Cardiac Response During Trumpet Playing

2010 ◽  
Vol 25 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Donald U Robertson ◽  
Lynda Federoff ◽  
Keith E Eisensmith
Keyword(s):  
College Students ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Response ◽  
Physiological Efficiency ◽  
Rest Periods ◽  
Upper Register

Heart rate, heart rate variability, stroke volume, and cardiac output were measured while six college students and six professionals played trumpet. One-minute rest periods were followed by 1 minute of playing exercises designed to assess the effects of pitch and articulation. Heart rate and heart rate variability increased during playing, but stroke volume decreased. Changes in heart rate between resting and playing were greater for students, although beat-to-beat variability was larger for professionals in the upper register. These results suggest that expertise is characterized by greater physiological efficiency.

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