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 hemodynamic and cardiometabolic effects of dopamine were evaluated in propoxyphene-induced circulatory shock in eight pentobarbital anesthetized pigs. Circulatory shock was induced by an infusion of propoxyphene chloride 15 mg . min-1 i.v. At shock, i.e. CI less than or equal to 2.0 l . min-1 . m-2 and/or MAP less than or equal to 60 mmHg, dopamine was infused at 10, 20, 40, 80 and 160 micrograms . kg-1 . min-1 with an interval between increments of 8 min. After 30 min at 160 micrograms . kg-1 . min-1, the infusion rate was reversibly decreased. The propoxyphene infusion of 15 mg . min-1 was continued throughout the study. Dopamine improved the circulation in seven animals; one animal died in refractory shock during dopamine infusion. Dopamine infusion at shock level resulted in an increase of the following variables (% of baseline value): MAP (69%), HR (109%), CI (138%) and SVI (129%). Normalisation was seen in MRAP (120%) and in MPAOP (100%). A profound decrease in systemic vascular resistance was unchanged. Increases were seen in left and right ventricular stroke work index, to 88% and 176% of baseline, respectively. Left ventricular dP/dt increased (170%). In the coronary circulation myocardial blood flow increased (133%) as did myocardial oxygen consumption (65%) concomitant with a decrease in myocardial oxygen uptake (41%), but coronary vascular resistance progressively decreased (38%). The myocardial propoxyphene extraction changed from +54% to -86% during peak dopamine infusion. In conclusion, dopamine reversed cardiac failure in propoxyphene overdose by a marked positive inotropic stimulation restoring contractility. A marked positive chronotropic stimulation maintained a sufficient cardiac index and a normal blood pressure in spite of a profound vasodilatation which was unresponsive to dopamine.
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PMID:The effects of dopamine on central hemodynamics and myocardial metabolism in experimental propoxyphene-induced shock. 406 Oct 11

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

Balloon-induced distention of the main pulmonary artery causes acute pulmonary hypertension and reflex pulmonary vasoconstriction in animals. Pulmonary artery pressure responses caused by MPA balloon inflation were measured in ten human newborn infants with cardiac failure (n = 5) or persistent fetal circulation (n = 5). During balloon inflation distal mean PAP increased significantly while cardiac rate remained unchanged. MPA distention caused greater increases of PAP in those infants with lower resting PAP. The greatest balloon-induced increases of PAP were observed in infants recovering from PFC. The existence of a pulmonary artery reflex and its possible role in the regulation of the human fetal and neonatal pulmonary circulation is discussed.
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PMID:Main pulmonary artery distention: a potential mechanism for acute pulmonary hypertension in the human newborn infant. 735 56

A 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation]. 771 33

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


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