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Biomedical subjects

T S Rector

Publications and source records attributed to T S Rector.

At least 37 records · Page 2Linked to original sources
PubMed1994

Endothelium-dependent vasodilation of peripheral conduit arteries in patients with heart failure.

Endothelium-dependent vasodilation of peripheral resistance vessels is abnormal in patients with heart failure, but there are little in vivo data on endothelium-dependent vasodilation of peripheral conduit vessels. This study assessed endothelium-dependent vasodilation of forearm conduit and resistance vessels in normal subjects and patients with heart failure. The effects of intraarterial endothelium-dependent and endothelium-independent vasodilators on both forearm conduit (brachial artery) and resistance vessels were assessed in 9 patients with New York Heart Association class II-III heart failure and 11 normal subjects of similar age. Brachial artery diameter was measured by two-dimensional, moderate-frequency (8 MHz) ultrasound, and forearm blood flow was measured by strain gauge plethysmography. The endothelium-dependent vasodilator, methacholine (0.3 and 1.5 micrograms/min), increased brachial artery diameter by 7.6 +/- 1.3% and 12.2 +/- 1.5% in normal subjects as compared to 6.9 +/- 2.1% and 10.4 +/- 2.4% in patients with heart failure (P = NS, normal vs heart failure). The endothelium-independent vasodilator, nitroglycerin (0.15 microgram), also produced similar increases in brachial artery diameter in the two groups (8.2 +/- 1.3% in normal subjects vs 11.1 +/- 1.4% in patients with heart failure, P = NS). In contrast, forearm blood flow responses to methacholine were significantly (P < .05) greater in normal subjects (4.1 +/- 0.5 and 9.2 +/- 1.4 mL/min/100 mL forearm volume) than in patients with heart failure (2.0 +/- 0.8 and 5.1 +/- 1.3 mL/min/100 mL forearm volume). Forearm blood flow responses to the endothelium-independent vasodilator, sodium nitroprusside, were similar between the two groups. This study suggests that endothelium-dependent and endothelium-independent vasodilation of the brachial artery is not impaired in patients with class II-III heart failure. This finding contrasts with abnormal endothelium-dependent vasodilation of forearm resistance vessels. These data suggest that there are regional differences in endothelial function in patients with heart failure.

Adult↗
PubMed1994

Effect of angiotensin II on noradrenaline release in the human forearm.

OBJECTIVE: The aim was to test the hypothesis that in normal humans angiotensin II would stimulate local release of noradrenaline under basal conditions or during a sympathetic stimulus provided by lower body negative pressure (LBNP). METHODS: Nine healthy volunteers received intra-arterial infusions of angiotensin II, 5 ng.min-1, into the non-dominant forearm. Forearm blood flow (strain gauge plethysmography) and regional noradrenaline spillover (using the tracer methodology of Esler) were measured during angiotensin II alone, LBNP alone, and LBNP plus angiotensin II. RESULTS: Angiotensin II and LBNP decreased forearm blood flow comparably: from 3.1(SD 1.5) to 2.4 (0.9) ml.100 g-1.min-1 during angiotensin II, p < 0.05; and from 3.3(1.5) to 2.5(1.0) ml.100 g-1.min-1 during LBNP, p < 0.05 (p = NS, A-II v LBNP). Angiotensin II had no effect on forearm venous noradrenaline or regional noradrenaline spillover. LBNP increased venous noradrenaline outflow from the forearm, from 1.6(0.40) to 2.1(0.6) nmol.min-1 (p < 0.05), while regional noradrenaline spillover tended to increase, rising from 1.5(0.8) to 2.0(1.0) nmol.100 ml-1.min-1. Angiotensin II did not enhance forearm blood flow or noradrenaline responses to LBNP. CONCLUSIONS: In the human forearm, mildly vasoconstrictor infusions of angiotensin II do not increase local release of noradrenaline, either alone or during mild LBNP. At least under these conditions, angiotensin II would not appear to be a potent influence on local sympathetic activity.

Angiotensin II↗
PubMed1994

Prognosis in congestive heart failure.

