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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intrarenal distribution of blood flow was measured by the 133xenon washout curve in 33 patients with heart disease. Plasma renin activity and sodium concentration were also measured on the day when the xenon study was performed. The patients were divided into three groups according to cardiac index: Group I whose cardiac index showed higher than 3.50 1/min/M2, BSA, group II whose index ranged from 2.50 to 3.50, and group III who had lower than 2.50. Total renal blood flow was significantly decreased in group II (p less than 0.001), as compared with normal controls. The percents of the total renal blood flow supplied to component I decreased significantly in group I, II (p less than 0.05) and group III (p less than 0.01). The flow rate in component I decreased significantly only in group II (p less than 0.05) and group III (p less than 0.01). There was a significant increase in the percent distribution of component II in group II (p less than 0.05) and in group III (p less than 0.01). The flow rate of component II showed a slight increase in group I and III. The study of autoradiographs done in dogs with heart failure demonstrated that component I corresponded to a cortical area having a relatively faster flow rate, whereas component II corresponded to the cortical area which was perfused more slowly. Accordingly, component III indicated outer medulla. There was no apparent relation between intrarenal distribution of blood flow and plasma renin activity although the latter tended to be elevated in patients treated with diuretics. In view of the data available it was concluded that outer cortical as well as outer medullary blood flow are decreased in chronic congestive heart failure and that there is no apparent correlation between outer cortical flow and plasma renin activity.
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PMID:Intrarenal distribution of blood flow and renin in chronic congestive heart failure. 111 37

Statistical analysis of the realtion between blood pressure and renal function in 421 patients with CGN, referred to the Second Internal Medicine at Nihon University Hospital, and in 253 Hypertensive patients with CGN by questionaires sent to 29 Medical Universities were investigated. The relationship between survival rate and blood pressure of 84 patients with CGN in Surugadai Nihon University Hospital was also examined. These data show that antihypertensive therapy for CGN with hypertension has an important effect on prognosis. Propranolol was given to 10 hypertensive patients with CGN and hypotensive effect on renal function was observed. Our experience suggests that propranolol may be useful for treating a high renin component in the hypertension with non renal failure, and renal function does not become worse. But in renal failure, propranolol therapy must be used carefully because of inducement to cardiac failure.
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PMID:Therapy and prognosis of hypertension in chronic nephritis. 115 36

Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, [Sar1, Ala8]AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.
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PMID:High-output heart failure in the dog: systemic and intrarenal role of angiotensin II. 116 74

In rats with unilateral renal artery stenosis, the malignant phase of hypertension is characterized by: systolic blood pressure above 180-190 mm Hg; sodium and water loss; polyuria and polydipsia; markedly activated renin-angiotensin-aldosterone system; impairment of renal function and malignant nephrosclerosis in the contralateral kidney; some rats exhibit signs of cerebral hemorrhage, heart failure, acute renal failure, and some rats die. After such a phase of malignant hypertension, a period of remission may occur, which is followed by another malignant phase, etc. When malignant hypertensive rats are offered, in addition to water, saline as drinking fluid, they compulsively drink the saline, BP falls transiently, and all signs of malignant hypertension nearly or completely disappear. These observations indicate that, at a critically high BP level, it is salt and water loss which, by activating the renin-angiotensin system, trigger the vicious circle of malignant renal hypertension in rats.
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PMID:Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. 119 18

To test the efficacy of exogenous prostaglandins for vasodilator therapy in heart failure, we studied the hemodynamic, hormonal, and renal effects of prostaglandin E2 (1.5-150 ng/kg/min) in six conscious dogs before and after induction of heart failure by right ventricular pacing (250 beats/min, 10 days). In healthy dogs, PGE2 decreased the mean arterial pressure (MAP) by a reduction in total peripheral resistance (TPR), increased cardiac output (CO), stroke volume (SV), and heart rate with no effect on right atrial pressure (RAP). Plasma levels of renin (PRC) and norepinephrine (NE) were increased at the highest dosage. Renal plasma flow (RPF) and sodium excretion (UNaV) were augmented without a change in the glomerular filtration rate (GFR) and urine flow (UF). In dogs with heart failure, PGE2 lowered the MAP and TPR and elevated the CO and SV without an effect on the RAP, PRC, and NE. The RPF and GFR were not changed, but the increase in UNaV was preserved and UF significantly augmented. In experimental heart failure, PGE2 increases the CO due to arteriolar dilation and afterload reduction without inducing further neurohumoral activation and exerts potent natriuretic and diuretic action. Therefore, PGE2 may have beneficial effects in heart failure therapy.
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PMID:Prostaglandin E2 in dogs with heart failure: hemodynamic, hormonal, and renal effects. 128 Jul 9

