Central Haemodynamics and Plasma Prostaglandin E2 in Borderline and Sustained Essential Hypertensive Patients before and after Indomethacin

1981 ◽  
Vol 61 (s7) ◽  
pp. 323s-325s ◽  
Author(s):  
M. E. Safar ◽  
A. F. Hornych ◽  
J. A. Levenson ◽  
A. Ch. Simon ◽  
G. M. London ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Before And After ◽  
Haemodynamic Changes ◽  
Normotensive Subjects ◽  
Pg E2

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 ± 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 ± 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 ± 1.4 pg/ml). 2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions. 3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index. 4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients. 5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment. 6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.

Haemodynamic Effects of Noise Exposure before and after β1-Selective and Non-Selective β-Adrenoceptor Blockade in Patients with Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 89s-91s ◽  
Author(s):  
L. Andrén ◽  
L. Hansson ◽  
M. Björkman
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Total Peripheral Resistance ◽  
Noise Exposure ◽  
Blood Pressure Response ◽  
Peripheral Resistance ◽  
Pressure Response ◽  
Arterial Blood ◽  
Before And After ◽  
Haemodynamic Changes

1. Noise stimulation (100 dBA) for 10 min caused a significant increase in diastolic (7.0%, P < 0.001) and mean arterial blood pressure (4.3%, P < 0.01) in patients with essential hypertension. 2. The blood pressure response to noise was due to an increase in total peripheral resistance (4.8%, P < 0.02); heart rate, stroke volume and cardiac output were unchanged. 3. β1-selective adrenoceptor blockade (metoprolol) did not change the haemodynamic reaction pattern induced by noise. 4. Noise exposure during non-selective β-adrenoceptor blockade (propranolol) caused an accentuated blood pressure response with increments of both systolic and diastolic blood pressure as well as a more pronounced rise in total peripheral resistance. 5. The haemodynamic changes induced by noise stimulation at 100 dBA totally disappeared after 5 min of quiet rest at 40 dBA.

Effect of Sotalol on Haemodynamics and Renin—Angiotensin—Aldosterone System in Hypertensive Patients

1976 ◽  
Vol 51 (1) ◽  
pp. 9-17 ◽  
Author(s):  
A. Verniory ◽  
M. Staroukine ◽  
F. Delwiche ◽  
M. Telerman
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Excretion Rate ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Receptor Blocking ◽  
Plasma Angiotensin

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.

Central and peripheral haemodynamic effects of hyperglycaemia, hyperinsulinaemia, hyperlipidaemia or a mixed meal

2003 ◽  
Vol 105 (6) ◽  
pp. 715-721 ◽  
Author(s):  
Andreas FUGMANN ◽  
Jonas MILLGÅRD ◽  
Mahziar SARABI ◽  
Christian BERNE ◽  
Lars LIND
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Mixed Meal ◽  
Hyperglycaemic Clamp ◽  
Calf Blood Flow ◽  
Haemodynamic Changes

The aim of the present study was to evaluate the haemodynamic changes during hyperinsulinaemia, hyperglycaemia or hypertriglyceridaemia in relation to those following a mixed meal. Ten subjects were subjected to hypertriglyceridaemia (3.9 mmol/l) for 2 h by an infusion of Intralipid® and heparin. Nine subjects received a hyperglycaemic clamp (12.5 mmol/l) with octreotide and low-dose insulin infusion to maintain normoinsulinaemia (10 m-units/l). Ten subjects received saline for 2 h as a control and, thereafter, 2 h of normoglycaemic hyperinsulinaemic clamp (80 m-units/l). Finally, ten subjects were evaluated for 2 h following an ordinary mixed meal. Calf blood flow was measured by venous occlusion plethysmography and cardiac index by thoracic bioimpedance. Both the mixed meal and normoglycaemic hyperinsulinaemia lowered total peripheral resistance, and increased calf blood flow and cardiac index, whereas blood pressure decreased (P<0.05-0.001). Both hyperglycaemia and hypertriglyceridaemia increased calf blood flow, but blood pressure was unchanged. Total peripheral resistance was unchanged in hypertriglyceridaemia, whereas hyperglycaemia induced a significant increase. Normoglycaemic hyperinsulinaemia induced a haemodynamic pattern similar, but to a lesser extent, to the pattern seen following a mixed meal. Hyperinsulinaemia seems to be a major mediator of the haemodynamic response, but other factors are obviously also of great importance. Hypertriglyceridaemia and hyperglycaemia induced haemodynamic responses that are not similar to those seen following a mixed meal.

