Chronic captopril and losartan (DuP 753) administration in rats with high-output heart failure

1992 ◽  
Vol 263 (3) ◽  
pp. H833-H840 ◽  
Author(s):  
G. Qing ◽  
R. Garcia
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Right Atrial ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
Regression Of Cardiac Hypertrophy ◽  
High Output

We investigated the role of atrial natriuretic factor (ANF) and the renin-angiotensin system as well as the effects of losartan in rats with aortocaval (AC) shunts. Right atrial and left ventricular end-diastolic pressures (LVEDP) were higher and mean arterial blood pressure (MAP) was lower in AC shunt animals than in their controls. AC shunt rats presented marked cardiac hypertrophy, decreased right atrial ANF concentration, and increased ventricular ANF content and concentration. Plasma ANF levels were elevated, and hematocrit was lower in AC shunt animals than in controls. Captopril or losartan treatment decreased MAP and returned LVEDP to sham-operated control values. A clear regression of cardiac hypertrophy was evident in both treated AC shunt groups, with plasma ANF levels tending to follow those in sham-operated rats. Plasma COOH-terminal ANF levels were decreased and urinary volume and hematocrit were increased in losartan-treated AC shunt animals. We conclude that chronic angiotensin converting enzyme inhibition and angiotension II receptor antagonism improved hemodynamic conditions, diminished water retention, reversed cardiac hypertrophy, and restored plasma and tissue ANF to more “normal” levels in rats with moderate high-output heart failure.

Atrial natriuretic factor release and natriuresis in rats with high-output heart failure

1990 ◽  
Vol 259 (5) ◽  
pp. H1374-H1379 ◽  
Author(s):  
R. Garcia ◽  
D. Lachance ◽  
G. Thibault
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Left Ventricular ◽  
Heart Weight ◽  
Main Peak ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

We investigated whether rats with high-output heart failure [aortocaval (AC) shunts] release atrial natriuretic factor (ANF) and excrete sodium after moderate volume expansion (VE) as do sham-operated controls. Mean arterial blood pressure was lower (92.5 +/- 4.4 vs. 114.0 +/- 1.3 mmHg) and relative heart weight was higher (545.6 +/- 35.1 vs. 253.8 +/- 9.8 mg/100 g body wt) in animals with AC shunts than in their controls. Central venous pressure (CVP) was elevated (3.61 +/- 0.36 vs. 0.37 +/- 0.94 mmHg) and heart rate decreased (332.5 +/- 8 vs. 370.0 +/- 9.9 beats/min) in AC rats. This group also presented lower basal urinary sodium excretion (UNaV), urinary volume, and hematocrit than their sham-operated controls. Basal plasma COOH- and NH2-terminal ANF levels were greatly elevated in AC shunt animals (165.43 +/- 55.73 and 1,692.98 +/- 305.63 fmol/ml, respectively) when compared with the controls (14.27 +/- 1.49 and 331.67 +/- 29.84 fmol/ml, respectively). VE was performed in conscious rats 3 times at 15-min intervals with human plasma protein fraction. The effect of VE on CVP, left-ventricular end-diastolic pressure, the increases in plasma COOH- and NH2-terminal ANF, and the diuretic and natriuretic responses were similar in both experimental groups. U(NA)V was positively correlated with plasma COOH- (r = 0.50, P less than 0.01) and NH2- (r = 0.60, P less than 0.001) terminal ANF only in the controls. One main peak of immunoreactive ANF corresponding to the elution time of a small peptide such as ANF-(99-126) was detected in the plasma of AC animals after VE. We conclude that ANF release and natriuresis are conserved after moderate VE in a rat model of moderate high-output experimental heart failure.

Systematic nocturnal atrial demand pacing results in high-output heart failure

1992 ◽  
Vol 72 (5) ◽  
pp. 1803-1809 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel ◽  
P. H. Chew
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Venous Pressure ◽  
Control Period ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Central Venous ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
High Output

Beat-to-beat parameters of heart rate (HR), intra-arterial blood pressure (BP), central venous pressure, and derived indexes of cardiac output and total peripheral resistance were recorded 18 h/day (from 1800 to 1200 h the following day) in four monkeys (Macaca mulatta) during 20 control days followed by 20 days of atrial demand pacing. The pacing rate was set at approximately 10 beats/min above the fastest hourly average HR recorded during the control period, i.e., sufficient to prevent the normal nocturnal fall in HR. Nocturnal pacing resulted in progressive weekly increases in central venous BP and arterial BP. Analyses of levels and diurnal trends in hemodynamic parameters and cardiac function curves across consecutive 5-day periods of nocturnal pacing revealed a hemodynamic pattern characteristic of high-output heart failure, which progressively increased (week by week) during the early morning hours (0500–0700). Sustained elevated left ventricular work resulting from the prevention of a nocturnal fall in HR may have been responsible for the reduction in cardiac function seen in this experimental model.