Prognostic variables such as the ejection fraction and peak oxygen consumption can be used to place patients with heart failure in risk strata. Some vasodilators have been shown to improve survival at all stages of heart failure with the probability of benefit increasing as the prognosis worsens. Quantitative estimates of survival among groups defined by prognostic variables and treatments should be used to make more informed benefit-to-risk assessments.

Death, Sudden, Cardiac↗
PubMed1993

Pulmonary and peripheral vascular factors are important determinants of peak exercise oxygen uptake in patients with heart failure.

OBJECTIVES: This study was conducted to determine the relations among exercise capacity and pulmonary, peripheral vascular, cardiac and neurohormonal factors in patients with chronic heart failure. BACKGROUND: The mechanisms of exercise intolerance in heart failure have not been fully clarified. Previous studies have indicated that peripheral factors such as regional blood flow may be more closely associated with exercise capacity than cardiac function, whereas the role of pulmonary function has received less attention. METHODS: Fifty patients with stable heart failure underwent a comprehensive assessment that included a symptom-limited maximal cardiopulmonary exercise test, right heart catheterization, pulmonary function tests, neurohormonal levels, radionuclide ventriculography and forearm blood flow at rest and after 5 min of brachial artery occlusion. Univariate and stepwise linear regression analyses were used to relate peak exercise oxygen uptake to indexes of cardiac, peripheral vascular, pulmonary and neurohormonal factors both alone and in combination. RESULTS: The mean ejection fraction was 19% and peak oxygen uptake was 16.5 ml/min per kg in this group of patients. By univariate analysis, there were no significant correlations between peak oxygen uptake and rest cardiac output, pulmonary wedge pressure, ejection fraction and pulmonary or systemic vascular resistance. In contrast, even in the absence of arterial desaturation during exercise, the forced expiratory volume in 1 s (r = 0.55, p < 0.001), forced vital capacity (r = 0.46, p < 0.01) and diffusing capacity for carbon monoxide (r = 0.47, p < 0.01) were all significantly associated with peak oxygen uptake. Peak postocclusion forearm blood flow (r = 0.45, p < 0.01), the corresponding minimal forearm vascular resistance (r = -0.56; p < 0.01) and plasma norepinephrine level at rest (r = -0.45; p < 0.01) were also significantly correlated with peak oxygen uptake. By multivariate analysis, minimal forearm vascular resistance and forced expiratory volume in 1 s were shown to be independently related to peak oxygen uptake, with a combined R value of 0.71. Other two-variate models included forced expiratory volume and plasma norepinephrine (R = 0.67) and forced expiratory volume and diffusing capacity (R = 0.65). Because forced vital capacity was highly correlated with forced expiratory volume in 1 s, it could be combined with the same variables to yield similar R values. Addition of any third variable did not improve these correlations. CONCLUSIONS: In comparison with rest indexes of cardiac performance, measures of pulmonary function and peripheral vasodilator capacity were more closely associated with peak exercise oxygen uptake in patients with heart failure. Furthermore, the associations were independent of each other and together accounted for 50% of the variance in peak oxygen uptake. These data suggest that pulmonary and peripheral vascular adaptations may be important determinants of exercise intolerance in heart failure.

Cardiac Catheterization↗
PubMed1993

Effects of cardiac transplantation on endothelium-dependent dilation of the peripheral vasculature in congestive heart failure.

