scholarly journals Cardiovascular effects of vasopressin following V1 receptor blockade compared to effects of nitroglycerin

2001 ◽  
Vol 281 (3) ◽  
pp. R887-R893 ◽  
Author(s):  
C. R. Cooke ◽  
B. M. Wall ◽  
K. M. Huch ◽  
T. Mangold
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Normal Subjects ◽  
Receptor Blockade ◽  
Hemodynamic Effects ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic subjects with impaired efferent sympathetic responses. Studies to compare the effects of AVP with the hemodynamic effects of nitroglycerin, an agent that primarily affects venous capacitance vessels, were also performed in normal subjects. Incremental infusions of AVP following V1-receptor blockade resulted in equivalent reductions in systemic vascular resistance (SVRI) in normal and in quadriplegic subjects. However, there were major differences in the effect on mean arterial pressure (MAP), which was reduced in quadriplegic subjects but did not change in normal subjects. This difference in MAP can be attributed to a difference in the magnitude of increase in cardiac output (CI), which was twofold greater in normal than in quadriplegic subjects. These observations are consistent with AVP-induced vasodilation of arterial resistance vessels with reflex sympathetic enhancement of CI and are clearly different from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP, CI, and indexes of cardiac preload, with only minor changes in SVRI.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Hemorrhage during Isoflurane–Nitrous Oxide Anesthesia

2004 ◽  
Vol 100 (4) ◽  
pp. 885-893 ◽  
Author(s):  
Claudia Höhne ◽  
Pia Vogler ◽  
Ilka Frerking ◽  
Roland C. E. Francis ◽  
Erik R. Swenson ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hormonal Regulation ◽  
Receptor Blockade ◽  
Angiotensin Ii Receptor ◽  
Oxide Anesthesia

Background The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia. Methods Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour. Results Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol. Conclusions ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

Beneficial or Detrimental Effects on Hemodynamics Depends on Dose of Dietary Potassium in Rapp Dahl Salt-Sensitive (DS) Rats.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 711-712
Author(s):  
William M Manger ◽  
Shlomoh Simchon ◽  
Kung-Ming Jan ◽  
Francis Haddy ◽  
Charles T Stier ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Aldosterone ◽  
Lower Blood Pressure ◽  
Hemodynamic Effects ◽  
Lower Blood ◽  
Dietary Potassium ◽  
Biphasic Effect

P103 Dietary K supplementation was reported to lower blood pressure and prevent strokes in humans and to prevent strokes in hypertensive DS rats. We report a biphasic effect as a function of KCl dose in DS rats that were fed 1% NaCl with increasing dietary KCl, namely, 0.7, 2.6, 4, and 8%. After 8 months on 1% NaCl supplemented with 0.7% KCl, mean arterial pressure (MAP), plasma volume (PV), cardiac output (CO), total peripheral, renal and cerebral vascular resistances (TPR, RVR, CVR) increased compared to salt-resistant DR rats; on 2.6% KCl all these parameters decreased compared with DS on 0.7% KCl diet. When KCl was increased to 4 and 8%, MAP, PV, CO and RVR progressively increased in DS and DR rats, without changing TPR; these changes were accompanied by parallel increases in plasma aldosterone. Only DS rats on the ”optimal“ 2.6% KCl supplement maintained hemodynamics most similar to control DR rats and thus prevented Na retention, hypertension, increases in RVR and CVR. These beneficial hemodynamic effects may explain stroke prevention.

Systemic hemodynamic effects of leukotrienes C4 and D4 in the rat

1983 ◽  
Vol 244 (4) ◽  
pp. H628-H633 ◽  
Author(s):  
M. A. Pfeffer ◽  
J. M. Pfeffer ◽  
R. A. Lewis ◽  
E. Braunwald ◽  
E. J. Corey ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Right Atrial ◽  
Moderate Pressure ◽  
Hemodynamic Effects ◽  
Systemic Hemodynamic ◽  
Leukotriene D4

Although local administration of the sulfidopeptide leukotrienes into cutaneous and coronary vascular beds indicates that these naturally occurring metabolites of arachidonic acid are vasoconstrictors, their systemic administration has produced both pressor and depressor responses. The systemic hemodynamic effects of intravenous leukotriene C4 (LTC4) and leukotriene D4 (LTD4) were assessed in ether-anesthetized rats and compared with the effects produced by equimolar doses (2 X 10(-10) to 4 X 10(-8) mol/kg) of norepinephrine and angiotensin. Mean arterial pressure, right atrial pressure, and cardiac output (electromagnetic flowmetry) were recorded during bolus administrations of these vasoactive compounds. LTC4 and LTD4 had similar hemodynamic effects that were characterized by moderate pressure elevations produced by dose-dependent increases in total peripheral resistance, since cardiac output declined. Although the peak mean arterial pressure levels produced by LTC4 and LTD4 (135 +/- 7 and 129 +/- 5 mmHg, respectively) were less than those by norepinephrine (157 +/- 3 mmHg) and angiotensin (174 +/- 5 mmHg), the peak total peripheral resistance values of LTC4 and LTD4 (2.23 +/- 0.32 and 1.86 +/- 0.17 mmHg X ml-1 X min-1, respectively) were between those of the well-known vasopressors, norepinephrine (1.50 +/- 0.09) and angiotensin (2.72 +/- 0.41). The pressor response to LTC4 and LTD4 was less marked than that to norepinephrine and to angiotensin because of the concomitant reduction in cardiac output. These results indicate that LTC4 and LTD4 are systemic vasoconstrictors with potencies similar to those of norepinephrine and angiotensin.