Captopril enhances renal responsiveness to ANF in dogs with compensated high-output heart failure

1992 ◽  
Vol 262 (3) ◽  
pp. R509-R516 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson
Keyword(s):  
Heart Failure ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Systemic Hemodynamic ◽  
Av Fistula ◽  
High Output Heart Failure ◽  
Converting Enzyme Inhibition ◽  
Control Infusion ◽  
High Output

The systemic hemodynamic, hormonal, and renal effects of chronic angiotensin-converting enzyme inhibition (CEI) with captopril and the responses to synthetic atrial natriuretic factor (ANF) infusions in the presence and absence of captopril were examined in normal dogs (n = 6) and in dogs with an arteriovenous (AV) fistula and compensated high-output heart failure (n = 6). This experimental model is characterized by normalization of the circulating renin-angiotensin-aldosterone system (RAAS) and persistent elevations in central filling pressures and plasma ANF. In both normal and AV-fistula dogs, oral captopril for 1 wk at 35 mg.kg-1.day-1 in three divided doses produced progressive reductions in arterial and atrial pressures (P less than 0.05), plasma ANF (P less than 0.05), and aldosterone (P less than 0.05). After 1-2 days of a modest increase in urinary sodium excretion (UNaV) (P less than 0.05), all of the dogs regained and maintained sodium balance during captopril administration. On the 8th day of the captopril regimen, synthetic ANF was infused at 15 and 30 ng.kg-1.min-1 for 75-min periods each. Control infusion experiments were performed in the same animals before captopril administration. The normal dogs exhibited dose-related elevations in UNaV (P less than 0.05) that were not augmented with captopril (P greater than 0.05). In contrast, in the AV-fistula dogs the observed renal unresponsiveness to synthetic ANF in the control experiments was reversed with chronic CEI, and ANF-induced UNaV achieved levels comparable to those obtained in the normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Underlying Causes of High Output Heart Failure

2020 ◽  
pp. 1-4
Author(s):  
Qiuhua Shen ◽  
Qiuhua Shen ◽  
John B. Hiebert ◽  
Janet D. Pierce
Keyword(s):  
Heart Failure ◽  
Neurohormonal Activation ◽  
Chronic Anemia ◽  
Output State ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
Underlying Causes ◽  
Venous Fistula ◽  
High Output ◽  
Pathophysiologic Mechanisms

In the U.S., each year, there are more than 500,000 new cases of all types of heart failure. With high output cardiac failure, there is an elevated cardiac output associated with several conditions and diseases, including obesity, chronic anemia, systemic arterio-venous fistula, hypercapnia, mitochondrial dysfunction, and hyperthyroidism. The underlying pathophysiologic mechanisms relate to a reduction in systemic vascular resistance from arterio-venous shunting or peripheral vasodilation. Often there is a decrease in systemic arterial blood pressure and neurohormonal activation leading to heart failure symptoms of dyspnea and fatigue. In a persistent high output state, patients may experience tachycardia, valvular abnormalities, and ventricular dilatation and/or hypertrophy. In this article, there is a review of high output heart failure, including the prevalence, pathophysiology, and common clinical causes of this disease.

