scholarly journals Influence of the ratio of mean arterial pressure to right atrial pressure on outcome after successful percutaneous edge-to-edge repair for severe mitral valve regurgitation

2021 ◽  
Vol 37 ◽  
pp. 100903
Author(s):  
Rico Osteresch ◽  
Kathrin Diehl ◽  
Patrick Dierks ◽  
Johannes Schmucker ◽  
Azza Ben Ammar ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Mitral Valve ◽  
Arterial Pressure ◽  
Mitral Valve Regurgitation ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Valve Regurgitation

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula

1992 ◽  
Vol 262 (6) ◽  
pp. H1802-H1808 ◽  
Author(s):  
M. Huang ◽  
R. L. Hester ◽  
A. C. Guyton ◽  
R. A. Norman
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hypertensive Rats

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

Vagally mediated regulation of renal function in conscious primates

1986 ◽  
Vol 250 (4) ◽  
pp. H546-H549
Author(s):  
S. F. Vatner ◽  
W. T. Manders ◽  
D. R. Knight
Keyword(s):  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rhesus Monkeys ◽  
Volume Expansion ◽  
Urine Flow ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Water Excretion

The effects of vagal denervation (VD) were examined on responses of Na+ and water excretion to acute volume expansion (18 ml/kg of 6% dextran in saline) in six conscious rhesus monkeys with chronic sinoaortic denervation (SAD). After SAD, volume expansion increased mean arterial pressure (from 95 +/- 6.6 to 119 +/- 7.5 mmHg), right atrial pressure (from 1.3 +/- 0.7 to 5.9 +/- 1.8 mmHg), urine flow (from 0.08 +/- 0.01 to 0.68 +/- 0.20 ml/min), and Na+ excretion (from 1.30 +/- 0.45 to 29.51 +/- 10.40 mueq/min). After VD, volume expansion increased mean arterial and right atrial pressures similarly, but induced significantly lower (P less than 0.05) increases in urine flow (from 0.05 +/- 0.01 to 0.19 +/- 0.03 ml/min) and Na+ excretion (from 0.87 +/- 0.27 to 11.50 +/- 6.13 mueq/min). Thus vagal mechanisms appear to play an important role in mediating excretion of Na+ and water in response to acute volume expansion in the conscious primate.

Hemorrhage effects on plasma ANP, NH2-terminal pro-ANP, and pressor hormones in anesthetized and conscious rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1933-R1943 ◽  
Author(s):  
H. Leskinen ◽  
H. Ruskoaho ◽  
P. Huttunen ◽  
J. Leppaluoto ◽  
O. Vuolteenaho
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Conscious Rats ◽  
Anesthetized Rats ◽  
Atrial Natriuretic

We examined the effect of hemorrhage on plasma NH2-terminal pro-atrial natriuretic peptide (NT-pro-ANP) and atrial natriuretic peptide (ANP) in anesthetized and conscious rats. Blood (1.5 ml/time point) was withdrawn at 0, 10, 20, and 30 min. In anesthetized rats it caused decrease in mean arterial pressure and led to bradycardia in 2 min. Right atrial pressure decreased significantly after 12 min. However, plasma ANP did not change, and NT-pro-ANP actually increased from 481 +/- 55 to 609 +/- 73 pmol/l (P < 0.01) at 20 min and to 696 +/- 82 pmol/l (P < 0.01) at 30 min. Also plasma arginine-8-vasopressin (AVP) and epinephrine increased significantly at 30 min. No significant changes in plasma endothelin and norepinephrine were found. The increase in NT-pro-ANP after hemorrhage was not blocked by AVP V1-receptor, alpha- and beta-catecholaminergic receptor, or muscarinic-receptor antagonists. The plasma 125I-ANP disappearance curve was shifted to the right after hemorrhage in anesthetized rats, suggesting that the elimination of ANP was decreased. In conscious rats, heart rate and right atrial pressure did not change significantly after hemorrhage, and mean arterial pressure did not decrease until 22 min. NT-pro-ANP decreased from 1,467 +/- 146 to 1,072 +/- 130 pmol/l (P < 0.01) at 20 min and to 941 +/- 41 pmol/l (P < 0.01) at 30 min. Plasma ANP did not respond to hemorrhage in conscious rats. In conclusion, we found no change in plasma ANP during hemorrhage in either anesthetized or conscious rats, but we did find a significant increase in plasma NT-pro-ANP levels in anesthetized rats and a significant decrease in conscious rats. We suggest that this divergence may be due to different hemodynamic responses to hemorrhage.

scholarly journals The Effect of Furosemide on Left Atrial Pressure in Dogs with Mitral Valve Regurgitation

2011 ◽  
Vol 25 (2) ◽  
pp. 244-250 ◽  
Author(s):  
S. Suzuki ◽  
T. Ishikawa ◽  
L. Hamabe ◽  
D. Aytemiz ◽  
H. Huai-Che ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Atrial ◽  
Mitral Valve Regurgitation ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Valve Regurgitation

Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output

1995 ◽  
Vol 269 (3) ◽  
pp. R678-R690 ◽  
Author(s):  
T. E. Lohmeier ◽  
G. A. Reinhart ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
R. Hester ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Pressure Control ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Renal Nerves ◽  
Sodium Retention

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

Echocardiographic Estimation of Left Atrial Pressure in Beagle Dogs with Experimentally-Induced Mitral Valve Regurgitation

2011 ◽  
Vol 73 (8) ◽  
pp. 1015-1024 ◽  
Author(s):  
Taisuke ISHIKAWA ◽  
Ryuji FUKUSHIMA ◽  
Shuji SUZUKI ◽  
Yuka MIYAISHI ◽  
Taiki NISHIMURA ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Atrial ◽  
Mitral Valve Regurgitation ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Valve Regurgitation ◽  
Beagle Dogs ◽  
Experimentally Induced

scholarly journals Daily Rhythms of Left Atrial Pressure in Beagle Dogs with Mitral Valve Regurgitation

2009 ◽  
Vol 23 (4) ◽  
pp. 824-831 ◽  
Author(s):  
T. Ishikawa ◽  
R. Tanaka ◽  
S. Suzuki ◽  
Y. Saida ◽  
A. Soda ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Atrial ◽  
Mitral Valve Regurgitation ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Valve Regurgitation ◽  
Beagle Dogs ◽  
Daily Rhythms

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

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