Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The haemodynamic effects of fazadinium were compared in two groups of elderly patients with class III functional heart failure about to undergo gastrointestinal surgery. Four patients were in sinus rhythm and four in atrial fibrillation. Following the assessment of baseline values fazadinium 1 mg kg-1 was injected i.v. and measurements obtained every 1 min for 15 min. In patients in sinus rhythm, fazadinium produced a decrease in total peripheral resistance, which was maximum at the 1st min (delta TPRI -738 +/- 88 dyn s cm-5 m2) and accompanied by a moderate decrease in arterial pressure (MAP -27 +/- 2.4 mm Hg) and cardiac index (delta CI -0.23 +/- 0.17 litre min-1 m-2) and a moderate increase in heart rate (delta HR +16 +/- 5.7 beat min-1). In patients in atrial fibrillation, a similar decrease in total peripheral resistance (delta TPRI -1160 +/- 174 dyn cm-5 m2) was accompanied by a significantly more pronounced tachycardia (delta HR +71 +/- 5.1 beat min-1) (P less than 0.001) and decreases in arterial pressure (delta MAP -51.7 +/- 5.9 mm Hg) (P less than 0.01) and stroke index (P less than 0.02).
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PMID:Influence of cardiac rhythm on the haemodynamic effects of fazadinium in patients with heart failure. 613 37

In low-output cardiac failure with hypertension developing early after aortocoronary surgery, the currently preferred vasodilators nitroglycerin and nitroprusside proved to be equally successful and safe for the closed-loop control of mean arterial pressure. With NP- and NTG-induced MAP reduction to the present level of 80 mm Hg cardiac index increased similarly from 2.0 +/- 0.35 to 2.4 +/- 0.3 l/min/m2 (p less than 0.05) and from 1.9 +/- 0.29 to 2.2 +/- 0.26 l/min/m2 (p less than 0.05), respectively. Once adequate blood pressure fall was obtained, the addition of dobutamine at 6 micrograms/kg/min resulted under maintenance doses of NP and NTG averaging 1.6 +/- 0.4 and 4.6 +/- 1.8 micrograms/kg/min, respectively. A further improvement of cardiac performance manifested itself by cardiac index rise to 3.4 +/- 0.4 l/min/m2 (p less than 0.005) and 3.3 +/- 0.3 l/min/m2 (p less than 0.001), respectively. The NP-Db and NTG-Db regimens induced comparable reductions of rate - pressure-products reflecting a decrease of myocardial oxygen demands and facilitation of myocardial work.
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PMID:Hemodynamic equivalence of automated nitroglycerin- and nitroprusside-infusions combined with dobutamine for augmentation of cardiac output in patients following aorta coronary bypass-operation. 643 93

The hypertension immediately after open heart surgery for coronary heart disease was chosen to evaluate the suitability of computer-controlled infusion sodium nitroprusside, to improve the circulatory state in heart failure by reducing the impedance to the left ventricular ejection. Sodium nitroprusside produced a prompt reduction of MAP to a preset level and a rise in cardiac index from an average of 2.1 +/- 0.3 to 2.4 +/- 0.4 when infused alone and to 3.1 +/- 0.5 1/min m2 (p less than 0.05, + 48%) after volume was infused to maintain LAP at a constant level to eliminate the effects of preload. The rise in cardiac index was associated with marked decrease in systemic vascular resistance from 2260 +/- 530 to 1415 +/- 280 and 1130 +/- 1130 +/- 270 dyns (p less than 0.005, 63%) respectively. The initial values of SVR correlated well with the fall of SVR (r = 0.78). Our results suggest that systemic vascular resistance is a strong indicator of the vascular responsiveness to vasodilation, the computer-controlled infusion of sodium-nitroprusside being suitable for the "titration" of the high systemic vascular resistance.
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PMID:[Hemodynamic effects of computer-guided blood pressure-lowering with nitroprusside sodium during the postoperative phase after aortocoronary bypass operations]. 698 28

Hemodynamic responses to different doses of hydralazine were evaluated in 18 patients with severe refractory resistant heart failure. There were no significant overall hemodynamic effects after 50 mg hydralazine. After 75 mg, CI increased slightly (+0.36 l/min/m2) with a 19% decrease in SVR. After 100 mg, there were substantial increases in CI (+0.60 l/min/m2) and decreases in SVR (31%) changes which were greater than those after 75 mg, but the decrease in MAP with 100 mg (-6.6 mm Hg) was of the same order as that after 75 mg (-5.0 mm Hg). LVFP and SWI improved significantly only with 100-mg doses. Seven patients in whom 100 mg hydralazine induced no hemodynamic effects all responded to single doses of 150 to 200 mg. The duration of action of hydralazine was longer (p less than 0.001) in patients with a CCr less than 35 ml/min (14.3 +/- 1.4 hr) than in patients with adequate renal function (7.9 +/- 0.5 hr). Thus, the dose and dosing interval of hydralazine needed to induce hemodynamic improvement in patients with severe heart failure are variable and require individualization.
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PMID:Hemodynamic evaluation of hydralazine dosage in refractory heart failure. 735 90

