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Biomedical subjects

M M Redfield

Publications and source records attributed to M M Redfield.

At least 55 records · Page 3Linked to original sources
PubMed1997

Congestive heart failure in elderly patients.

The prevalence of congestive heart failure (CHF) is increasing. Most patients with CHF are elderly, and CHF is the most common dismissal diagnosis in elderly hospitalized patients. As many as 50% of elderly patients with heart failure may have normal systolic function and isolated diastolic heart failure. Assessment and management of elderly patients are complicated by comorbidities, increased susceptibility to side effects, and concerns about the appropriate use of costly and invasive procedures. The basics of the approach to the evaluation and management of heart failure in elderly patients are reviewed.

Age Distribution↗
PubMed1996

Noninvasive doppler echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: a simultaneous Doppler echocardiographic and cardiac catheterization study.

OBJECTIVES: The purpose of this study was to examine the relation of the mitral flow velocity curves to left ventricular filling pressures in patients with two different types of myocardial problems: hypertrophic cardiomyopathy and severe left ventricular systolic dysfunction. BACKGROUND: Previous studies have suggested that assessment of Doppler-derived mitral flow velocity curves can be used to predict left ventricular filling pressures in specific disease entities. However, it is unclear whether information derived from specific mitral flow velocity curves obtained from one disease entity can be valid in other disease states. METHODS: The study group consisted of 42 patients with left ventricular systolic dysfunction (group A) and 55 patients with hypertrophic cardiomyopathy (group B); both groups underwent simultaneous cardiac catheterization and were studied by Doppler echocardiography. High fidelity measures of left atrial and left ventricular pressures were obtained simultaneously with mitral flow velocity curves. RESULTS: There was a significant relation between the Doppler echocardiographic variables and mean left atrial pressure in group A patients. The left atrial pressure was directly related to the E/A ratio (r = 0.49, p = 0.004) and inversely related to the deceleration time (r = 0.73, p < 0.001). The sensitivity and specificity of the deceleration time, < 180 m/s, which indicated a mean left atrial pressure > or = 20 mm Hg, were both 100%. In group B patients, there was no significant relation between mean left atrial pressure and deceleration time. CONCLUSIONS: Doppler echocardiographic mitral flow velocity curves are useful in predicting and estimating left ventricular filling pressures in patients with left ventricular dysfunction. However, because of the complexity of the multiple interrelated factors that determine diastolic filling of the left ventricle, these flow velocity curves cannot be used in patients with other disease entities, such as hypertrophic cardiomyopathy. Future studies of different disease states are necessary to fully understand the role of Doppler echocardiography in the assessment of diastolic filling.

Adult↗
PubMed1996

Assessment of mean left atrial pressure from the left ventricular pressure tracing in patients with cardiomyopathies.

The direct measurement of mean left atrial pressure is difficult and the ability to assess mean left atrial pressure from the left ventricular (LV) pressure tracing obtained at cardiac catheterization is clinically useful. The current study describes the limitations of using LV pre-a-wave pressure or LV end-diastolic pressure to estimate mean left atrial pressure and describe another index, mean LV diastolic pressure, which provides a better assessment of mean left atrial pressure.

Atrial Function, Left↗
PubMed1996

Cardiac secretion of adrenomedullin in human heart failure.