Patients with congestive heart failure demonstrate attenuated endothelium-dependent vasodilation of the peripheral vasculature, but there are no data regarding the effect of therapies on this abnormality or whether this abnormality is reversible. This study was performed to address the hypothesis that abnormalities in endothelium-dependent vasodilation in heart failure are improved by heart transplantation. Forearm blood flow responses to the intraarterial administration of a dose range of methacholine, an endothelium-dependent vasodilator, and nitroprusside, an endothelium-independent vasodilator, were examined in 2 separate protocols. In protocol 1, forearm blood flow responses to methacholine in 14 heart transplant recipients were 5.02 +/- 3.11, 11.55 +/- 7.20 and 11.61 +/- 10.24 ml/min/100 ml forearm volume. These responses were significantly greater than those in 10 patients with heart failure (2.23 +/- 1.22, 4.60 +/- 3.43 and 6.70 +/- 4.91 ml/min/100 ml forearm volume; p < 0.05). In contrast, the responses to nitroprusside were nearly identical in the 2 groups. In protocol 2, six patients were studied before and 4 months (range 1 to 11) after transplantation. Methacholine responses before transplantation were 2.5 +/- 1.3, 5.2 +/- 1.5 and 7.3 +/- 1.5 ml/min/100 ml forearm volume and were significantly improved after transplantation to 5.7 +/- 1.2, 12.1 +/- 3.0 and 14.2 +/- 2.2 ml/min/100 ml forearm volume (p < 0.05). Peak reactive hyperemia responses increased significantly from 19.0 +/- 3.7 to 44.8 +/- 6.4 ml/min/100 ml forearm volume (p < 0.01) after transplantation. These data demonstrate that heart transplantation was associated with a significant improvement in the forearm blood flow responses to methacholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Assurance against drug-induced death in patients with heart failure.

Several recent studies of medications for heart failure have observed increased mortality in the treatment group. Historically, adequate data on mortality have not been provided to regulatory agencies, physicians, and patients. Simple confidence interval calculations suggest that from 5000 to more than 13,000 patients, depending on the mortality rate in the control group, would have to be studied in randomized controlled trials to exclude a risk of two to three drug-induced deaths per 100 patients treated. A sample size of less than 1000 patients would be needed to be confident that the incidence of drug-induced death is less than 10 per 100 treated if an agent truly had no effect on mortality. Guidelines for studies to provide estimates of the effect of a medication on mortality should be developed based in part on the relative values given to the benefits of an agent versus an increased risk of mortality.

Drug-Related Side Effects and Adverse Reactions↗
PubMed1993

Effects of norepinephrine on endothelium-dependent vasodilation of forearm resistance vessels.

BACKGROUND: Endothelium-dependent dilatation of forearm resistance vessels is attenuated in patients with heart failure. Activation of the sympathetic nervous system could cause this abnormality by way of vasoconstriction and chemical inactivation of nitric oxide. METHODS AND RESULTS: The effects of concurrent intra-arterial norepinephrine infusions (25, 50 and 100 ng/min) on forearm blood flow responses to equipotent doses of an endothelium-dependent vasodilator, methacholine (0.3 and 1.5 micrograms/min), and an endothelium-independent vasodilator, nitroprusside (1 and 5 micrograms/min), were studied in 12 normal subjects. Norepinephrine infusions increased the mean plasma norepinephrine from 255 pg/ml at baseline to 460, 629, and 1089 pg/ml, respectively. Basal forearm blood flow was reduced from 2.9 to 1.6 ml/min/100 ml of forearm volume at the highest dose (p < 0.01). The average response to the lowest dose of methacholine (4.5 ml/min/100 ml) was not significantly reduced by concurrent infusion of norepinephrine (4.4, 4.2, and 4.3 ml/min/100 ml, respectively), whereas the response to the higher dose of methacholine (8.9 ml/min/100 ml) tended to be lower (7.2, 6.7, and 7.4 ml/min/100 ml, respectively) but did not attain statistical significance. Methacholine induced vasodilation was not more sensitive to norepinephrine than nitroprusside responses. Lower body negative pressure (-20 mm Hg) also significantly reduced baseline forearm flow and increased plasma norepinephrine but did not effect either methacholine or nitroprusside induced vasodilation. CONCLUSION: Sympathetic stimulation induced by infusion of norepinephrine or lower body negative pressure is not a potent antagonist to endothelium-dependent vasodilation of the forearm vasculature. These data suggest that sympathetic activation does not completely explain the abnormal endothelium-dependent vasodilation seen in patients with heart failure.

Adult↗
PubMed1993

Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. The V-HeFT VA Cooperative Studies Group.