Ventricular arrhythmias and disturbed autonomic control, as reflected by abnormal heart rate variability (HRV), are related to hemodynamic impairment in chronic heart failure (CHF). We investigated the effects of orally (p.o.) administered isomazole, a new phosphodiesterase (PDE) inhibitor with calcium-sensitizing properties, on hemodynamics, ventricular arrhythmias, and HRV and examined a possible interaction between these parameters. Hemodynamic measurements and ambulatory ECG monitoring were performed in 12 patients with stable CHF class III-IV after single doses of isomazole 5-30 mg. Pulmonary wedge pressure decreased after 5, 10, 20, and 30 mg, but cardiac output, (CO) increased only after the higher doses [20 mg, + 20% (p = 0.031)] of isomazole. HR did not change. Mean arterial and pulmonary artery pressure, (MAP, PAP) decreased significantly in the 10- and 20-mg groups [10 mg, -6% (p = 0.035) and -14% (p < 0.001) respectively; 20 mg, -13% (p = 0.047) and -31% (p = 0.006), respectively]. Isomazole did not exert a significant effect on ventricular arrhythmias in the subsequent 24 h after acute dosing. Analysis of HRV showed that rMSSD and pNN50 (parameters of vagal tone) tended to increase after isomazole administration. Normalized high-frequency power during the day increased from 17.4 to 22.3 nu (p < 0.05), whereas low frequency tended to decrease from 52.7 to 48.2 nu (p = 0.06). Acute isomazole administration improves hemodynamics but has no effect on ventricular arrhythmias. The HRV variability data suggest development of an increase in vagal control of HR, parallel to the acute hemodynamic improvement after isomazole. Withdrawal of vagal control of HR in CHF may be a reversible process.
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PMID:Exploratory study of the effects of single doses of isomazole on hemodynamics and heart rate variability parameters in chronic heart failure. 772 57

Cardiac functions are regulated by both contractile proteins and calcium regulatory proteins. In cardiac hypertrophy, an increase in protein synthesis can be partitioned into an increase in both capacity and efficiency of synthesis. beta-cardiac myosin heavy chain (beta-MHC) isoform is predominantly expressed while alpha-MHC is suppressed in pressure overload hypertrophy. The SR Ca(2+)-ATPase is also markedly decreased in pressure overloaded hearts, while in thyrotoxic hearts both are increased. The signal transduction system in cardiac hypertrophy can be examined by stretching cardiac myocytes grown up on deformable membranes. In our analysis, stretching myocytes stimulated protein kinase C, MAP-II kinase and S6 kinase, all of which may lead to the induction of fetal-type cardiac genes and accelerated protein synthesis. Analyses of the subcellular mechanisms of cardiac hypertrophy will provide important insights into understanding of the molecular basis of heart failure.
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PMID:[Molecular basis for heart failure]. 833 89

It is well accepted that sympathetic tone is elevated in chronic heart failure (HF) and that the cardiac sympathetic afferent reflex is a sympathoexcitatory reflex. There have been no studies designed to examine the role of this reflex in control of sympathetic outflow in the HF state. In this study we tested the hypothesis that cardiac sympathetic afferent reflexes are enhanced in HF and are, therefore, capable of contributing to the increase in sympathetic outflow in this disease state. Ventricular pacing was carried out in 14 dogs until signs of HF were evident. Fourteen sham dogs served as controls. At the time of the acute experiment the dogs were anesthetized with alpha-chloralose. The hemodynamic [arterial pressure and heart rate (HR)] and renal sympathetic nerve activity (RSNA) responses to left ventricular epicardial application of two doses of bradykinin (BK) and capsaicin (Cap) were determined in the sinoaortic-denervated and vagotomized state. The MAP, RSNA, and HR responses to BK were greater in the HF group compared with the sham group. The RSNA response to BK (50 micrograms) in the HF group was significantly increased (34.0 +/- 5.9 vs. 11.5 +/- 4.2%, P < 0.05). The MAP, RSNA, and HR responses to Cap in the HF group were similar to the responses to BK. The RSNA response to Cap in the HF group was significantly increased (29.8 +/- 11.3 vs. 13.8 +/- 2.3% for 10 micrograms, P < 0.05 and 46.5 +/- 10.7 vs. 18.7 +/- 3.1% for 100 micrograms, P < 0.05). The cyclooxygenase blocker indomethacin (5 mg/kg i.v.) attenuated the reflex responses to BK in the HF group. These data suggest that the enhanced cardiac sympathetic afferent reflex to epicardial BK in HF appears to be mediated by altered levels of prostaglandin synthesis. Blockade of cardiac sympathetic afferents with topical lidocaine reduced baseline of RSNA significantly more in the HF state than in the normal state (-24.2 +/- 3.6 vs. -4.3 +/- 4.5%, P < 0.05). We conclude from these data that the cardiac sympathetic afferent reflex is sensitized in the HF state and speculate that this enhanced cardiac sympathetic afferent reflex may contribute to the sustained higher sympathetic tone in chronic HF.
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PMID:Cardiac sympathetic afferent reflex in dogs with congestive heart failure. 885