ANF and postprandial control of sodium excretion in dogs with compensated heart failure

1990 ◽  
Vol 258 (1) ◽  
pp. R232-R239
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
M. W. Brands
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Right Atrial ◽  
Av Fistula ◽  
Feeding Experiments ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
Series Of Experiments ◽  
High Output ◽  
Atrial Natriuretic

The changes in plasma immunoreactive atrial natriuretic factor (iANF) and urinary Na excretion that occur in response to an oral load of Na and to infusion of synthetic atrial natriuretic factor (ANF) were examined in conscious dogs with an arteriovenous (AV) fistula and chronic compensated high-output heart failure. After ingestion of a meal containing 125 meq Na, plasma iANF and right atrial pressure increased from high basal levels of 506 +/- 46 pg/ml and 96 +/- 5 mmH2O to peak responses of 728 +/- 43 pg/ml (P less than 0.05) and 104 +/- 6 mmH2O (P less than 0.05). These increases were associated with a brisk postprandial natriuresis and diuresis of a magnitude previously observed in normal dogs. Synthetic ANF infusions that achieved plasma iANF levels of similar and higher magnitude to those observed during the feeding experiments did not produce a significant natriuresis in these AV fistula dogs. In separate series of experiments, chronic effects of normal and low-Na diets on daily Na excretion and postabsorptive plasma iANF, renin, and aldosterone were studied in normal and AV fistula dogs. During the normal Na diet of 40 meq/day, both groups had normal levels of renin and aldosterone, but Na balance was achieved in AV fistula animals in the presence of a fourfold elevation in plasma iANF compared with normal dogs (P less than 0.05). During 2 wk of Na restriction, cumulative negative Na balance and marked stimulation of renin and aldosterone were similar in normal and AV fistula animals, but plasma iANF did not change significantly in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Haemodynamic and Neurohumoral Changes in Spontaneously Hypertensive Rats with Aortocaval Fistulae

1993 ◽  
Vol 84 (5) ◽  
pp. 531-535 ◽  
Author(s):  
Tamiko Oka ◽  
Hikaru Nishimura ◽  
Masakuni Ueyama ◽  
Jiro Kubota ◽  
Keishiro Kawamura
Keyword(s):  
Heart Failure ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Left Ventricular ◽  
Heart Weight ◽  
Stroke Index ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Output Heart Failure ◽  
High Output

1. Our aim was to evaluate the effects of an aortocaval fistula (1 mm) on cardiorenal haemodynamics, cardiac hypertrophy and neurohumoral factors in spontaneously hypertensive rats and to compare the results with those observed in Wistar rats at 2 weeks after fistulae placement. Sham-operated spontaneously hypertensive rats and Wistar rats served as controls. 2. Heart weight was significantly increased in spontaneously hypertensive rats (34%) and in Wistar rats (43%) at 2 weeks after fistula creation. Left ventricular systolic pressure and dp/dtmax. were significantly decreased (both P <0.01) in spontaneously hypertensive rats with fistulae which had higher left ventricular end-diastolic pressure than Wistar rats with fistulae (P <0.01). Signs of circulatory congestion (ascites, tachypnoea, prostration) were observed only in the overloaded spontaneously hypertensive rats (45%). Cardiac index was comparably increased in both fistulae groups due to an increase in stroke index, since heart rate was not increased. 3. Fistulae placement decreased renal blood flow and kidney weight, and increased blood urea nitrogen to a greater degree in spontaneously hypertensive rats (all P <0.05); serum creatinine levels were unaltered. Plasma noradrenaline concentration was increased in spontaneously hypertensive rats with fistulae (P <0.05), whereas plasma renin activity was not changed. 4. Thus, spontaneously hypertensive rats with fistulae developed overt haemodynamic signs of high-output heart failure with frequent ascites and dyspnoea, whereas most of these findings were milder or absent in Wistar rats. This model provides an opportunity to evaluate the pathophysiological and pharmacological responses in high-output heart failure.

scholarly journals Inhibition of Brainstem Endoplasmic Reticulum Stress Rescues Cardiorespiratory Dysfunction in High Output Heart Failure

Hypertension ◽  
2020 ◽  
Author(s):  
Hugo S. Díaz ◽  
David C. Andrade ◽  
Camilo Toledo ◽  
Karla G. Schwarz ◽  
Katherin V. Pereyra ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Potential Role ◽  
Renin Angiotensin System ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
High Output Heart Failure ◽  
High Output