BACKGROUND: Congestive heart failure is a clinical syndrome characterized by neuroendocrine activation. Measurements of plasma norepinephrine and plasma renin activity were performed in the Vasodilator-Heart Failure Trial II (V-HeFT II) to characterize the effect of therapy on neuroendocrine activation and to examine the responses to therapy among patients with different degrees of activation. METHODS AND RESULTS: The baseline median plasma norepinephrine value (n = 743) was 490 pg/mL and the baseline median plasma renin activity (n = 737) was 6.9 ng.mL-1 x hr-1. Baseline plasma renin activity and plasma norepinephrine correlated poorly with each other (r = 0.12), implying that these two neuroendocrine systems are being activated by separate processes. By univariate analysis, the logarithms of the plasma norepinephrine (p < 0.0001) and the plasma renin activity (p = 0.01) were significantly related to all-cause mortality. In a multivariate analysis that included other significant univariate prognostic variables (i.e., baseline ejection fraction, peak oxygen consumption during exercise, and cardiothoracic ratio), log plasma norepinephrine but not plasma renin activity remained a significant (p = 0.02) predictor of mortality. Baseline plasma norepinephrine correlated poorly with baseline left ventricular ejection fraction (r = -0.18), peak oxygen consumption (r = -0.15), and cardiothoracic ratio (r = 0.11). Neither the plasma norepinephrine (r = 0.09) nor the plasma renin activity (r = 0.18) was closely associated with a quality of life assessment at baseline. The baseline plasma norepinephrine level in patients randomized to enalapril (mean, 593 +/- 388 [SD] pg/mL; n = 372) and to hydralazine and isosorbide dinitrate (mean, 544 +/- 297 pg/mL; n = 371) were similar. Thirteen weeks after randomization, plasma norepinephrine did not change (-5 +/- 393 pg/mL) in 312 patients randomized to enalapril but increased significantly by 74 +/- 311 pg/mL (p < 0.0001) in 300 patients assigned to hydralazine-isosorbide dinitrate. The plasma norepinephrine increased significantly more in patients assigned to hydralazine-isosorbide dinitrate than those on enalapril at both 13 weeks (p = 0.01) and at 1 year (p = 0.04) (90 +/- 302 pg/mL [n = 240] versus 14 +/- 376 pg/mL [n = 265]). Based on previous reports and examination of survival among several plasma norepinephrine strata, the baseline plasma norepinephrine data were grouped into three relatively homogeneous strata for further analysis. The cumulative mortality was significantly different between the three strata (p < 0.0001). The patients with plasma norepinephrine > 900 pg/mL had a higher mortality than those with corresponding values from 601 to 900 pg/mL or < 600 pg/mL. The survival benefit of enalapril compared with hydralazine-isosorbide dinitrate was most evident in those patients with a plasma norepinephrine value > 900 pg/mL. Although the plasma renin activity was not strongly associated with survival, patients in the upper quartile (> 16 ng.mL-1 x hr-1) had the worst prognosis. Among this group, the patients on enalapril demonstrated significantly better survival than those on hydralazine-isosorbide dinitrate (p = 0.02). CONCLUSIONS: This study confirms that plasma norepinephrine is an independent predictor of prognosis in patients with congestive heart failure. Hydralazine-isosorbide dinitrate treatment, unlike enalapril treatment, was associated with increased plasma norepinephrine concentration during the first year of follow-up. The enalapril group had a significantly lower mortality, and this survival benefit of enalapril as compared with hydralazine-isosorbide dinitrate was most evident among patients with the most marked neuroendocrine activation. Neuroendocrine activation is an important prognostic factor for patients with congestive heart failure and is an important determinant of the differential response to vasodilators.

Drug Therapy, Combination↗
PubMed1993

Evaluation by patients with heart failure of the effects of enalapril compared with hydralazine plus isosorbide dinitrate on quality of life. V-HeFT II. The V-HeFT VA Cooperative Studies Group.

BACKGROUND: Two new questionnaires concerning the quality of life of patients with heart failure were used in a randomized, controlled trial to determine if the patients' perceptions of the effects of enalapril on their daily activities and sense of well-being were different from those of a group treated with hydralazine and isosorbide dinitrate. METHODS AND RESULTS: The questionnaires were completed at baseline and at 3 months, 6 months, and subsequently every 6 months during follow-up, which averaged 2.5 years (range, 0.5-5.7 years). Data from the questionnaires were reliable as indicated by correlation coefficients between repeated baseline scores of 0.88 and 0.87. Both treatment groups showed a progressive deterioration in quality of life as measured by both questionnaires. The questionnaire scores of the two treatment groups were not significantly different at any follow-up visit. Furthermore, there were no differences between treatments among subgroups defined by baseline questionnaire scores, peak oxygen consumption, ejection fraction, previous vasodilator use, and plasma norepinephrine concentration. CONCLUSIONS: Although several factors may limit the generalization of these results, the lack of a difference with regard to patients' quality of life is an important consideration for the evaluation of the relative therapeutic efficacy of these vasodilators.