Adrenomedullin (ADM) is a newly discovered endogenous vasorelaxing and natriuretic peptide. Recently, we have reported that plasma ADM is increased in severe congestive heart failure (CHF) in humans and that increased immunohistochemical staining is observed in the failing human ventricular myocardium. The present study was designed to test the hypothesis that the failing human ventricle secretes ADM and that circulating ADM progressively increases with the severity of clinical CHF. Plasma ADM was significantly increased in human CHF (39.8 +/- 3.6 pg/ml, P < 0.001 vs. normal) as compared with normal subjects (14.4 +/- 2.7 pg/ml). Plasma ADM was increased in mild CHF (NYHA class II, 30.1 +/- 3.4 pg/ml, P < 0.01 vs. normal), moderate CHF (NYHA class III, 31.5 +/- 3.0 pg/ml, P < 0.01 vs. normal), and severe CHF (NYHA class IV, 66.1 +/- 9.4 pg/ml, P < 0.001 vs. normal). In 13 patients with CHF in whom plasma samples were obtained from aorta (AO), coronary sinus (CS) and anterior interventricular vein (AIV), there was a significant step-up in plasma ADM between AO and AIV (50.6 +/- 9.3 pg/ml and 62.1 +/- 11.1 pg/ml, respectively, P < 0.01) and between AO and CS (50.6 +/- 9.3 pg/ml and 58.6 +/- 11.4 pg/ml, respectively, P < 0.05). The current study demonstrates that the failing human heart secretes ADM in human CHF suggesting contribution to the increase in plasma ADM, and indicates for the first time an additional endocrine system of cardiac origin which is activated in human CHF and may function in cardiorenal regulation.

Adrenomedullin↗
PubMed1996

Doppler evaluation of patients with constrictive pericarditis: use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction.

OBJECTIVES: This study sought to examine the value of analyzing Doppler echocardiographically derived tricuspid regurgitation signals during respiration in relation to the diagnosis of constrictive pericarditis. BACKGROUND: A physiologic hallmark of constrictive pericarditis is enhanced ventricular interdependence, which produces reciprocal changes in right and left ventricular filling and ejection dynamics during the respiratory cycle. It was hypothesized that these changes could be detected noninvasively by analyzing Doppler echocardiographically derived tricuspid regurgitation signals and that this information could assist in noninvasively diagnosing constrictive pericarditis. METHODS: Simultaneous Doppler echocardiography and catheterization studies of the right and left sides of the heart with high fidelity pressure manometers were performed in 5 patients with surgically confirmed constrictive pericarditis and 12 patients (control subjects) with heart failure due to other causes. RESULTS: Changes observed in tricuspid regurgitation Doppler echocardiographic variables from onset to peak inspiration in patients with constrictive pericarditis were significantly different from those in control subjects. Mean (+/- SD) percent change in maximal tricuspid regurgitation velocity was 13% +/- 6% and -8% +/- 7% in the constrictive pericarditis and control groups, respectively (p < 0.0001); mean percent change in tricuspid regurgitation signal duration was 18% +/- 2% and -2% +/- 7%, respectively (p < 0.0001); mean percent change in tricuspid regurgitation time velocity integral was 27% +/- 15% and -10% +/- 12%, respectively (p < 0.0001). CONCLUSIONS: Respiratory changes in Doppler echocardiographically derived tricuspid regurgitation peak velocity and velocity duration are increased in patients with constrictive pericarditis and may be helpful in diagnosing this condition noninvasively.

Aged↗
PubMed1996

Analysis of left ventricular diastolic function.

Our understanding of left ventricular diastolic function has evolved with our understanding of Doppler echocardiographic assessment of left ventricular filling dynamics. Left ventricular diastolic function consists of several variables which affect the Doppler echocardiographic recordings in a complex way. While there are still limitations with the non-invasive assessment of left ventricular diastolic function and filling pressures by Doppler echocardiography, great progress has been made and careful interpretation of properly obtained Doppler recordings can give clinically relevant information concerning left ventricular diastolic function, filling pressures, and prognosis in patients with cardiac disease.

Diastole↗
PubMed1996

Ventricular remodeling during development and recovery from modified tachycardia-induced cardiomyopathy model.