Inhibition of the Cardiovascular Effects of Acupuncture (Moxibustion) by Phenotolamine in Dogs During Halothane Anesthesia

1976 ◽  
Vol 04 (02) ◽  
pp. 153-161 ◽  
Author(s):  
Myung O. Lee ◽  
Do Chil Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Blocking Agent ◽  
Halothane Anesthesia

The cardiovascular effects of acupuncture, moxibustion by electrocautery, at Jen Chung (Go-26) and phentolamine (0.1 mg/kg-i.v.) alone were compared to phentolamine (0.1 mg/kg-i.v.) prior to moxibustion at Go-26 in groups of ten dogs under 0.75 percent halothane anesthesia. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressue, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two hour period. A significant increase (5% level) in cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure and significant decrease in total peripheral resistance were observed following acupuncture, moxibustion with electrocautery, at Jen Chung (Go-26) in dogs under halothane anesthesia. These effects were inhibited by pretreatment with the alpha blocking agent, phentolamine (0.1mg/kg-i.v.). The cardiovascular effects of phentolamine (0.1mg/kg-i.v.) alone were similar to those of dogs in which phenotolamine was administered prior to moxibustion.

Increased cardiac output following occlusion of the descending thoracic aorta in dogs

1982 ◽  
Vol 243 (1) ◽  
pp. R152-R158 ◽  
Author(s):  
J. K. Stene ◽  
B. Burns ◽  
S. Permutt ◽  
P. Caldini ◽  
M. Shanoff
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Superior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Mean Systemic Pressure ◽  
Extracorporeal Bypass

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

Evaluation of cardiac output variations with the peripheral pulse pressure to mean arterial pressure ratio

2018 ◽  
Vol 33 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Audrey Tantot ◽  
Anais Caillard ◽  
Arthur Le Gall ◽  
Joaquim Mateo ◽  
Sandrine Millasseau ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Peripheral Pulse

Abstract P154: Ultrasound Imaging for Serial Measurements of Venous Diameters in Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Teresa Krieger-Burke ◽  
Bridget M Seitz ◽  
Gregory D Fink ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Real Time ◽  
Ultrasound Imaging ◽  
Imaging System ◽  
Sprague Dawley ◽  
Reliable Technique ◽  
Venous Capacitance ◽  
Anesthetized Rats

The purpose of our study was to investigate serial ultrasound imaging in rats as a means to quantify the diameters of splanchnic veins in real time and the effect of drugs on venous capacitance. A 21 MHz probe ( Vevo 2100 imaging system,Visual Sonics Inc.) was used to collect images containing the portal vein (PV) and the superior mesenteric vein (SMV) in anesthetized male Sprague-Dawley rats maintained at 37°C. Stable landmarks were established and we were able to repeatedly locate specific cross-sections of PV and SMV. When controlled for respiratory and cardiac cycles during measurements, respective diameters of these vessels remained within 0.75±0.15% and 0.2±0.10% of baseline (PV: 2.02±0.15 mm; SMV: 1.67±0.05 mm) when located and measured every 5 minutes over 45 minutes (n=3 rats). PV and SMV remained within 1.0±0.6% and 0.38±0.9% from baseline, respectively, when measured on separate days over 10 weeks in a preliminary study using 2 rats. The consistency of raw vessel measurements allowed these vessels to serve as their own control during subchronic pharmacologic interventions. In a second study, the vasodilator sodium nitroprusside (2 mg/kg, i.v. bolus) was administered to anesthetized rats (n=3) following collection of baseline vessel measurements. PV and SMV diameters increased 37.23±2.4% and 29.77±8.8% from baseline by 30 minutes post drug administration while mean arterial pressure decreased 10.32±1.7 mmHg. Conversely, the administration of the venoconstrictor sarafotoxin (S6C) (5 ng/kg, i.v. bolus) to other anesthetized rats (n=3) decreased PV and SMV diameters 22.10±2.4% and 9.44±1.6% from baseline within 5 minutes, associated with an increase in mean arterial pressure of 12.85±3.2 mmHg. Together these results support serial ultrasound imaging as a reliable technique to accurately measure acute and subchronic changes in the diameter of splanchnic veins concurrent with blood pressure changes in intact rats. The ability to follow rat abdominal vein diameters in real time will assist in determining the role of the venous circulation in blood pressure regulation.

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