Angiotensin-converting enzyme (ACE) inhibitors are established in the treatment of hypertension and heart failure; both conditions are complicated by resistance to insulin-mediated glucose disposal. The defect in essential hypertension is both tissue and pathway specific, i.e., confined to nonoxidative (glycogen synthetic) routes of intracellular glucose utilization in skeletal muscle, whereas heart failure and non-insulin-dependent diabetes mellitus (NIDDM) are associated with more widespread abnormalities of carbohydrate and lipid metabolism. Thus, the mechanisms of the insulin resistance in hypertension, NIDDM, and heart failure are fundamentally different, so metabolic responses to drug therapy may not be the same in all insulin-resistant states. There have been conflicting reports about the effects of ACE inhibitors on insulin sensitivity and glycemic control. A number of studies, both with captopril and with enalapril, have shown small increases in insulin sensitivity, and there is evidence that this is due to enhanced glucose uptake into skeletal muscle. The interpretation of these studies, however, is often compromised by poor trial design, lack of full placebo data, various indirect measurements of insulin sensitivity, and heterogeneous patient populations in whom the biochemical mechanisms of insulin resistance (and drug responses) may not be the same. Overall, there probably is a modest class effect of ACE inhibitors that enhances insulin-mediated glucose disposal; the mechanism of this effect is likely to be a combination of increased muscle blood flow, local renin-angiotensin system blockade, and elevated kinin levels.
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PMID:Angiotensin-converting enzyme inhibitors and insulin sensitivity: metabolic effects in hypertension, diabetes, and heart failure. 128 42

Preventive therapy by angiotensin-converting-enzyme (ACE) inhibitors is considered in hypertension and, more recently, in chronic heart failure. The mechanism of action of ACE-inhibitors is complex; most extensively studied, however, is their inhibitory effect on angiotensin-II production. ACE-inhibitors may act as vasodilators, reducing pre- and afterload. On the other hand, local renin-angiotensin systems may control growth processes both in myocardial and in smooth muscle cells. This may be another site of action for ACE-inhibitors. ACE-inhibitors are reliable antihypertensive drugs and may have additional specific effects on the heart and vascular smooth muscle. Clear evidence is, however, missing for their superiority above other drugs in preventing cardiovascular complications of hypertension. Most recently, the data of the "study of left-ventricular dysfunction" (SOLVD) and "survival and ventricular enlargement" (SAVE) study became available. These studies showed that ACE-inhibitors could prevent the incidence of heart failure in about one-third of patients with severe left-ventricular dysfunction during 3 years of observation when compared with placebo treated patients. A new indication, therefore, for ACE-inhibitors could be left ventricular dysfunction after myocardial infarction. It remains unclear 1) what could be the adequate diagnostic procedures to identify patients for preventive treatment, 2) when therapy should be started, 3) about the duration of therapy, 4) about the doses of ACE-inhibitors for this indication, 5) what will be the side-effects when used in a broader population, and 6) will this prevention of heart failure be a specific effect of ACE-inhibitors?
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PMID:[Prevention with angiotensin-converting enzyme (ACE) inhibitors]. 129 Mar

ACE-inhibitors improve symptoms and prognosis in patients with heart failure. The V-Heft II trial has demonstrated that the beneficial effect of these agents is superior to unspecific vasodilators. Besides sustained arterial and venous vasodilation the inhibition of the neurohumoral axis is thought to play an important role. Angiotensin II and catecholamines not only exert vasoconstrictor effects, but might also contribute to vascular and myocardial growth. Thus, it may not be surprising that the beneficial effects of ACE inhibitors in heart failure only emerge during long-term therapy rather than after short-term administration. It has been shown that these agents improve blood flow to skeletal muscle during exercise after chronic therapy (not acutely), and there is some preliminary evidence that improvement of endothelial function might be involved in this effect, i.e., by reducing the degradation of bradykinin, an endothelial vasodilator. ACE inhibitors reduce LV hypertrophy, an important risk factor for cardiovascular disease and prognosis. Moreover, there is experimental evidence that ACE inhibitors can prevent and even reverse interstitial fibrosis in the left ventricle. Although the plasma renin activity may be normal in patients with chronic heart failure, recent data using polymerase chain reaction indicate that the tissue cardiac renin angiotensin system is activated in the failing human heart as assessed by measurements of angiotensin converting enzyme mRNA and angiotensinogen mRNA which may be an important target for ACE-inhibition.
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PMID:[The value of ACE inhibitors in heart failure (mechanism of action)]. 129 Mar 8

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

Treatment with angiotensin-converting enzyme (ACE) inhibitors can begin at any time when a left ventricular dysfunction has been diagnosed. In the absence of rare contra-indications (renal artery stenosis, connective tissue disease, severe renal failure), all patients with asymptomatic or, a fortiori, symptomatic chronic heart failure can benefit from ACE inhibitors, whatever the origin of the heart failure. Among the ACE inhibitors now available, the benefits of captopril (3 daily doses) and of enalapril (2 daily doses) on all the targets of cardiac failure treatment are now well established. The effects of lisinopril on mortality are not yet known, but the haemodynamic and symptomatic benefits of this drug are also well established (with the advantage of once daily administration). Other ACE inhibitors with less numerous and less convincing trial reports can be used or rejected depending on the physician's faith in the effects of this pharmaceutical class. With all ACE inhibitors the initial dose must be very low, to be gradually increased over several days or even weeks until the highest dose tolerated is reached. ACE inhibitors can be associated with the classical treatment of cardiac failure. A previous diuretic treatment with sodium depletion may increase the risks of first dose effect and renal intolerance due to the introduction of the ACE inhibitors. Theoretically, the combination of ACE inhibitors and spironolactone is to be avoided for fear of hyperkalaemia and renal deterioration. Yet, provided some precautions are taken this combination may improve the benefits of ACE inhibition when the renin-angiotensin-aldosterone system inhibition is not optimal. However, this has yet to be demonstrated by prospective clinical trials.
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PMID:[Management of the treatment with converting enzyme inhibitors in chronic heart failure]. 129 41


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