scholarly journals Relaxin Modifies Systemic Arterial Resistance and Compliance in Conscious, Nonpregnant Rats

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3289-3296 ◽  
Author(s):  
Kirk P. Conrad ◽  
Dan O. Debrah ◽  
Jackie Novak ◽  
Lee A. Danielson ◽  
Sanjeev G. Shroff
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Therapeutic Potential ◽  
Muscle Tone ◽  
Arterial Compliance ◽  
Renal Arteries ◽  
Conscious Rat ◽  
Systemic Hemodynamic ◽  
Arterial Load ◽  
Passive Mechanics

Abstract Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices—AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.

Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans

2003 ◽  
Vol 285 (2) ◽  
pp. H614-H620 ◽  
Author(s):  
Denis Chemla ◽  
Isabelle Antony ◽  
Yves Lecarpentier ◽  
Alain Nitenberg
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Reliable Estimate ◽  
Arterial Elastance ◽  
Total Arterial Compliance ◽  
Arterial Load ◽  
Effective Arterial Elastance

The respective contribution of systemic vascular resistance ( R) and total arterial compliance ( C) to the arterial load remains to be established in humans. Effective arterial elastance ( Ea), i.e., the left ventricular end-systolic pressure (LVESP)-over-stroke volume ratio, is a reliable estimate of arterial load. It is widely accepted that Ea mainly relates to mean aortic pressure (MAP) and thus to the R-to- T ratio ( R/ T ratio), where T is cycle length. We tested the contribution of R/ T and 1/ C to Ea in 20 normotensive and 46 hypertensive subjects (MAP range: 84–160 mmHg). The multilinear model applied ( Ea = 1.00 R/ T + 0.42/ C – 0.04; r2 = 0.97). The sensitivity of Ea to a change in R/ T was 2.5 times higher than to a similar change in 1/ C in both normotensive and hypertensive adults. The LVESP was more strongly related to systolic aortic pressure (SAP; r2 = 0.94) than to MAP ( r2 = 0.83), and LVESP matched 90% SAP (bias = 0 ± 5mmHg). An alternative model of Ea is proposed, in which Ea is proportional to the heart rate × SAP product-over-cardiac index ratio whatever the MAP.

Abstract 15631: The Hemodynamic Determinants and Physiologic Correlates of QTc Interval Using Impedance Cardiography in Heart Failure

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Fadi Khraim ◽  
Rodolfo Pike ◽  
Jennifer Williams ◽  
Salah S Al-Zaiti
Keyword(s):  
Heart Failure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Impedance Cardiography ◽  
Arterial Compliance ◽  
Qtc Interval ◽  
Cardiac Events ◽  
Heart Failure Patients ◽  
Qrs Duration ◽  
Duration Effect

Background: Prolonged QTc interval is a known risk factor for adverse cardiac events, including sudden and non-sudden cardiac death. Understanding the determinants and physiologic correlates of QTc can guide the proper strategy for the primary prevention of sudden death in high risk patients. Methods & Results: This was an observational study that recruited ambulatory heart failure patients (NYHA I-III) from an outpatient clinic in NL, Canada. In supine resting position, consented participants underwent non-invasive 12-lead ECG and hemodynamic monitoring using BioZ Dx Impedance Cardiography (Sonosite Inc., WA, USA). ECGs were evaluated by a reviewer blinded to clinical data. Participants with pacing (n=12) or left bundle branch block (n=9) were excluded. Three measures of interest were automatically computed: (1) QTc interval (i.e., from QRS onset to T offset), (2) QRS duration (i.e., from QRS onset to QRS offset), and (3) JTc (i.e., QTc interval minus QRS duration). Effect sizes were computed using Pearson’s r coefficients. The final sample (n=23) was 62±13 years of age and 70% male with LVEF of 34±10%. The mean QTc was 441±39 milliseconds, and 10 patients (43%) had prolonged QTc (≥450 milliseconds). QTc interval negatively correlated with cardiac output (r= -0.57), and positively correlated with systemic vascular resistance (r= +0.57), as well as thoracic fluid content (r= +0.43). QRS duration alone was not specifically associated with any hemodynamic parameter, but JTc interval positively correlated with total arterial compliance (r=+0.42). Conclusions: In heart failure patients, we interestingly found that increased systemic vascular resistance results in QTc interval prolongation, where repolarization time is specifically influenced by arterial compliance. This suggests potential benefit from antihypertensive therapy targeted at lowering systemic vascular resistance in those with prolonged QTc/JTc. Nevertheless, these intervals need to be interpreted with caution in patients with thoracic fluid overload (e.g., pulmonary edema).

