Effect of Sublingual Nitroglycerin in Emergency Treatment of Severe Pulmonary Edema

Bussmann, W.‐D.; Schupp, D.

doi:10.1097/00132586-197906000-00008

Cited by 9 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…GTN has been used in the treatment of heart failure and relieves the symptoms of pulmonary congestion (6,33,44). The results of the present study in the rat and previous studies in the dog show that GTN has significant vasodilator activity in the pulmonary vascular bed and that pulmonary vasodilator responses are enhanced when vasoconstrictor tone is increased (28).…”

Section: Discussionsupporting

confidence: 64%

Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat

Badejo

Hodnette

Dhaliwal

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

PJ. Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat. Am J Physiol Heart Circ Physiol 299: H819 -H826, 2010. First published June 11, 2010; doi:10.1152/ajpheart.00959.2009.-It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds. However, the role of nitric oxide (NO) formed from nitrite in mediating the response to GTN in the pulmonary vascular bed is uncertain. The purpose of the present study was to determine if nitrite plays a role in mediating vasodilator responses to GTN. In this study, intravenous injections of GTN and sodium nitrite decreased pulmonary and systemic arterial pressures and increased cardiac output. The decreases in pulmonary arterial pressure under baseline and elevated tone conditions and decreases in systemic arterial pressure in response to GTN and sodium nitrite were attenuated by cyanamide, an ALDH2 inhibitor, whereas responses to the NO donor, sodium nitroprusside (SNP), were not altered. The decreases in pulmonary and systemic arterial pressure in response to GTN and SNP were not altered by allopurinol, an inhibitor of xanthine oxidoreductase, whereas responses to sodium nitrite were attenuated. GTN was ϳ1,000-fold more potent than sodium nitrite in decreasing pulmonary and systemic arterial pressures. These results suggest that ALDH2 plays an important role in the bioactivation of GTN and nitrite in the pulmonary and systemic vascular beds and that the reduction of nitrite to vasoactive NO does not play an important role in mediating vasodilator responses to GTN in the intact chest rat. mitochondrial aldehyde dehydrogenase; xanthine oxidoreductase; nitric oxide; glyceryl trinitrate; sodium nitrite; sodium nitroprusside; allopurinol; cyanamide; U-46619; N G -nitro-L-arginine methyl ester GLYCERYL TRINITRATE (GTN) and, to a lesser extent, amyl nitrite have been used in the treatment of angina and heart failure for more than a century (4, 5, 38). However, the molecular mechanism by which GTN relaxes vascular smooth muscle is still the subject of current investigation and remains unknown. Although it is well established that nitric oxide (NO) activates soluble guanylyl cyclase, increases cGMP formation, and relaxes vascular smooth muscle, the role of NO release in mediating the vasorelaxant response to GTN is uncertain (11,17,21,26,30,37,39). Although studies in the literature provide evidence that NO is released from GTN, other studies show that NO is not released and suggest that the activation of guanylyl cyclase is mediated by a closely related but not currently identified chemical species with NO-guanylyl cyclase stimulating properties (2, 11, 16, 23, 25, 29 -31, 36, 39). There is substantial evidence in the literature that mitochondrial aldehyde dehydrogenase (ALDH2) plays an i...

show abstract

Section: Discussionsupporting

confidence: 64%

Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat

Badejo

Hodnette

Dhaliwal

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…3-5 min after 0.8-1.6 mg of sublingual nitroglycerin left ventricular filling pressure declines by 30-50% [3], Cardiac output rises significantly and clinical symptoms of pul monary edema improve dramatically. Ele vated arterial blood pressure is lowered.…”

Section: Nitrates In Acute Heart Failurepulmonary Edemamentioning

confidence: 97%

Nitrate Therapy in Heart Failure

Schneider¹,

Bussmann²,

Hartmann³

et al. 1991

Cardiology

View full text Add to dashboard Cite

Nitrates are drugs of first choice in patients with acute heart failure. Acute pulmonary edema can be successfully treated with single or repeated doses of sublingual nitroglycerin. In cases of prolonged acute heart failure, e.g. in the setting of acute myocardial infarction, nitroglycerin or isosorbide dinitrate can be given by the intravenous route for up to 24 h. Patients with acute myocardial infarction usually benefit from nitrate therapy if filling pressures are high and/or left ventricular function is compromised. Nitrate therapy can be considered safe if arterial blood pressure is maintained above 95 mm Hg. With these precautions nitrates can reduce infarct size and the incidence of complications as well as improve long-term prognosis. In the chronic treatment concern has risen with regard to possible nitrate tolerance. Thus, therapy schedules allowing for nitrate-poor phases are generally recommended. Therapy schedules with constant-rate delivery of drugs achieved with patches or intravenous administration of nitrates should be used with caution.

show abstract

“…This contributes to a partial off-loading of the ventricle with a reduction in end-diastolic volume and a decrease in pulmonary capillary wedge pressure (PCWP). 19,20 At higher doses (i.e, ≥ 150–250 mcg/min) arteriolar dilatation occurs which helps to improve cardiac output through a reduction in afterload and diminished impedance to forward flow. 21–23 This effect may be more pronounced when systemic vascular resistance is severely elevated 24 and appears to be mediated through a dose-dependent, differential effect on the amplified pressure wave reflected back to the central circulation from the periphery when arterioles recoil (a facet of the ventricular/vascular coupling relationship termed the augmentation index).…”

Section: Specific Targets Of Therapymentioning

confidence: 99%

Acute Heart Failure Treatment

Levy

Bellou

2013

Curr Emerg Hosp Med Rep

View full text Add to dashboard Cite

Dyspnea is the predominant symptom for patients with acute heart failure and initial treatment is largely directed towards the alleviation of this. Contrary to conventional belief, not all patients present with fluid overload and the approach to management is rapidly evolving from a solitary focus on diuresis to one that more accurately reflects the complex interplay of underlying cardiac dysfunction and acute precipitant. Effective treatment thus requires an understanding of divergent patient profiles and an appreciation of various therapeutic options for targeted patient stabilization. The key principle within this paradigm is directed management that aims to diminish the work of breathing through situation appropriate ventillatory support, volume reduction and hemodynamic improvement. With such an approach, clinicians can more efficiently address respiratory discomfort while reducing the likelihood of avoidable harm.

show abstract

Effect of Sublingual Nitroglycerin in Emergency Treatment of Severe Pulmonary Edema

Cited by 9 publications

References 0 publications

Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat

Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat

Nitrate Therapy in Heart Failure

Acute Heart Failure Treatment

Contact Info

Product

Resources

About