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.

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. H2511-H2517 ◽  
Author(s):  
Ming Yu ◽  
Venkat Gopalakrishnan ◽  
Thomas W. Wilson ◽  
J. Robert McNeill
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hemodynamic Responses ◽  
Hypertensive Group ◽  
Time Flow ◽  
Before And After ◽  
Vascular Responsiveness

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

Cardiac Output by the Dye Dilution Technique Under Thiopental Sodium-Oxygen and Ether Anesthesia

1956 ◽  
Vol 186 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Esther M. Greisheimer ◽  
Dorothy W. Ellis ◽  
George Stewart ◽  
Lydia Makarenko ◽  
Nadia Oleksyshyn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Stroke Index ◽  
Ether Anesthesia ◽  
Dye Dilution ◽  
Arterial Blood ◽  
Thiopental Sodium

One hundred-twenty determinations of cardiac output by the dye dilution technic utilizing the cuvette oximeter were made on 20 dogs. Of these, 60 were done under thiopental sodium-oxygen analgesia and 60 were done after supplementing with ether. Arterial blood pressure was recorded by strain gauge. Electrocardiograms were taken periodically. Concentrations of thiopental and ether in arterial blood were determined. Cardiac output began to increase under thiopental analgesia and continued to increase when ether was administered. Arterial blood pressure and heart rate decreased slightly when ether was administered. Stroke index increased when ether was administered. Total peripheral resistance decreased markedly under thiopental analgesia, and continued to decrease when ether was administered. When compared with an earlier study in which cyclopropane was used as the supplementing agent, it was found that cyclopropane and ether exert opposite effects on cardiac output and peripheral resistance despite the fact that the effect on arterial blood pressure is similar under the two agents. Increase in cardiac output was found to be parallel with decrease in total peripheral resistance in this study. Amount of dye injected did not influence cardiac output. Under the conditions of this study, cardiac output was in no way dependent on the concentration of thiopental in the blood nor on the amount injected. Level of ether in the blood did not show much effect, if any, on cardiac output. It is probable that the changes observed in this study are comparable with those which obtain clinically when thiopental-oxygen analgesia is supplemented with ether. Systolic blood pressure is not an infallible guide to other cardiovascular functions since it may remain fairly steady while cardiac output and peripheral resistance undergo marked changes under anesthesia.

Peripheral Resistance Changes and Blood Pooling After Endotoxin in Eviscerated Dogs

1958 ◽  
Vol 195 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert P. Gilbert ◽  
Hiroshi Kuida ◽  
Maurice B. Visscher
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Endotoxin Shock ◽  
E Coli ◽  
Arterial Blood ◽  
Later Phase

Studies were performed on eviscerated dogs maintained with a constant cardiac inflow with and without injections of lethal amounts of E. coli endotoxin. Continuous recordings of mean arterial blood pressure and total venous return permitted determination of changes in total peripheral resistance and extent of vascular pooling. A significant fall in mean arterial blood pressure occurs within 30 minutes after endotoxin in the eviscerated dog with constant cardiac inflow. There is therefore a decrease in total peripheral resistance. There is also a small but significant increase in vascular pooling exceeding that seen without endotoxin but much reduced from that observed in noneviscerated animals given endotoxin. It is concluded that a decrease in vascular tone occurs after endotoxin and that it probably plays a significant role in the later phase of endotoxin shock in the dog.