This study was designed to characterize left ventricular (LV) function and mass in a modified cardiomyopathy model in the dog in which right ventricular pacing rates are gradually increased throughout 38 days. On the last day of the pacing protocol, ejection fraction was reduced (25 +/- 3 vs. 60 +/- 1%) and LV end-diastolic diameter index (a ratio of LV end-diastolic diameter to body weight, 2.09 +/- 0.02 vs. 1.79 +/- 0.08 mm/kg) and LV mass index (a ratio of LV mass to body weight, 5.2 +/- 0.3 vs. 4.3 +/- 0.2 g/kg) were greater than in the normal dogs (P < 0.05, respectively). Cardiac filling pressures increased, and LV diastolic function and coronary blood flow were impaired. After 4 wk of recovery from the progressive pacing protocol, LV end-diastolic diameter index (2.12 +/- 0.06 mm/kg) and LV mass index (5.6 +/- 0.2 g/kg) remained increased. Ejection fraction was improved (38 +/- 4%) but still depressed. LV diastolic function, coronary blood flow, and cardiac filling pressures returned to levels seen in the normal dogs. This modified cardiomyopathy model associated with LV hypertrophy complements the conventional tachycardia-induced cardiomyopathy model without LV hypertrophy.

Animals↗
PubMed1996

Angiotensin II in the evolution of experimental heart failure.

Although angiotensin II (Ang II) has been implicated in the pathophysiology of congestive heart failure, its temporal and regional changes during the development and progression of the disease are poorly defined. Our objective was to assess circulating, renal, cardiac, and vascular Ang II in a canine model of rapid ventricular pacing-induced heart failure that evolves from early left ventricular dysfunction to overt congestive heart failure. Ang II was measured by radioimmunoassay with low cross-reactivity to other angiotensins. Control, early left ventricular dysfunction, and overt congestive heart failure dogs were studied. Early left ventricular dysfunction was characterized by impaired cardiac function, cardiac enlargement, preserved renal perfusion pressure, maintained urinary sodium excretion, and normal plasma renin activity. Overt congestive heart failure was characterized by further impaired cardiac function and cardiac enlargement, reduced renal perfusion pressure, urinary sodium retention, and increased plasma renin activity and plasma Ang II. In early left ventricular dysfunction dogs, renal cortical, renal medullary, ventricular, and aortic Ang II were unchanged, and atrial Ang II was decreased. In overt congestive heart failure dogs, Ang II was increased in the kidney and heart compared with normal dogs and in all tissues compared with early left ventricular dysfunction dogs. The greatest increase in tissue Ang II occurred in the renal medulla. We conclude that early increases in local renal, myocardial, and vascular Ang II do not occur in this model of early left ventricular dysfunction and may even be suppressed. In contrast, increased myocardial and particularly renal Ang II in association with increased circulating Ang II are hallmarks of overt experimental congestive heart failure. These studies provide new insights into the temporal and regional alterations in Ang II during the progression of experimental congestive heart failure.

Angiotensin II↗
PubMed1996

Superiority of brain natriuretic peptide as a hormonal marker of ventricular systolic and diastolic dysfunction and ventricular hypertrophy.