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 Influence of critical closing pressure on systemic vascular resistance and total arterial compliance: A clinical invasive study

2017 ◽  
Vol 110 (12) ◽  
pp. 659-666 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Philippe Hervé ◽  
Sandrine Millasseau ◽  
Mabrouk Brahimi ◽  
...  
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Total Arterial Compliance ◽  
Critical Closing Pressure ◽  
Closing Pressure

Arterial Stiffness Is Associated With QTc Interval Prolongation in Patients With Heart Failure

2017 ◽  
Vol 20 (3) ◽  
pp. 255-263
Author(s):  
Salah Al-Zaiti ◽  
Samir Saba ◽  
Rodolfo Pike ◽  
Jennifer Williams ◽  
Fadi Khraim
Keyword(s):  
Heart Failure ◽  
Arterial Stiffness ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Qtc Interval ◽  
Interval Prolongation ◽  
Indirect Measure ◽  
Total Arterial Compliance ◽  
Qtc Interval Prolongation

Background: A prolonged corrected QT (QTc) interval is a known risk factor for adverse cardiac events. Understanding the determinants and physiologic correlates of QTc is necessary for selecting proper strategies to reduce the risk of adverse events in high-risk patients. We sought to evaluate the role of arterial stiffness in heart failure as a determinant of QTc prolongation. Method: This was an observational study that recruited ambulatory heart failure patients (New York Heart Association Classes I–II) from an outpatient heart failure clinic. In the supine resting position, consented patients underwent noninvasive 12-lead electrocardiograph (ECG) and hemodynamic monitoring using BioZ Dx impedance cardiography. ECGs were evaluated by a reviewer blinded to clinical data, and QTc interval was automatically computed. Patients with pacing or bundle branch block (BBB) were analyzed separately. Strengths of associations were evaluated using Pearson’s r coefficients and multivariate linear regression. Results: The final sample ( N = 44) was 62 ± 13 years of age and 64% male with ejection fraction of 34% ± 12%. At univariate level, QTc interval moderately ( r > .50) correlated with cardiac output, left cardiac work index, systemic vascular resistance, and total arterial compliance in patients with intrinsically narrow QRS complexes. At the multivariate level, increasing systemic vascular resistance and decreasing total arterial compliance remained independent predictors of widening QTc interval in this group ( R2 = .54). No significant correlations were seen in patients with pacing or BBB. Conclusions: In the absence of conduction abnormalities, magnitude of arterial stiffness, an indirect measure of endothelial dysfunction, is associated with QTc interval prolongation.

Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation

1995 ◽  
Vol 78 (5) ◽  
pp. 1642-1650 ◽  
Author(s):  
C. F. Pilati ◽  
M. B. Maron ◽  
F. J. Bosso
Keyword(s):  
Pulmonary Edema ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Edema Formation ◽  
Systemic Hemodynamic ◽  
Lv Dysfunction ◽  
The Right

This study was undertaken to determine whether endothelium-derived relaxing factor (EDRF) modulates the pulmonary and systemic hemodynamic responses to massive sympathetic nervous system (SNS) activation and, in so doing, also modulates the degree of SNS-induced left ventricular (LV) dysfunction and the likelihood for pulmonary edema formation. The SNS of 13 anesthetized untreated rabbits and 14 anesthetized rabbits pretreated with the EDRF inhibitor, N omega-nitro-L-arginine (L-NNA, 20 mg/kg), was massively activated with an intracisternal injection of veratrine. Pulmonary and systemic arterial pressures increased to the same extent in both groups, but LV end-diastolic pressure was significantly lower in untreated rabbits. During this time, cardiac output decreased by 37% in L-NNA pretreated rabbits compared with 8% in untreated animals. Peak systemic and pulmonary vascular resistances increased significantly in L-NNA rabbits, whereas only systemic vascular resistance increased significantly in untreated rabbits. However, this increase in systemic vascular resistance was threefold less than that observed for L-NNA-treated animals. Although the degree of LV dysfunction was greater in the L-NNA rabbits, pulmonary edema developed less frequently in this group. We suggest that when EDRF release is inhibited during massive SNS activity, pulmonary vascular resistance increases markedly, which causes the right ventricle to fail. We further suggest that the reduced right ventricular output maintains pulmonary microvascular pressure below levels required for edema development.

scholarly journals Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

2015 ◽  
Vol 46 (4) ◽  
pp. 1178-1189 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Yves Papelier ◽  
Pierre Attal ◽  
Philippe Hervé
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Arterial Compliance ◽  
Pulmonary Arteries ◽  
Transpulmonary Pressure ◽  
Total Arterial Compliance ◽  
Arterial Load ◽  
Pulmonary Arterial

Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is “constant” in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects. Furthermore, reported RC-times in the literature have consistently demonstrated significant scatter around the mean. In precapillary PH, the true PVR can be overestimated if one uses the standard PVR equation because the zero-flow pressure may be significantly higher than pulmonary arterial wedge pressure. Furthermore, SV/PApp may also overestimate true C. Further studies are needed to clarify some of the inconsistencies of pulmonary RC-time, as this has major implications for our understanding of the arterial load in diseases of the pulmonary circulation.

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