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

2008 ◽  
Vol 294 (1) ◽  
pp. H293-H301 ◽  
Author(s):  
Xiaoxiao Chen ◽  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Rafat I. Elahi ◽  
...  
Keyword(s):  
Impulse Response ◽  
Mathematical Analysis ◽  
Total Peripheral Resistance ◽  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Noninvasive Measurements ◽  
Extended Technique ◽  
Arterial Blood ◽  
Before And After ◽  
Cardiovascular Simulator

We previously developed a mathematical analysis technique for estimating the static gain values of the arterial total peripheral resistance (TPR) baroreflex ( GA) and the cardiopulmonary TPR baroreflex ( GC) from small, spontaneous beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we extended the mathematical analysis so as to also estimate the entire arterial TPR baroreflex impulse response [ hA( t)] as well as the lumped arterial compliance (AC). The extended technique may therefore provide a linear dynamic characterization of TPR baroreflex systems during normal physiological conditions from potentially noninvasive measurements. We theoretically evaluated the technique with respect to realistic spontaneous hemodynamic variability generated by a cardiovascular simulator with known system properties. Our results showed that the technique reliably estimated hA( t) [error = 30.2 ± 2.6% for the square root of energy ( EA), 19.7 ± 1.6% for absolute peak amplitude ( PA), 37.3 ± 2.5% for GA, and 33.1 ± 4.9% for the overall time constant] and AC (error = 17.6 ± 4.2%) under various simulator parameter values and reliably tracked changes in GC. We also experimentally evaluated the technique with respect to spontaneous hemodynamic variability measured from seven conscious dogs before and after chronic arterial baroreceptor denervation. Our results showed that the technique correctly predicted the abolishment of hA( t) [ EA = 1.0 ± 0.2 to 0.3 ± 0.1, PA = 0.3 ± 0.1 to 0.1 ± 0.0 s−1, and GA = −2.1 ± 0.6 to 0.3 ± 0.2 ( P < 0.05)] and the enhancement of GC [−0.7 ± 0.44 to −1.8 ± 0.2 ( P < 0.05)] following the chronic intervention. Moreover, the technique yielded estimates whose values were consistent with those reported with more invasive and/or experimentally difficult methods.

Studies on the Mechanism of Mineralocorticoid-Induced Blood Pressure Increase in Man

1979 ◽  
Vol 57 (s5) ◽  
pp. 303s-305s ◽  
Author(s):  
A. Distler ◽  
T. Philipp ◽  
B. Lüth ◽  
G. Wucherer
Keyword(s):  
Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Pressure Rise ◽  
Sympathetic Tone ◽  
Plasma Noradrenaline ◽  
Steroid Administration ◽  
Arterial Blood ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration

1. To gain insight into the mechanism of mineralocorticoid-induced blood pressure rise in man we performed haemodynamic studies in six normotensive volunteer subjects before and during administration of the synthetic steroid 9α-fluorocortisol (0·8 mg daily) for a period of 6 weeks. In a further study, performed in seven subjects, plasma noradrenaline concentration and reactivity to exogenous noradrenaline were determined before and during administration of the mineralocorticoid. 2. Within the first week of steroid administration an increase in mean arterial blood pressure could be demonstrated, which was due to an increase in cardiac output. After the sixth week the elevated blood pressure was the consequence of an increased total peripheral resistance. 3. Plasma noradrenaline concentration decreased and reactivity to exogenous noradrenaline increased during steroid administration. 4. The mechanism underlying the increase in total peripheral resistance during long-term mineralocorticoid administration remains unclear. Increased sympathetic tone does not seem to be a factor since plasma noradrenaline decreased considerably. Pressor response to noradrenaline increased probably due to decreased sympathetic tone.

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