Atrial and brain natriuretic peptides (ANP and BNP) are produced by the heart, and their plasma concentrations are increased in human chronic congestive heart failure. Although separate studies have suggested that circulating levels of the biologically active C-terminal ANP, the biologically inactive N-terminal ANP, and BNP may have diagnostic utility in the detection of left ventricular systolic dysfunction or left ventricular hypertrophy, no studies have directly assessed the relative value of these peptides prospectively. We therefore designed this study to compare the relative ability of the different natriuretic peptides to detect abnormal left ventricular systolic and diastolic function and left ventricular hypertrophy. Using a prospective study design, we investigated 94 patients referred for cardiac catheterization and 15 age-matched normal subjects. The diagnostic abilities of elevated plasma C-terminal ANP, N-terminal ANP-(1-30), and BNP concentrations to identify systolic dysfunction (ejection fraction < 45%), diastolic dysfunction (time constant of left ventricular relaxation > 55 milliseconds, left ventricular end-diastolic pressure > 18 mm Hg), and left ventricular hypertrophy (left ventricular mass index > 120 g/m2) were objectively compared by receiver operating characteristic analysis. The areas under the receiver operating characteristic curve of BNP for detecting each of these abnormalities ranged from 0.715 to 0.908 and were significantly greater than those of C-terminal ANP or N-terminal ANP-(1-30). The sensitivity and specificity of an elevated plasma BNP, which we defined as greater than the mean + 3 SD of the 15 age-matched normal subjects, were 0.83 and 0.77, respectively, for detecting ejection fraction less than 45%, 0.85 and 0.70 for detecting the time constant of left ventricular relaxation greater than 55 milliseconds, 0.63 and 0.76 for detecting left ventricular end-diastolic pressure greater than 18 mm Hg, and 0.81 and 0.85 for detecting left ventricular mass index greater than 120 g/m2. The use of BNP and one other peptide increased sensitivity (0.90 to 0.96), albeit with lower specificity (0.56 to 0.71). An elevated plasma BNP was a more powerful marker of left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and left ventricular hypertrophy than C-terminal ANP or N-terminal ANP-(1-30) in this population of patients with suspected cardiac disease. Measurement of BNP alone or in combination with C-terminal ANP or N-terminal ANP-(1-30) has potential utility for the detection of altered left ventricular structure and function in a patient population at risk for cardiovascular disease.

Aged↗
PubMed1995

Effect of low dose aspirin on cardiorenal function and acute hemodynamic response to enalaprilat in a canine model of severe heart failure.

OBJECTIVES: This study examined the effect of low dose aspirin on cardiorenal and neurohumoral function and on the acute hemodynamic response to enalaprilat in a canine model of heart failure. BACKGROUND: Low dose aspirin is frequently prescribed for patients with systolic dysfunction who also benefit from angiotensin-converting enzyme inhibition. Although high doses of potent cyclo-oxygenase inhibitors cause fluid retention and vaso-constriction and antagonize the effects of angiotensin-converting enzyme inhibitors, the effects of low dose aspirin in heart failure are unknown. METHODS: A model of heart failure was produced in 11 mongrel dogs by rapid ventricular pacing (250 beats/min for 12 to 14 days). Five dogs received 325 mg aspirin/day for the final 4 days of pacing before the acute experiment; six control dogs received no aspirin. Cardiorenal and neurohumoral function was measured during chloralose anesthesia. Hemodynamic and renal responses to enalaprilat were assessed. RESULTS: Both groups demonstrated severe heart failure with decreased cardiac output; increased atrial pressures and systemic resistance; activation of plasma renin activity, aldosterone and atrial natriuretic factor; and sodium retention. Low dose aspirin had no detrimental effect on cardiorenal or neurohumoral function. Mean arterial pressure, pulmonary capillary wedge pressure and systemic vascular resistance decreased to a similar degree with enalaprilat in both groups. There was no difference between the groups with respect to renal response to enalaprilat. CONCLUSIONS: The present study demonstrates that low dose aspirin has no adverse effect on hemodynamic, neurohumoral or renal function in heart failure. Furthermore, aspirin has no adverse effect on the acute response to enalaprilat. These findings suggest that there is no contraindication to concomitant treatment with low dose aspirin and angiotensin-converting enzyme inhibitors in humans with heart failure.

Aldosterone↗
PubMed1995

Long-term outcome of patients with biopsy-proved myocarditis: comparison with idiopathic dilated cardiomyopathy.

