Haemodynamic Effects of Captopril in Hypertensive Patients: Comparison with Saralasin

1979 ◽  
Vol 57 (s5) ◽  
pp. 131s-134s ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
P. Lijnen ◽  
T. Reybrouck
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Acute Administration ◽  
Ang Ii ◽  
Hypertensive Patients ◽  
Plasma Angiotensin

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.

Prevention of fatal hemorrhagic shock in dog by pretreatment with chronic high-salt diet

1985 ◽  
Vol 249 (3) ◽  
pp. H577-H584
Author(s):  
A. P. Rocchini ◽  
K. P. Gallagher ◽  
M. J. Botham ◽  
J. H. Lemmer ◽  
C. A. Szpunar ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Chloride ◽  
Hemorrhagic Shock ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Flows

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.

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
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Systemic Effects ◽  
Base Line ◽  
Uterine Blood Flow ◽  
Vascular Responses ◽  
Uterine Arteries ◽  
Systemic Responses

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)

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

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)

scholarly journals Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Spinal Anesthesia ◽  
Cesarean Delivery ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Preeclampsia

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.

Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 119s-121s
Author(s):  
S. N. Hunyor ◽  
H. Larkin ◽  
Janet Rowe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Heart Rate Effect

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern. 2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume. 3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others. 4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects. 5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases. 6. No heart rate effect was seen with saralasin. 7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.

Combined Pre- and after-Load Reduction in Hypertensive Patients with Cardiomegaly and Normal Filling Pressure

1981 ◽  
Vol 61 (s7) ◽  
pp. 113s-116s ◽  
Author(s):  
S. N. Hunyor ◽  
G. I. Nelson ◽  
G. L. Donnelly
Keyword(s):  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Isometric Exercise ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Load Reduction ◽  
Blocking Drug ◽  
Isometric Handgrip ◽  
Hypertensive Patients

1. Twelve hypertensive patients with cardiomegaly were treated with equivalent antihypertensive doses of prazosin (11 weeks) and β-adrenoceptor-blocking drug (9 weeks) in random crossover fashion. 2. At the end of each treatment period haemodynamic assessment included the response to isometric handgrip exercise (4 min at 30% of maximum voluntary contraction). 3. Resting cardiac index and heart rate were higher on prasozin although the latter was only 65 beats/min. Systemic vascular resistance and left ventricular filling pressure were insignificantly higher on β-adrenoceptor-blocking drug. 4. During isometric handgrip the blood pressure rise was similar on the two regimens, but the mechanism whereby it was achieved was quite different. On prazosin an increase in cardiac output accounted for the pressor response with virtually no change in systemic vascular resistance, whereas on β blockade there was a flat cardiac output response with a marked increase in the systemic vascular resistance. 5. Ventricular function curves indicated a predominant utilization of the Frank-Starling mechanism during β blockade, whereas enhanced contractility played a major role during prazosin treatment. 6. The isometric exercise response pattern during prazosin treatment resembles that in normal subjects whereas in the β blockade phase it corresponded to that in untreated hypertensive patients with left ventricular hypertrophy or cardiomegaly or to that in congestive heart failure patients. 7. There was no evidence of harmful effects of combined pre- and after-load reduction in hypertensive patients with cardiomegaly and normal filling pressure, even under conditions of moderately severe cardiac loading with isometric exercise.

scholarly journals Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat

2015 ◽  
Vol 309 (4) ◽  
pp. H605-H614 ◽  
Author(s):  
Daniel Yoo ◽  
Ryan C. Jupiter ◽  
Edward A. Pankey ◽  
Vishwaradh G. Reddy ◽  
Justin A. Edward ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Potassium Channels ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Tissue ◽  
Sinus Node ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure

Hydrogen sulfide (H2S) is an endogenous gaseous molecule formed from L-cysteine in vascular tissue. In the present study, cardiovascular responses to the H2S donors Na2S and NaHS were investigated in the anesthetized rat. The intravenous injections of Na2S and NaHS 0.03–0.5 mg/kg produced dose-related decreases in systemic arterial pressure and heart rate, and at higher doses decreases in cardiac output, pulmonary arterial pressure, and systemic vascular resistance. H2S infusion studies show that decreases in systemic arterial pressure, heart rate, cardiac output, and systemic vascular resistance are well-maintained, and responses to Na2S are reversible. Decreases in heart rate were not blocked by atropine, suggesting that the bradycardia was independent of parasympathetic activation and was mediated by an effect on the sinus node. The decreases in systemic arterial pressure were not attenuated by hexamethonium, glybenclamide, Nw-nitro-l-arginine methyl ester hydrochloride, sodium meclofenamate, ODQ, miconazole, 5-hydroxydecanoate, or tetraethylammonium, suggesting that ATP-sensitive potassium channels, nitric oxide, arachidonic acid metabolites, cyclic GMP, p450 epoxygenase metabolites, or large conductance calcium-activated potassium channels are not involved in mediating hypotensive responses to the H2S donors in the rat and that responses are not centrally mediated. The present data indicate that decreases in systemic arterial pressure in response to the H2S donors can be mediated by decreases in vascular resistance and cardiac output and that the donors have an effect on the sinus node independent of the parasympathetic system. The present data indicate that the mechanism of the peripherally mediated hypotensive response to the H2S donors is uncertain in the intact rat.

scholarly journals Blood pressure control during exercise in the Atlantic cod, Gadus morhua

1986 ◽  
Vol 126 (1) ◽  
pp. 225-236 ◽  
Author(s):  
M. Axelsson ◽  
S. Nilsson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Atlantic Cod ◽  
Plasma Concentrations ◽  
Blood Samples ◽  
Blood Pressures ◽  
Mixed Venous

