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

Water, sodium, and potassium balance and urinary excretion of norepinephrine and aldosterone were investigated in rats with left ventricular failure due to left ventricular infarction, and measurements were obtained of plasma levels of atrial natriuretic factor (ANF). Increased plasma levels of ANF in relation to the size of the infarction and to the right atrial and left ventricular end-diastolic pressure were found. The augmented levels of ANF were not able to prevent an accumulation of sodium in the rats with myocardial infarction in which urinary excretion of norepinephrine and aldosterone was unchanged in comparison to control values. Plasma levels of ANF in the pulmonary artery, aorta, and renal vein of six conscious dogs were studied during the development of heart failure due to rapid right ventricular pacing. A threefold increase in ANF was found: ANF levels did not differ between the pulmonary artery and the aorta, but a reduction in ANF of about 30% was reported in the renal vein in comparison to the arteries. A close positive correlation between right atrial pressure and plasma levels of ANF was noted. No correlation could be demonstrated between mean pulmonary arterial pressure and ANF or between the stimulated plasma renin concentration and plasma ANF values.
 ...
PMID:Atrial natriuretic factor in acute and chronic cardiac failure. 248 23

A randomized, single-blind controlled study intended to assess the potential benefits of intravenous amiodarone in anterior myocardial infarction is presented. Three hundred nineteen patients entered the study, 159 received amiodarone infusion, and 160 received glucose-insulin-potassium (GIK) infusion. Basal characteristics were similar in the two experimental groups, who were randomized on a consecutive basis. Exclusion criteria were shock or pulmonary edema, hypotension, inferoposterior infarction, bradycardia, antrioventricular block, severe diabetes, and other major diseases. Patients aged 27 to 70 years, with a Q-wave anterior infarction, initiated 12-40 hours earlier at the time of admission, entered the trial. Other entry criteria were heart rate higher than 80 beats/min and systolic blood pressure higher than 100 mmHg. Amiodarone was administered in saline infusion 10-20 mg/kg, within 4 to 10 hours, through a central vein. GIK infusion consisted of 150-300 g of glucose, 25-50 IU of insulin, and 80-120 mEq of KCl in 1000 cc of water at a rate of 1.5-2.0 ml/g/hour. Both groups received digitalis, nitrates, sedatives, and diuretics as needed. Although individually the major endpoints of death, reinfarction, and sustained supraventricular and ventricular arrhythmias did not differ significantly, each was less in the amiodarone group than in the control, and the sum of all adverse events was significantly lower for the amiodarone patients (p less than 001). Heart failure and conduction disturbances were not different in the two groups. This study shows that amiodarone, with its vasodilating and antiarrhythmic properties, may be beneficial in acute anterior infarction, but further studies on larger populations will be necessary in order to show a reduction of mortality rate.
 ...
PMID:Intravenous amiodarone in acute anterior myocardial infarction: a controlled study. 248 93

Fatigue, that cardinal symptom of heart failure, expresses muscle deconditioning and is becoming the main complaint of our patients. Dyspnoea also is, at least partially, a consequence of muscle deconditioning; however, the wide use of diuretics which reduce water and salt retention has improved the "pump" function an therefore dyspnoea. The "muscle deconditioning" syndrome in heart failure has two causes: reduction of the nutritive blood flow in skeletal muscle, and specific alteration of mitochondrial oxidative metabolism. The syndrome appears only after a lasting reduction of physical activities. Its anatomical substrate is a mild muscular fibrosis and, mainly, reduced area of oxidative mitochondrial cristae. It remains for approximately three months, which accounts for the delayed improvement of exercise tolerance under vasodilatator treatment with angiotensin-converting enzyme inhibitors. This syndrome explains the success of retraining techniques which, in ou opinion, should become part of our therapeutic armamentarium.
 ...
PMID:[The syndrome of "muscle deconditioning" in chronic cardiac insufficiency]. 250 99