Attitude to Health↗
PubMed1992

Impaired forearm vasodilation to hyperosmolal stimuli in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy.

Patients with congestive heart failure (CHF) have impaired peripheral vasodilation during exercise. Hyperosmolality is one local stimulus that produces vasodilation during exercise in normal subjects. This study addressed the hypothesis that vasodilation to hyperosmolal stimuli is impaired in patients with CHF. Forearm blood flow responses to intrabrachial artery infusions of isoosmolar (280 mosm/kg) and hyperosmolal (480 and 660 mosm/kg) solutions of saline and glucose were compared in 9 patients with CHF and 13 normal subjects. Forearm blood flow was measured by strain gauge plethysmography. In the normal subjects, hyperosmolal infusions of 480 and 660 mosm/kg increased forearm blood flow by 3.12 +/- 0.40 and 6.80 +/- 0.67 ml/min/100 ml forearm volume, respectively (both p < 0.001 compared with isoosmolal infusions). In contrast, in the patients with CHF, these infusions increased forearm blood flow by 2.19 +/- 0.44 and 4.06 +/- 0.92 ml/min/100 ml forearm volume (p < 0.05 normal vs CHF). The impaired forearm blood flow responses in heart failure occurred despite significantly greater (p < 0.05, normal vs CHF) increases in venous osmolality (17.3 +/- 6.5 vs 9.6 +/- 1.3 mosm/kg for the 660 mosm/kg infusion). There were no differences between groups in forearm venous hematocrit, calcium, and sodium or potassium changes during hyperosmolal infusions. It is concluded that peripheral vasodilation to hyperosmolal stimuli is impaired in patients with CHF.

Adult↗
PubMed1992

Assessment of patient outcome with the Minnesota Living with Heart Failure questionnaire: reliability and validity during a randomized, double-blind, placebo-controlled trial of pimobendan. Pimobendan Multicenter Research Group.

To determine the reliability and validity of a patient outcome questionnaire for chronic heart failure, a randomized, double-blind, placebo-controlled, 3-month trial of pimobendan, an investigational medication with inotropic and vasodilator activities, was performed. Evaluated were 198 ambulatory patients with primarily New York Heart Association (NYHA) class III heart failure from 20 referral centers. Baseline therapy included digoxin, diuretics and, in 80%, a converting enzyme inhibitor. Oral pimobendan at 2.5 (n = 49), 5.0 (n = 51), or 10 (n = 49) mg daily or matching placebo (n = 49) was administered. The Minnesota Living with Heart Failure (LIhFE) questionnaire was a primary outcome measure, along with an exercise test. Interitem correlations identified subgroups of questions representing physical and emotional dimensions. Repeated baseline scores were highly correlated (r = 0.93), as were the physical (r = 0.89) and emotional (r = 0.88) dimension scores. Placebo did not have a significant effect with median (25th, 75th percentile) changes from baseline scores of 1 (-3, 5), 1 (-2, 3), and 0 (-1, 2), respectively (all p values greater than 0.10). The 5 mg dose significantly improved the total score, 7.5 (0, 18; p = 0.01) and the physical dimension, 4 (0, 8; p = 0.01), compared with placebo. Changes in the total (r = 0.33; p less than 0.01) and physical (r = 0.35; p less than 0.01) scores were weakly related to changes in exercise times, but corresponded well with changes in patients' ratings of dyspnea and fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1991

Local forearm vasodilation with intra-arterial administration of enalaprilat in humans.

