Local and systemic estradiol-17 beta: effects on uterine and systemic vasodilation

1989 ◽  
Vol 256 (4) ◽  
pp. E536-E542 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Rosenfeld

Systemic estradiol-17 beta (E2 beta) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2 beta-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 micrograms E2 beta into both uterine arteries followed 120 min later by systemic E2 beta, 1 microgram/kg. At 120 min after local E2 beta, UBF increased from 26 +/- 5 to 161 +/- 21 ml/min (P less than 0.05); uterine vascular resistance (UVR) decreased 83 +/- 2.5% (P less than 0.05); and systemic parameters were unchanged. At 120 min after systemic E2 beta, UBF remained elevated and CO had increased gradually from 4.4 +/- 0.2 to 5.5 +/- 0.32 l/min (26 +/- 3.4%, P less than 0.05), reflecting a 37 +/- 3.9% (P less than 0.05) increase in HR; mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 +/- 3.1% (P less than 0.05) fall in systemic vascular resistance (SVR), with % delta SVR less than % delta UVR (P less than 0.05). Base-line PRA and angiotensin II, 1.31 +/- 0.2 ng.ml-1.h-1 and 10.3 +/- 2.1 pg/ml, respectively, were unchanged by local E2 beta; systemic E2 beta caused increases to 3.56 +/- 0.51 ng.ml-1.h-1 (P less than 0.05) and 34.1 +/- 11.3 pg/ml (P less than 0.05), respectively. E2 beta-induced uterine hyperemia occurs independent of its systemic effects and is not responsible for systemic cardiovascular alterations, and the relative uterine vascular responses exceed systemic responses.(ABSTRACT TRUNCATED AT 250 WORDS)

1979 ◽  
Vol 57 (s5) ◽  
pp. 131s-134s ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
P. Lijnen ◽  
T. Reybrouck

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P < 0·001) and mean brachial artery pressure (MBAP) by 18·7 mmHg (P < 0·001) within 75 min in 26 hypertensive patients. After 2 months (on 150–600 mg/day) MBAP had decreased by 27·1 mmHg (n = 18) with no further change of plasma ANG II. δMBAP was significantly related to control log plasma renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11·2 mmHg greater (P < 0·001) than δMBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+ 3·3 beats/min; P < 0·005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P < 0·01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P < 0·01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P < 0·001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.


Author(s):  
Tat’yana A. Fisher ◽  
◽  
Svetlana S. Kolyvanova

The aim of this paper was to study changes in the haemodynamic and psychophysiological parameters of working age men as a result of repeated exposure to contrasting temperatures, depending on the type of autonomic regulation. Materials and methods. The research involved 14 men (aged 34.77 ± 5.66 years; office workers) divided into two groups according to Kérdö index: those with the sympathetic (n = 8) and parasympathetic (n = 6) types of self-regulation. Cold conditioning followed a certain plan of exposure to contrasting temperatures. The haemodynamic and psychophysiological parameters as well as adaptive potential were assessed 20 minutes before and 20 minutes after the exposure (alternating temperature cycles). We examined the following parameters: heart rate, systolic and diastolic blood pressure, pulse and mean arterial pressure, stroke volume, cardiac output, vascular resistance, and adaptive potential according to Baevsky. Integral psychophysiological parameters were determined using the Lüscher express method. Results. Subjects with predominance of sympathetic regulation both before and after the exposure to contrasting temperatures had higher values of heart rate and cardiac output and lower vascular resistance than the parasympathicotonic group. Individuals with predominance of parasympathetic regulation showed decreased cardiac output and a significant increase in vascular resistance after the exposure compared with the initial data. We found statistically significant differences in the integral parameters “heteronomy/autonomy” and “balance of personal traits” between the groups under study before the conditioning procedures. The research indicates that repeated exposure to contrasting temperatures not only affects the haemodynamic parameters, but also changes the psychophysiological parameters, motivated behaviour in particular. For citation: Fisher T.A., Kolyvanova S.S. Effect of Repeated Exposure to Contrasting Temperatures on the Body of Working Age Men with Different Types of Autonomic Regulation. Journal of Medical and Biological Research, 2021, vol. 9, no. 4, pp. 394–404. DOI: 10.37482/2687-1491-Z077


1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel

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.


1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.


1985 ◽  
Vol 69 (2) ◽  
pp. 207-214 ◽  
Author(s):  
D. P. Worth ◽  
J. N. Harvey ◽  
J. Brown ◽  
M. R. Lee

1. γ-l-Glutamyl-l-dopa was given by intravenous infusion to eight normal subjects at doses of 12.5 and 100 μg min−1 kg−1. 2. Both doses of the dipeptide resulted in an increase in mean urinary sodium excretion. 3. Mean effective renal plasma flow rose at both doses, but mean glomerular filtration rate increased only at the lower dose. 4. There was a fall in mean plasma renin activity after the infusion of both 12.5 and 100 μg min−1kg−1. 5. Mean urine free dopamine excretion increased by 280- and 2500-fold at infusion rates of 12.5 and 100 μg min−1 kg−1 respectively. 6. Mean plasma free dopamine rose at both doses but the increase at 12.5 μg min−1 kg−1 was not to a level previously associated with systemic effects of the catecholamine. 7. On administration of the dipeptide at 12.5 μg min−1 kg−1 there were no changes in blood pressure or heart rate, but at the higher dose there was a fall in diastolic blood pressure. 8. At a dose of 12.5 μg min−1 kg−1 in man, there is kidney specific conversion of gludopa to dopamine.