Aging is associated with hypertension and electrolyte disturbances. The purpose of this study was to determine the effect of aging upon secretion and renal actions of atrial natriuretic peptide (ANP). Rats were anesthetized and received tracheal, jugular vein, carotid artery, and bilateral uretheral catheterization. One set of young (2-3 mo) rats (Group 2, n = 9) and one set of old (18-21 mo) rats (Group 4, n = 7) received bilateral atrial appendectomies. Control young (Group 1, n = 8) and old (Group 3, n = 8) rats received a sham appendectomy. All rats were infused (iv) with 6% albumin in Krebs buffer, sufficient to increase blood volume by 15%. Finally, each rat was injected with ANP (1 microgram/kg). Sodium excretion rate (U(Na+)V) in response to volume expansion was significantly decreased in all groups compared to Group 1 (young control, p < .05). All groups demonstrated a striking increase in U(Na+)V with the ANP injection, but the response was greatest in young control rats when factored by body weight (p < .05). There were no significant differences in MAP between the groups, suggesting that the differences in U(Na+)V observed were not the result of hemodynamic factors. Isolated perfused atria from young (n = 9) and old (n = 8) rats were subjected to stretch and endothelin stimulation (50 nM). Atria from young rats showed a dramatic increase in ANP secretion in response to atrial stretch and a further marked increase in secretion in response to endothelin, whereas both of these responses were markedly attenuated in old rats (p < .05). These results suggested that the secretion and renal effects of ANP are impaired in aging. Changes in secretion and actions of ANP in aging could contribute to the development of hypertension or heart failure.
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PMID:Alterations in atrial natriuretic peptide (ANP) secretion and renal effects in aging. 922 24

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.
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PMID:Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment. 927 26

This study examined the cardiovascular effects of 17beta-estradiol in ovariectomized rats with heart failure. Two groups (50-60 days old) were implanted with 60-day-release pellets containing 17beta-estradiol (25 microg/day) or vehicle at 7 days before ligation of the left coronary artery. Another group was sham operated and given vehicle pellets. After 7 wk, they were studied under pentobarbital anesthesia. Relative to sham-operated rats, ligated rats had reduced mean arterial pressure (MAP, -24 +/- 6 mmHg), cardiac output (-27 +/- 4 ml/min), left ventricular (LV) end-systolic pressure (-29 +/- 8 mmHg), depressor responses to ACh (-6 +/- 4 mmHg at 7.2 microg/kg) and sodium nitroprusside (SNP, -22 +/- 6 mmHg at 9 microg/kg), and pressor responses to NG-nitro-L-arginine methyl ester (L-NAME, -14 +/- 6 mmHg at 8 mg/kg) and increased LV end-diastolic pressure (LVEDP, 10.3 +/- 0.8 mmHg) but no change in total peripheral resistance (TPR). Treatment of ligated rats with 17beta-estradiol reduced TPR (-0.19 +/- 0.06 mmHg . min . ml-1), LVEDP (-3.6 +/- 1 mmHg), and responses to ACh (-16 +/- 4 mmHg) and augmented responses to L-NAME (14 +/- 3 mmHg) but did not alter other variables. Therefore, 17beta-estradiol reduces preload and afterload and restores the vasodilator role of basal nitric oxide in ovariectomized rats with chronic heart failure.
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PMID:Estrogen restores role of basal nitric oxide in control of vascular tone in rats with chronic heart failure. 984 36


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