The natriuretic, diuretic, and hypotensive effects of atrial natriuretic peptide (ANP) were examined in rats 4 wk after myocardial infarction induced by left coronary artery ligation. Synthetic rat ANP (fragment 1-28) was infused intravenously in doses of 0.1, 0.3, and 1.0 micrograms.kg-1.min-1 for 30 min. There was a significant decrease in systolic blood pressure in controls and rats with infarction, although only in control rats was there a significant decrease in diastolic blood pressure. Changes in systolic and diastolic blood pressure were attenuated in rats with infarction compared with controls (P less than 0.01). The diuretic and natriuretic effects of ANP were observed in both groups of rats, but the effects were significantly less in rats with infarction (P less than 0.01). The ANP infusion did not induce significant changes in heart rate or hematocrit in controls or rats with infarction. The results indicate that rats with chronic left heart failure are less sensitive to the natriuretic, diuretic, and hypotensive effects of ANP when compared with controls. The attenuated renal response to ANP may contribute to the impaired sodium and water excretion in chronic heart failure, although other mechanisms are involved.
 ...
PMID:Attenuated response to atrial natriuretic peptide in rats with myocardial infarction. 252 77

It is apparent therefore that a large variety of neurohumoral influences affect renal hemodynamics and the renal tubular reabsorption of sodium and water in response to cardiac failure and thereby contribute to the development of a "salt-avid" kidney, circulatory congestion, and edema formation. These influences are summarized schematically in Figure 1.
 ...
PMID:Sodium retention in heart failure. 252 41

Plasma levels of atrial natriuretic peptide (ANP) and renal responses to ANP were examined in rats with chronic cardiac failure produced by coronary artery ligation and in sham-operated controls. Plasma ANP levels were elevated in the rats with severe cardiac failure as compared with the controls (P less than 0.001). ANP injections at the doses of 1, 5, 25 and 50 micrograms/kg increased water and sodium excretion significantly at all but the lowest dose in the controls; only the two largest doses caused clear diuresis and natriuresis in the heart failure group. The diuretic and natriuretic effects of ANP were significantly weaker at the doses of 5 and 25 micrograms/kg in the rats with heart failure as compared with the controls. We conclude, that natriuretic and diuretic effects of ANP are attenuated in this chronic heart failure mode.
 ...
PMID:Attenuated diuretic and natriuretic effects of atrial natriuretic peptide in rats with heart failure. 252 89

Atrial natriuretic peptide levels are elevated in heart failure. However, the hemodynamic responses to exogenous atrial natriuretic peptide infusion in heart failure are blunted. To determine if captopril can restore hemodynamic responsiveness to atrial natriuretic peptide infusion in rats with heart failure, studies were performed in a rat model of heart failure after coronary artery ligation. Rats with heart failure received either captopril (2 g/l drinking water) or placebo for 4 weeks and then were treated with an infusion of atrial natriuretic peptide (0.3 microgram/kg/min). Captopril treatment alone improved hemodynamics. Left ventricular end-diastolic pressure, mean aortic pressure, and mean circulatory filling pressure decreased from 22 +/- 2 to 14 +/- 1, from 106 +/- 4 to 76 +/- 3, and from 10.5 +/- 0.6 to 8.8 +/- 0.4 mm Hg, respectively. Heart rate, right atrial pressure, and hematocrit were unchanged. Total blood volume decreased from 66.0 +/- 1.0 to 60.0 +/- 1.0 ml/kg; venous compliance increased from 2.1 +/- 0.1 to 2.7 +/- 0.1 ml/kg/mm Hg. Atrial natriuretic peptide alone had minimal hemodynamic effects on rats with heart failure. There was no change in right atrial pressure, mean aortic pressure, left ventricular end-diastolic pressure, mean circulatory filling pressure, and total blood volume. However, atrial natriuretic peptide infusion increased venous compliance from 2.1 +/- 0.1 to 2.4 +/- 0.1 ml/kg/mm Hg. Heart rate and hematocrit increased from 323 +/- 5 to 359 +/- 8 beats/min and from 48 +/- 1% to 51 +/- 1%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Captopril restores hemodynamic responsiveness to atrial natriuretic peptide in rats with heart failure. 253 77