Recent evidence shows that chronic activation of catecholaminergic neurons of the rostral ventrolateral medulla is crucial in promoting autonomic imbalance and cardiorespiratory dysfunction in high output heart failure (HF). Brainstem endoplasmic reticulum stress (ERS) is known to promote cardiovascular dysfunction; however, no studies have addressed the potential role of brainstem ERS in cardiorespiratory dysfunction in high output HF. In this study, we assessed the presence of brainstem ERS and its potential role in cardiorespiratory dysfunction in an experimental model of HF induced by volume overload. High output HF was surgically induced via creation of an arterio-venous fistula in adult male Sprague-Dawley rats. Tauroursodeoxycholic acid (TUDCA), an inhibitor of ERS, or vehicle was administered intracerebroventricularly for 4 weeks post-HF induction. Compared with vehicle treatment, TUDCA improved cardiac autonomic balance (LF HRV /HF HRV ratio, 3.02±0.29 versus 1.14±0.24), reduced cardiac arrhythmia incidence (141.5±26.7 versus 35.67±12.5 events/h), and reduced abnormal respiratory patterns (Apneas: 11.83±2.26 versus 4.33±1.80 events/h). TUDCA administration (HF+Veh versus HF+TUDCA, P <0.05) attenuated cardiac hypertrophy (HW/BW 4.4±0.3 versus 4.0±0.1 mg/g) and diastolic dysfunction. Analysis of rostral ventrolateral medulla gene expression confirmed the presence of ERS, inflammation, and activation of renin-angiotensin system pathways in high output HF and showed that TUDCA treatment completely abolished ERS and ERS-related signaling. Taken together, these results support the notion that ERS plays a role in cardiorespiratory dysfunction in high output HF and more importantly that reducing brain ERS with TUDCA treatment has a potent salutary effect on cardiac function in this model.

Atrial natriuretic factor secretion in dogs with experimental high-output heart failure

1987 ◽  
Vol 252 (4) ◽  
pp. H692-H696 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
K. M. Verburg ◽  
R. C. Vari
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Sodium Balance ◽  
Av Fistula ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output

The temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (iANF) were studied in six conscious dogs with an arteriovenous (AV) fistula, a model of chronic high-output heart failure. Following the creation of the AV fistula, the dogs retained sodium avidly for 5 days, and plasma renin activity, plasma aldosterone concentration, and right atrial pressure increased significantly from controls. During this initial stage, iANF increased only modestly. From day 6 to 14, the dogs increased their daily sodium excretion and approached sodium balance. This natriuretic response was associated with a significant rise in iANF, with the return of renin and aldosterone levels to base line, and with a progressive significant elevation in right atrial pressure. Thus, in dogs with an AV fistula and cardiac volume overload, chronic increases in atrial pressure appear to be a sustained stimulus for the release of ANF. It is suggested that following the initial period of sodium retention in this experimental mental model of heart failure, chronic endocrine adjustments for the reestablishment of sodium balance involve an increase in ANF which subsequently can exert a tonic inhibitory action on the renin-aldosterone axis. It is concluded that the ANF endocrine system might function as an effective chronic compensatory mechanism to help promote sodium and water excretion in dogs with an AV fistula through the suppression of the renin-aldosterone system and possibly through its direct renal actions.

scholarly journals External assessment of the EUROMACS right-sided heart failure risk score

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hirak Shah ◽  
Thomas Murray ◽  
Jessica Schultz ◽  
Ranjit John ◽  
Cindy M. Martin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Risk Score ◽  
Pressure Ratio ◽  
Area Under The Curve ◽  
Left Ventricular ◽  
Right Atrial ◽  
Risk Scores ◽  
External Assessment ◽  
Failure Risk

AbstractThe EUROMACS Right-Sided Heart Failure Risk Score was developed to predict right ventricular failure (RVF) after left ventricular assist device (LVAD) placement. The predictive ability of the EUROMACS score has not been tested in other cohorts. We performed a single center analysis of a continuous-flow (CF) LVAD cohort (n = 254) where we calculated EUROMACS risk scores and assessed for right ventricular heart failure after LVAD implantation. Thirty-nine percent of patients (100/254) had post-operative RVF, of which 9% (23/254) required prolonged inotropic support and 5% (12/254) required RVAD placement. For patients who developed RVF after LVAD implantation, there was a 45% increase in the hazards of death on LVAD support (HR 1.45, 95% CI 0.98–2.2, p = 0.066). Two variables in the EUROMACS score (Hemoglobin and Right Atrial Pressure to Pulmonary Capillary Wedge Pressure ratio) were not predictive of RVF in our cohort. Overall, the EUROMACS score had poor external discrimination in our cohort with area under the curve of 58% (95% CI 52–66%). Further work is necessary to enhance our ability to predict RVF after LVAD implantation.

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