To determine whether converting enzyme inhibitors could produce peripheral vasodilation through a local mechanism, we infused enalaprilat, 2 micrograms/min/dl forearm volume (FAV), into the brachial artery of normal subjects and measured changes in forearm blood flow (FBF) with strain-gauge plethysmography. Enalaprilat produced a peak increase in FBF of 2.82 +/- 0.54 ml/min/dl FAV (78% increase) at 1 minute (p less than 0.01 versus vehicle) and an increase of 1.11 +/- 0.28 ml/min/dl FAV at 4 minutes (p less than 0.05 versus vehicle). Blood pressure and plasma renin activity measured at the completion of infusion did not change. Intravenous enalaprilat infusion at the same dose in seven additional normal subjects did not increase FBF. Pretreatment of seven subjects with 75 mg oral indomethacin attenuated the peak response to enalaprilat (4.13 +/- 1.52 versus 0.58 +/- 0.32 ml/min/dl; p less than 0.05). We conclude that intra-arterial enalaprilat produces an increase in FBF in normal subjects. This peripheral vasodilation is caused by a local effect independent of circulating renin-angiotensin system inhibition. This response is attenuated by indomethacin, suggesting that prostaglandins contribute to the vasodilator response.

Blood Pressure↗
PubMed1991

Endothelium-dependent vasodilation is attenuated in patients with heart failure.

BACKGROUND: Endothelial cells produce a number of substances, collectively termed endothelium-derived relaxing factor (EDRF), that promote local relaxation of vascular smooth muscle. Although studies have demonstrated defects in endothelium-dependent vasodilation in animal models of hypertension, atherosclerosis, and heart failure, there are only limited data from human subjects because of the difficulty in obtaining fresh vascular segments. METHODS AND RESULTS: To address the hypothesis that endothelium-dependent vasodilation is attenuated in patients with heart failure, we measured forearm blood flow responses to the intra-arterial administration of methacholine, a known stimulus of EDRF release through muscarinic receptors. In 14 normal subjects, a dosage range of methacholine increased forearm blood flow by 5.26 +/- 0.63, 10.50 +/- 0.63, and 13.22 +/- 0.86 ml/min/100 ml forearm volume (FAV); these responses were 1.98 +/- 0.46, 5.48 +/- 0.79, and 8.50 +/- 1.53 ml/min/100 ml FAV in 14 patients with heart failure. When pooled over all doses, the responses were strikingly less in the patients with heart failure (5.32 +/- 0.31 versus 9.52 +/- 0.60 ml/min/100 ml FAV; p = 0.0003). In a second study, the average difference in forearm blood flow responses between patients with heart failure and normal subjects with methacholine was significantly greater than the average difference between the groups with nitroprusside (4.04 +/- 1.10 versus 2.20 +/- 0.71 ml/min/100 ml FAV; p = 0.04). The decreased methacholine responses in the patients with heart failure were not related to age (r = 0.39; p = NS) or etiology because there was no difference in the responses between patients with ischemic heart disease and those with idiopathic cardiomyopathy. CONCLUSIONS: These data suggest that endothelium-dependent vasodilation is attenuated in patients with heart failure. Although the mechanisms of the decreased endothelium-dependent responses in heart failure are not known, this impaired local vasodilation may contribute to abnormalities in vasoconstriction that are characteristic of heart failure.

Adult↗
PubMed1990

Cardiovascular and neurohormonal effects of atrial natriuretic peptide in conscious dogs with and without chronic left ventricular dysfunction.

Atrial natriuretic peptide (hANP 4-28) was infused for 1 h (0.3 microgram/kg/min) in 11 normal awake dogs and seven awake dogs with chronic left ventricular dysfunction, induced 16 weeks earlier by repetitive DC shock. The responses were similar in the two groups and included decreases in arterial pressure (107-99 mm Hg), heart rate (83-72 beats/min), and cardiac output (3.6-2.8 L/min), without changes in right or left ventricular filling pressures. Systemic vascular resistance (SVR) tended to rise during the infusion and was significantly increased (2,847-3,442 dyn s cm-5, p less than .05) during the postinfusion recovery period. Regional blood flows (microspheres) during infusion revealed a decrease in skin and splanchnic flow. Despite the apparent vasoconstrictor effect, plasma norepinephrine (PNE), renin activity (PRA), and arginine vasopressin (AVP) levels all fell during ANP infusion. These data suggest that ANP exerts a cardioinhibitory effect, possibly similar to that of arginine vasopressin (AVP), and that the net systemic vasoconstrictor effect of ANP in these dogs is mediated by a complex interrelationship between direct vascular effects, neurohormonal inhibition, and central reflex activation.