1964 ◽  
Vol 19 (4) ◽  
pp. 639-643 ◽  
Author(s):  
M. H. Frick ◽  
Timo Somer

Cardiac output was measured with dye dilution in normal subjects at rest in horizontal position, at rest supine with the legs on the pedals, and during increasing work loads. Experiments were designed to clarify the effect of leg raising on comparisons of stroke volume at various levels of exercise. Leg raising evoked a 19% increase in stroke volume and a decrease in heart rate. Oxygen uptake and A-V O2 difference remained unaltered. In comparing stroke volume at mild exercise with leg-raised resting position, no change occurred contrasting the significant rise when compared with horizontal position. At mild exercise cardiac output response was relatively flat, whereas A-V O2 difference rose sharply. At heavier exercise cardiac output rose more steeply and approximately linear to oxygen consumed. Stroke volumes at these loads were significantly higher than levels in both of the resting positions. Ignorance of the effect of leg raising results in misinterpretation of the stroke volume data at low levels of supine exercise when greatly enhanced tissue extraction of oxygen allows smaller blood flow increments. base line in exercise; exercise stroke volume; stroke volume, exercise; stroke volume, base line; supine exercise Submitted on December 13, 1963


1985 ◽  
Vol 249 (3) ◽  
pp. H577-H584
Author(s):  
A. P. Rocchini ◽  
K. P. Gallagher ◽  
M. J. Botham ◽  
J. H. Lemmer ◽  
C. A. Szpunar ◽  
...  

The ability of a chronic high-salt diet to prevent fatal hemorrhagic shock was examined in 36 mongrel dogs. Twenty-one dogs received a dietary supplement of 9 g sodium chloride/day for 6 wk, and 15 dogs received the same basic diet for 6 wk but without the sodium chloride supplement. Hemorrhagic shock was induced in all dogs by bleeding into an overhanging sealed reservoir. After 3 h of shock, salt-pretreated dogs had a lower systemic vascular resistance of 0.70 +/- 0.02 versus 1.44 +/- 0.04 mmHg X ml-1 X min X kg (P less than 0.01) and a higher cardiac output of 53 +/- 3 versus 26 +/- 3 ml X min-1 X kg-1 (P less than 0.01) than was observed in controls. At 2.5 h of shock, the salt-pretreated dogs also experienced an increase in gastrointestinal (P less than 0.01), hepatic arterial, (P less than 0.05), kidney (P less than 0.05), brain (P less than 0.01), and heart blood flows (P less than 0.001) compared with 0.5 h of shock, whereas the control dogs experienced no increased flow during this same period. We also observed that after 3 h of hypotension there was a significantly smaller increase in plasma renin activity in the salt-pretreated dogs. Administration of 0.1 U X kg-1 X min-1 of hog renin eliminated the differences in systemic vascular resistance, cardiac output, and survival in five salt-pretreated dogs.


1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)


2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.


1989 ◽  
Vol 256 (3) ◽  
pp. H641-H647 ◽  
Author(s):  
A. L. Gest ◽  
A. A. Moise ◽  
T. N. Hansen ◽  
S. Kaplan

The purpose of this project was to study the effects of increased plasma concentrations of arginine vasopressin (AVP) on hemodynamics and lung fluid balance in lambs. We studied 16 unanesthetized newborn lambs during a base-line period and while infusing AVP into a hindlimb vein at 1.65 +/- 0.12 and 2.98 +/- 0.15 mU.kg-1.min-1. We measured aortic, pulmonary arterial, and left atrial pressures and heart rate continuously and cardiac output at frequent intervals. In five additional experiments, we collected samples of pure lung lymph during a base-line period and while infusing AVP at 2.02 +/- 0.15 mU.kg-1.min-1. AVP infusion increased plasma concentrations of AVP to 11.3 +/- 5.2 and 19.9 +/- 5.2 microU/ml at the low and high rates of infusion, respectively. Both aortic and left atrial pressures increased at the low rate of infusion (11 and 3 Torr, respectively) but remained unchanged at the higher rate. Systemic vascular resistance increased, and heart rate and cardiac output decreased at each rate of infusion. In fact, at the higher rate of infusion cardiac output decreased 38% when compared with base line. Neither pulmonary artery pressure nor pulmonary vascular resistance was affected by infusion of AVP. Despite the increase in left atrial pressure, the rate of lung lymph flow was not affected by the infusion of AVP, whereas the lymph-to-plasma protein ratio decreased slightly but significantly from 0.64 +/- 0.02 to 0.60 +/- 0.02.(ABSTRACT TRUNCATED AT 250 WORDS)


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