Atlantic cod were subjected to 12–15 min swimming exercise at 2/3 body lengths s-1 in a Blazka-type swim tunnel. Pre- and postbranchial blood pressures, cardiac output (ventral aortic blood flow) and heart rate were continuously recorded, and blood samples for measurement of arterial and mixed venous oxygen tension were taken before and at the end of the exercise period. In a second group of fish, subjected to similar exercise regimes, blood samples were taken for analysis of the plasma concentrations of catecholamines. Pre- and postbranchial blood pressures and cardiac output increase during exercise, while the mixed venous oxygen tension decreases. The effect on cardiac output is due to an increase of both heart rate and stroke volume. There are no significant changes in either systemic or branchial vascular resistances, or in the plasma concentrations of catecholamines. Injection of the adrenergic neurone-blocking drug bretylium produces a decrease in postbranchial blood pressure in resting cod, due to a decrease in the systemic vascular resistance. Exercising cod treated with bretylium have a significantly lower pre- and postbranchial blood pressure than exercising control cod. This is due mainly to a dramatic reduction in the systemic vascular resistance. The alpha-adrenoceptor antagonist phentolamine does not further affect the blood pressure in cod treated with bretylium. It is concluded that the exercise hypertension observed in cod depends on the effect of adrenergic vasomotor fibres maintaining the systemic vascular resistance, and also on the increase in cardiac output. An adrenergic innervation of the heart may play some role in the control of cardiac performance both at rest and during exercise, but the main cardioregulatory mechanism is likely to be non-adrenergic, most probably including cardiac control via variation of the cholinergic vagal cardioinhibitory tonus.

Abstract 323: Acute Reduction of Ambient Air Pressure Lowers Systemic Vascular Resistance and Improves Cardiac Output in Mice in-vivo

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Anmol Shahid ◽  
Vaibhav B Patel ◽  
Gavin Y Oudit ◽  
Michael S McMurtry
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Atmospheric Pressure ◽  
Arterial Compliance ◽  
Ambient Air ◽  
Left Ventricular ◽  
Air Pressure

Background: Humans have lower risk for myocardial infarction and stroke at higher altitudes. The mechanism is unknown. We previously demonstrated that acute reductions in ambient air pressure result in enhanced arterial vasodilation ex vivo using a myograph model of murine resistance arteries. Enhanced vasodilation might increase effective arterial compliance in vivo , thus we further hypothesized a reduction in systemic vascular resistance in vivo as a result of lowered ambient air pressure. Methods: In-vivo Pressure Volume Loops: A novel hypobaric chamber was designed and constructed with the capacity to hold a single anaesthetized mouse and simulate a variety of lowered air pressures within the chamber. The design of the chamber allowed for monitoring of murine heart rate, respiratory rate, & blood oxygen saturation at all times. Using inhaled isoflurane to anesthetize the animal, a closed-chest left-ventricular catheterization procedure was performed within the chamber on free-breathing adult male C57-WT mice (n=8) during consecutive acute exposures to the three air pressure steps: 754 mmHg (control or room atmospheric pressure), 714 mmHg (p1) and 674 mmHg (p2). Results: In-vivo : Total systemic vascular resistance was reduced by acute exposure to lower air pressure (10.09±0.15 mmHg*min/μL at control vs. 8.11±1.45 and 8.18±1.24 mmHg*min/μL at p1 and p2, respectively; p<0.05). Cardiac output was significantly improved by lowering atmospheric pressure below room pressure (7.36±0.15 mL/min at control versus 9.71±1.45 mL/min and 9.59±1.77 mL/min at p1 and p2, respectively; p<0.05). Significant increases in stroke volume with a reduction in air pressure were also observed (p<0.05 for p1 and p2 vs. control). We did not note significant changes in heart rate, mean arterial pressure, or contractility of the mice with lowered atmospheric pressure. Conclusion: Acute reductions in ambient air pressure lower systemic vascular resistance, and increase cardiac output and stroke volumes in vivo .

Central and regional hemodynamic effects during infusion of Big endothelin-1 in healthy humans

1996 ◽  
Vol 80 (6) ◽  
pp. 1921-1927 ◽  
Author(s):  
G. Ahlborg ◽  
A. Ottosson-Seeberger ◽  
A. Hemsen ◽  
J. M. Lundberg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Endothelin 1 ◽  
Healthy Humans ◽  
Arterial Blood

Big endothelin-1 (Big ET-1) was given intravenously to six healthy men to study uptakes and vascular effects. Blood samples were taken from systemic and pulmonary arterial and internal jugular and deep forearm venous catheters. Arterial Big ET-1-like immunoreactivity (Big ET-1-LI) increased from 5.43 +/- 0.60 to 756 +/- 27 pmol/l, and ET-1-LI increased from 4.67 +/- 0.08 to 6.67 +/- 0.52 pmol/l (P < 0.001). Skeletal muscle fractional extraction of Big ET-1-LI was 15 +/- 4%. ET-1-LI release did not increase in the studied vascular beds. Heart rate fell by 17% (P < 0.001), cardiac output fell by 26% (P < 0.001), and stroke volume fell by 11% (P < 0.05). Mean arterial blood pressure increased 18%, systemic vascular resistance increased 65%, and pulmonary vascular resistance increased 57% (P < 0.01-0.001). Pulmonary blood pressures, forearm blood flow, arterial pH, arterial PCO2, and systemic arterial-internal jugular venous O2 difference remained unchanged. No specific Big ET-1 receptors were found in human pulmonary membranes. The half-maximal inhibitory concentration for the receptor antagonist bosentan was 181 nM. In summary, circulating Big ET-1 elicits greater increases in mean arterial blood pressure and systemic vascular resistance and decreases in heart rate and cardiac output compared with an equimolar ET-1 infusion (26).

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