Animals↗
PubMed1990

Atrial natriuretic factor attenuates sympathetic reflexes during lower body negative pressure in normal men.

To assess further the effects of atrial natriuretic factor on autonomic nervous system reflexes in normal humans, the hemodynamic and neurohormonal responses to lower body negative pressure were measured at control and during infusions of atrial natriuretic factor and nitroglycerin in nine normal male subjects. The control -20 mm Hg lower body negative pressure was characterized by significant reductions in right atrial and pulmonary wedge pressures, as well as stroke volume and cardiac output. This was associated with a reflex increase in forearm vascular resistance and plasma norepinephrine. During the infusion of atrial natriuretic factor, the same -20 mm Hg lower body negative pressure produced a larger decrease in mean arterial pressure of 7.9 +/- 3.9 mm Hg (p less than 0.05), as well as a larger decrease in stroke volume (41.3 +/- 4.2 ml/beat) and cardiac output (2.0 +/- 0.3 L/min). Atrial natriuretic factor infusion did not affect the increase in forearm vascular resistance during lower body negative pressure, but did attenuate the increase in plasma norepinephrine. To control for nonspecific vasodilator actions, lower body negative pressure was also repeated during nitroglycerin infusion. Nitroglycerin infusion did not significantly change the responses of blood pressure, cardiac output, stroke volume, forearm vascular resistance, or plasma norepinephrine during lower body negative pressure. Thus, these data demonstrate that atrial natriuretic factor infusion can attenuate sympathetic nervous system reflexes evoked during lower body negative pressure. These inhibitory effects on the sympathetic nervous system may contribute to many of the observed hemodynamic actions of atrial natriuretic factor.

Aged↗
PubMed1990

Outcome assessment: functional status measures as therapeutic endpoints for heart failure.

The role of measures of patients' functional status during chronic heart failure is to bridge the outcome information gap between physiologic assessments and the goal of medical care, which is to prolong the patient's life with minimal disability due to the syndrome and subsequent health care. The methods of rigorously developing and applying patient questionnaires as outcome measures will be unfamiliar to many health care providers. Many health care providers trained with different perspectives probably have an incredulous view of patient evaluations. What have we accomplished, though, if patients cannot perceive a net benefit from our services? In the final analysis, the patients' outcome assessments, collected in a systematic and unbiased manner, rather than the proxy measures used by health care providers, are the bottom line.

Activities of Daily Living↗
PubMed1990

Impact of a drug-use review program intervention on prescribing after publication of a randomized clinical trial.

The effect of a drug-use review (DUR) program intervention on physician prescribing after the results of a randomized clinical trial were published was studied. A Veterans Administration (VA) cooperative study published in June 1986 showed that congestive heart failure (CHF) patients who had hydralazine and isosorbide added to their drug therapy had less mortality than patients given digoxin and diuretics with or without prazosin. Physicians with at least one CHF patient who was receiving the less effective therapy were randomly assigned to intervention and control groups. In September 1986, intervention-group physicians (n = 288) were mailed a letter and questionnaire from the DUR program coordinator, the journal article, and a drug history profile of a CHF patient who might benefit from the information. Control physicians received no mailing. The questionnaire asked whether the physicians already knew about the VA study, intended to alter their prescribing, and could identify factors that would affect their decision. Two thirds of intervention-group physicians were already aware of the VA study. One third indicated that they intended to alter drug therapy based on the study results; factors significantly associated with the intent to adopt a change were physician training and experience, comments by peers, new drug availability, and the size of the reduction in mortality. During four months after the intervention, only 5 physicians in the two groups switched their patients to both hydralazine and isosorbide (full change); 23 switched them to at least one of the drugs or discontinued prazosin (partial change). There was no significant difference in the number of full or partial changes between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Attitude of Health Personnel↗