OBJECTIVES: The study objectives were 1) to assess the long-term outcome of patients with biopsy-proved lymphocytic myocarditis (Dallas criteria), and 2) to compare the outcome of these patients with that of patients with idiopathic dilated cardiomyopathy. BACKGROUND: Endomyocardial biopsy is frequently performed in patients presenting with dilated cardiomyopathy to identify lymphocytic myocarditis. Most previous studies of the natural history of myocarditis were performed before the establishment of the Dallas criteria. Thus, it is important to evaluate the prognostic value of positive endomyocardial biopsy findings in patients presenting with dilated cardiomyopathy, using standardized criteria for lymphocytic myocarditis. METHODS: All endomyocardial biopsy results from the Mayo Clinic (October 1979 to April 1988) with a diagnosis of myocarditis were reclassified according to the Dallas criteria. Patients whose biopsy specimens showed borderline or lymphocytic myocarditis were included in the study group; those with systemic inflammatory diseases known to be associated with myocardial involvement were excluded. Study group survival was compared with that for a cohort of patients with idiopathic dilated cardiomyopathy seen at the Mayo Clinic from 1976 to 1987 who had endomyocardial biopsy findings negative for myocarditis. RESULTS: Biopsy specimens from 41 patients met the Dallas criteria for a diagnosis of myocarditis (n = 28) or borderline myocarditis (n = 13). Of these 41 patients, 9 were excluded because of the presence of systemic diseases known to be associated with myocarditis, and 5 patients were excluded because of lack of available follow-up data. The myocarditis study group therefore included 27 patients (10 with borderline myocarditis, 17 with myocarditis). Fifty-eight patients with a diagnosis of idiopathic dilated cardiomyopathy who underwent endomyocardial biopsy served as the comparison cohort. Ejection fraction was lower in patients with idiopathic dilated cardiomyopathy ([mean +/- SD] 25 +/- 11%) than in those with myocarditis (38 +/- 19%, p = 0.001), even though a higher proportion of myocarditis group patients were in New York Heart Association functional class III or IV (63%) than patients in the dilated cardiomyopathy group (30%, p = 0.005). There was no difference in 5-year survival rate between the myocarditis and idiopathic dilated cardiomyopathy groups (56% vs. 54%, respectively). CONCLUSIONS: This study demonstrates that the long-term outcome of patients with biopsy-proved myocarditis seen in a referral setting is poor, although no different from that of patients with idiopathic dilated cardiomyopathy. With the current lack of proved effective treatment for lymphocytic myocarditis and no demonstration of survival benefit for patients with myocarditis, these data suggest that endomyocardial biopsy performed to exclude myocarditis is of limited prognostic value in the routine evaluation of dilated cardiomyopathy.

Adult↗
PubMed1995

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50 +/- 11 vs. 158 +/- 37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4 +/- 2.4 vs. 0.6 +/- 0.4 ng/ml per h, P < 0.05) and aldosterone (36.4 +/- 12.5 vs. 2.5 +/- 0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion and regulation of the RAAS in experimental ELVD.

Aldosterone↗
PubMed1994

Clearance receptor-mediated control of atrial natriuretic factor in experimental congestive heart failure.

Circulating atrial natriuretic factor (ANF) is regulated by clearance receptors (ANFR-C). C-ANF-(4-23) is a ring-deleted analogue of ANF, which binds specifically to ANFR-C. The present studies were undertaken to determine total metabolic (TMCR), pulmonary (PCR), and renal clearance rates (RCR) of ANF in a group of seven mongrel dogs in chronic congestive heart failure (CHF) in comparison with a control group (n = 6). TMCR was not altered in CHF [1,534 +/- 319 vs. control: 1,735 +/- 208 ml/min; P = not significant (NS)] in association with an elevation of circulating endogenous ANF (206 +/- 44 vs. control: 36 +/- 10 pg/ml; P < 0.01). Infusion of C-ANF-(4-23) reduced TMCR in both groups similarly (CHF: 753 +/- 134 vs. control: 972 +/- 156 ml/min; P = NS). PCR was lower in CHF (286 +/- 431 vs. 1,672 +/- 407 ml/min; P < 0.05), whereas RCR was not different (10 +/- 24 vs. control: 15 +/- 25 ml/min; P = NS). ANFR-C blockade did not facilitate urinary sodium excretion in CHF. These studies demonstrate that 1) TMCR does not contribute to elevated endogenous ANF in CHF; 2) total functional activity of the clearance receptor pathway is preserved in CHF; and 3) renal ANF metabolism and the clearance receptor pathway are not linked to the avid sodium retention and renal ANF resistance observed in chronic CHF.