The non-osmotic stimulation of release of arginine vasopressin (AVP) seems to be the main determinant of the impaired water excretion and hyponatraemia in patients with cardiac failure. This non-osmotic stimulation of AVP release could be secondary to a decrease in stroke volume to which the ventricular receptors respond by decreasing the vagal afferent input to the hypothalamus via the mid-brain. Improvement of cardiac stroke volume would then decrease AVP release and improve water excretion. In cardiac failure, the non-osmotic stimulation of AVP release is not clearly modulated by the renin-angiotensin system or by the atrial natriuretic peptide plasma concentration. Nevertheless, physiological concentrations of atrial natriuretic peptide could inhibit the renal epithelial water transport at the collecting duct level. Water-loading and osmotic-loading experiments in patients with cardiac failure indicated that the release of AVP is still under osmotic control and favoured the concept that volume depletion in general and cardiac failure in particular may lower the osmotic threshold and increase the osmotic sensitivity to vasopressin release. Experiments using a specific vasopressin antagonist rarely indicated a vasoconstrictor role for endogenous AVP in either experimental or clinical cardiac failure. Intrarenal factors also contributed to the impaired water excretion observed in patients with cardiac failure: increased central sympathetic efferent discharge and stimulation of the renin-angiotensin-aldosterone system would be expected as a consequence of the decreased effective arterial blood volume. These effects could then decrease maximal reabsorption of solute further impairing the ability of the kidney to excrete free water. The impaired water excretion is correlated with the severity of the cardiac deterioration and thus has prognostic implications.
 ...
PMID:Water disturbances in cardiac failure. 253 70

Rats treated with the alkaloid monocrotaline developed right ventricular hypertrophy with a left:right ventricle weight ratio of 1.35 +/- 0.10 (mean +/- s.e.m., n = 25) compared with 3.83 +/- 0.40 (n = 14) in diet-matched controls (P less than 0.001). Urine volume and sodium content were reduced and body water increased consistent with heart failure. In 10 out of 26 treated rats pleural, pericardial or peritoneal effusions were present. Urine norepinephrine content was significantly raised (P less than 0.02) but epinephrine was unchanged. Plasma norepinephrine levels were raised though not significantly. Myocytes isolated from the right ventricle had a reduced myosin Ca2+-activated ATPase (P less than 0.05) activity and a shift towards slower V2 and V3 myosin isoforms. There was no decrease in maximum contraction amplitude with calcium or isoproterenol in either left or right ventricular cells of treated rats. Right ventricular cells from treated rats showed a reduced rate of contraction in maximum isoproterenol (P less than 0.05) and a significant rightward shift in PD2 (P less than 0.05) representing a two-fold increase in EC50 for isoproterenol compared with right ventricular cells from control animals. There was no shift in EC50 for isoproterenol in left ventricle cells. In parallel experiments, myocytes isolated from both ventricles of rats treated with isoproterenol for one week showed a rightward shift of more than 50-fold in the isoproterenol concentration-response curve and a depressed response to maximum isoproterenol. In the rat monocrotaline model of right-sided cardiac hypertrophy and failure, changes in sensitivity to beta-adrenoceptor agonists are slight, and present only in the right ventricle. The lack of change in the left ventricle seems to suggest that this functional desensitisation is not a consequence of raised circulating catecholamines.
 ...
PMID:Isoproterenol sensitivity of isolated cardiac myocytes from rats with monocrotaline-induced right-sided hypertrophy and heart failure. 255 26

Congestive heart failure is a complex clinical syndrome characterized by circulatory and metabolic abnormalities. It has been apparent for more than 25 years that the sympathetic nervous system and the renin-angiotensin-aldosterone system are markedly activated in the late stages of heart failure. These two systems interact to facilitate sympathetic drive and promote salt and water retention. Circumstantial evidence is now accumulating to indicate that excessive sympathetic drive and angiotensin II activity may contribute to the pathophysiology of heart failure. These observations suggest that a dual strategy of modulating sympathetic nervous system activity to the heart while blocking angiotensin II activity may provide a rational therapeutic approach to the treatment of heart failure. Xamoterol, a beta 1 partial agonist, may enhance myocardial contractile force in the steady state, while acting to inhibit excessive sympathetic drive during exercise or severe heart failure. The concomitant use of a converting-enzyme inhibitor would be expected to blunt the detrimental effects of excessive angiotensin II activity. Modulation of adrenergic drive coupled with inhibition of marked angiotensin II activity may be potentially more effective in the treatment of congestive heart failure than either strategy used alone.
 ...
PMID:The relationship of the sympathetic nervous system and the renin-angiotensin system in congestive heart failure. 257 May 21


<< Previous 1 2 3 4 5 6 7 8 9 10