The role of vasodilator therapy in heart failure

Chatterjee, Kanu; Parmley, William W.

doi:10.1016/0033-0620(77)90006-8

Cited by 307 publications

(39 citation statements)

References 104 publications

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“…Hypoxia-induced alterations in the oxidative stress indices of rats with acute pulmonary edema were observed in the present study, and the effects on the activity level of the antioxidant enzyme SOD, and the levels of the lipid peroxidation product MDA and IL-6 in were investigated the lung tissue, so as to explore their effects and related mechanisms in a rat model of acute pulmonary edema (23,24). The results of the present study demonstrated that the antioxidant capacity and associated SOD enzyme activity of the lung tissue significantly decreased when the duration of pulmonary edema was extended; whereas the levels of the MDA lipid peroxidation product significantly increased, and the levels of IL-6 in the plasma and lung tissue significantly increased, which suggested that the induction of oxidative stress may have an important role in the pulmonary tissue damage associated with acute pulmonary edema.…”

Section: A B C D Discussionmentioning

confidence: 76%

Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

Gao

Tian

Wang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and interleukin (IL)-6 in the lung tissue of a rat model of acute pulmonary edema induced by acute hypoxia, and its pathophysiological significance. A total of 48 adult Wistar rats were randomly divided into group A, a normal group; group B, a model of acute pulmonary edema induced by hypoxia for 24 h; group C, a model of acute pulmonary edema induced by hypoxia for 48 h; and group D, a model of acute pulmonary edema induced by hypoxia for 72 h. The rats in groups B-D were intraperitoneally injected with 6% ammonium chloride to establish the model of acute pulmonary edema, and were subsequently sacrificed following successful modeling for 24, 48 and 72 h. The plasma of rats was isolated and the lungs of the rats were removed. Subsequently, a 10% lung homogenate was prepared and the contents and the activities of MDA, SOD and IL-6 in the lung tissue and IL-6 in the plasma were detected by enzyme-linked immunosorbent assay. MDA and IL-6 expression levels increased and SOD activity decreased in the lung tissue in group B as compared with group A; however the difference did not reach significance (P>0.05). MDA, IL-6 and SOD levels in the lung tissue of rats were significantly altered following the increased duration of pulmonary edema in groups C and D, as compared group A (P<0.05). The plasma IL-6 levels of the rats in groups B-D significantly increased, as compared with those in group A (P<0.05). In conclusion, the results of the present study demonstrated that the incidence of acute pulmonary edema may be associated with oxidative stress. Furthermore, decreased antioxidant capacity and increased free radical levels may be associated with pulmonary edema, as in the present study the levels of IL-6, SOD and MDA in the lung tissue were observed to be associated with the pathological changes of the disease.

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Section: A B C D Discussionmentioning

confidence: 76%

Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

Gao

Tian

Wang

et al. 2015

Experimental and Therapeutic Medicine

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“…As congestive heart failure is usually a chronic condition, it is appropriate that recent attention has focused on the long-term effectiveness of vasodilators (Chatterjee & Parmley, 1977;Taylor, 1980;Cohn, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…This increase in systemic vascular resistance, however, also leads to an increase in the left ventricular outflow resistance, which can further reduce cardiac output (Cohn, 1973;Zelis etal., 1970). Thus, a vicious cycle may develop that will ultimately lead to a lower steady state level with a reduced cardiac output and inappropriately high systemic vascular resistance (Chatterjee & Parmley, 1977).…”

Section: Introductionmentioning

confidence: 99%

“…Vasodilators can improve cardiac performance and decrease preload or afterload by affecting the precapillary resistance or the postcapillary capacitance of the vascular bed (Chatterjee & Parmley, 1977;Taylor, 1980;Cohn, 1981). Stimulation of the adrenergic system and development of secondary aldosteronism are important compensatory mechanisms in heart failure (Kramer et al, 1968).…”

Section: Introductionmentioning

confidence: 99%

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Sustained haemodynamic and clinical effects of captopril in long‐term treatment of severe chronic congestive heart failure.

Ricci¹,

Zaniol²,

Teglio³

et al. 1982

Brit J Clinical Pharma

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1 The angiotensin‐converting‐enzyme inhibitor captopril is known to produce beneficial haemodynamic effects in patients with chronic congestive heart failure. 2 Twelve patients with chronic congestive heart failure were conventionally treated with digitalis and diuretic therapy plus oral captopril (75‐150 mg/day), and 14 patients were used as a control group. 3 There was no improvement in functional and haemodynamic values in the controls, but the patients treated with captopril showed a significant functional improvement (increase of exercise time and improvement in New York Heart Association functional class), a definitive decrease in systemic vascular resistance (20%), and a significant increase in the cardiac index and ejection fraction (18% and 28% respectively).

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“…Reduction of preload, on the other hand, lowers left ventricular filling pressure but does not consistently result in improved stroke volume (10,15,18). In some patients, a preload decrease such as that resulting with potent diuretics or venodilator agents like nitrates, while reducing congestion may result in a decline in cardiac output (7). Thus, it is often necessary to precisely titrate a given agent's variable effects on preload and afterload according to the individual patient's hemodynamic responses.…”

Section: Introductionmentioning

confidence: 99%

Non‐parenteral combined afterload and preload reduction therapy in congestive heart failure

Mehta

Pepine

Conti

et al. 1978

Clinical Cardiology

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Summary:It has been shown that hydralazine is beneficial in chronic heart failure by virtue of its afterload reducing effect. Nitroglycerin paste results in venodilation and fall in left ventricular fIlling pressure (L VFP). Thirteen patients with chronic heart failure were given a combination of oral hydralazine and nitroglycerin paste. With oral hydralazine (75 to 100 mg every 8 h), left ventricular stroke work increased and L VFP slightly fell. Following addition of 2 % nitroglycerin paste, an additional decline in mean pulmonary artery and LVFP was observed without significant changes in heart rate and arterial pressure. There were no untoward side effects from either therapy. Eight patients followed for three to eight months (mean five months) reported subjective improvement in shortness of breath and other symptoms related to ventricular dysfunction. This study shows that in certain patients with chronic heart failure, hydralazine and nitroglycerin paste combination produces salutary clinical effects on long term probably through afterload and preload reduction, respectively.

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The role of vasodilator therapy in heart failure

Cited by 307 publications

References 104 publications

Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

Sustained haemodynamic and clinical effects of captopril in long‐term treatment of severe chronic congestive heart failure.

Non‐parenteral combined afterload and preload reduction therapy in congestive heart failure

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