Animals↗
PubMed1993

Atrial natriuretic peptide in heart failure.

Atrial natriuretic peptide hormone of cardiac origin, which is released in response to atrial distension and serves to maintain sodium homeostasis and inhibit activation of the renin-angiotensin-aldosterone system. Congestive heart failure is a clinical syndrome characterized by increased cardiac volume and pressure overload with an inability to excrete a sodium load, which is associated with increased activity of systemic neurohumoral and local autocrine and paracrine mechanisms. Circulating atrial natriuretic peptide is greatly increased in congestive heart failure as a result of increased synthesis and release of this hormone. Atrial natriuretic peptide has emerged as an important diagnostic and prognostic serum marker in congestive heart failure. In early heart failure, it may play a key role in preserving the compensated state of asymptomatic left ventricular dysfunction. Despite increased circulating atrial natriuretic peptide in heart failure, the kidney retains sodium and is hyporesponsive to exogenous and endogenous atrial natriuretic peptide. The mechanism for the attenuated renal response is multifactorial and includes renal hypoperfusion, activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. Therapeutic strategies to potentiate the biologic actions of atrial natriuretic peptide may prolong the asymptomatic phase and delay progression to overt congestive heart failure.

Animals↗
PubMed1993

Natural history of idiopathic dilated cardiomyopathy: effect of referral bias and secular trend.

OBJECTIVES: The current study was designed to determine the effect of secular trend and referral bias on the natural history of idiopathic dilated cardiomyopathy. BACKGROUND: In a previous study of 104 patients with idiopathic dilated cardiomyopathy conducted in a referral population at the Mayo Clinic between 1960 and 1973, the 1- and 5-year mortality rates were 31% and 64%, respectively. A recent study of 40 patients with idiopathic dilated cardiomyopathy conducted in a population-based cohort at the Mayo Clinic between 1975 and 1984 reported 1- and 5-year mortality rates of 5% and 20%, respectively. We hypothesized that improvements in diagnosis and therapy have occurred since the original referral cohort was described and that these improvements have altered the apparent natural history of the disease. We refer to this effect as secular trend. Alternatively, the presence of more advanced disease in the referral population (referral bias) may also contribute to the differences in survival. METHODS: Two sequential referral populations with idiopathic dilated cardiomyopathy seen at the Mayo Clinic between 1976 and 81 (n = 85) and 1982 and 1987 (n = 137) were identified. Outcome was compared between these cohorts and the 1960-1973 referral cohort to examine the effect of secular trend. Outcomes were compared with that of the population-based cohort to examine the effect of referral bias. RESULTS: Survival in the 1976-1981 referral cohort did not differ from that in the 1960-1973 referral cohort, suggesting little impact of secular trend during these time periods. Survival in the more recent 1982-1987 referral cohort was significantly better than that in the earlier referral cohorts, suggesting that improvements in diagnosis and treatment in the 1980s altered the natural history of idiopathic dilated cardiomyopathy. Survival in the 1982-1987 referral cohort was still worse than that of the population-based cohort, suggesting an effect of referral bias on studies of the natural history of idiopathic dilated cardiomyopathy. CONCLUSIONS: The current study demonstrates that secular trend and referral bias affect the apparent natural history of idiopathic dilated cardiomyopathy. Survival in referral patients with this disease is significantly better than previously described.

Bias↗
PubMed1993

Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.

BACKGROUND: Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin-aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably "asymptomatic" ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. METHODS AND RESULTS: ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48 +/- 2 to 29 +/- 4%), cardiac output (4.64 +/- 0.29 to 2.89 +/- 0.17 L/min), and mean arterial pressure (119 +/- 4 to 108 +/- 4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60 +/- 19 to 165 +/- 27 pg/mL) and norepinephrine (382 +/- 127 to 690 +/- 211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion before producing ALVD. CONCLUSIONS: The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

Animals↗